Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety

In the paper

“both acute chlordiazepoxide and chronic fluoxetine decreased stress-induced c-Fos increases in the BNSTL, providing some of the first evidence that the potential anxiolytic effects of both compounds may be mediated by actions in the BNST (Bechtholt et al, 2008).”

What the sources say

• Disputed

  Split into 2 atoms — 0 confirmed, 0 partially supported, 2 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  Checked by a reasoning model — may be wrong.

  cites Bechtholt et al, 2008 sourceExperimental — accuracy not yet measured

In the paper

“large, dose-dependent increases in startle amplitude that began ∼30 min after CRF infusion, grew steadily over the course of a 2-h test period, and lasted for several hours thereafter.”

What the sources say

• Partly supported

  The Results report a dose-dependent increase beginning about 30 minutes after infusion, and the Discussion says the effect lasted at least 6 hours. However, the Discussion places its maximum at about 80–90 minutes, so the claim that startle grew steadily throughout the 2-hour test overstates the time course. (LLM, conf=0.85)

  cites Liang et al, 1992b sourceExperimental — accuracy not yet measured

In the paper

“The longer the duration of the trace interval, the less predictable the US becomes, resulting in greater context conditioning (Marlin, 1981).”

What the sources say

• Partly supported

  The paper’s summary (INTERSTIMULUS INTERVAL (SEC), page not available) says that increasing trace intervals reduce conditioning to the CS and increase conditioning to contextual cues. It does not say that the US becomes less predictable; the discussion instead calls the CS “perfectly predictive of the US” and emphasizes its changing temporal relationship to the US. (LLM, conf=0.85)

  cites Marlin, 1981 sourceExperimental — accuracy not yet measured

In the paper

“These increases were prevented by pretreatment with α-helical CRF (αhCRF9–41), a CRF antagonist, and were reversed by delayed αhCRF9–41 infusions”

What the sources say

• Supported

  The paper’s opening summary states that α-helical CRF blocked CRF-enhanced startle when infused five minutes before CRF and reversed it when given 90 minutes afterward. The Results section also reports reversal after the delayed infusion. Page numbers are not supplied in our copy. (LLM, conf=0.94)

  cites Liang et al, 1992b source
• ?Not checked — no full text of the sourcecites Swerdlow et al, 1989 source

In the paper

“context is not necessarily a spatial location but a set of static background stimuli present during training”

What the sources say

• Supported

  The Discussion defines contexts as static background stimuli present during training rather than necessarily the place where events occurred. The Introduction also describes olfactory cues distinguishing contexts within a single chamber. (LLM, conf=0.95)

  cites Otto and Poon, 2006 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Rescorla and Wagner, 1972

In the paper

“The effects of intra-cerebroventricular (i.c.v.) infusions were mimicked by intracisternal (fourth ventricle) but not by intrathecal (in the space around motor neurons in the spinal cord) CRF infusions and were not disrupted by lesions of the PVT”

What the sources say

• Partly supported

  Experiment 1 reports that intracisternal CRF produced an increase in startle similar to i.c.v. CRF, while intrathecal CRF produced a smaller, more rapid increase—not no effect. The lesion results concern the paraventricular nucleus of the hypothalamus (PVN), not the PVT named in the citing sentence; those PVN lesions did not alter i.c.v. CRF-enhanced startle. (LLM, conf=0.91)

  cites Liang et al, 1992a sourceExperimental — accuracy not yet measured

In the paper

“CRF1 knockout mice showed a complete abolition of context-potentiated startle assessed immediately after conditioning, but normal fear-potentiated startle to a 30-s light/tone compound CS that had been paired with footshock 24 h earlier.”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites Risbrough et al (2009) source

In the paper

“CRF2 knockout mice also showed normal fear-potentiated startle to the discrete CS, but also some attenuation of context-potentiated startle.”

What the sources say

• Supported

  The Results (Fear-Potentiated Startle, Experiment 2; page unavailable) report no difference between CRF2 knockout and wild-type mice in startle potentiation to the discrete cue. The Results (Shock-Potentiated Startle, Experiment 2; page unavailable) report that knockout mice still showed increased startle after shock, but significantly less than wild-type mice; the paper identifies this shock-potentiated response as dependent on contextual cues. (LLM, conf=0.93)

  cites Risbrough et al (2009) source

In the paper

“We also found that local infusion into the BNST of this CRF1 antagonist blocked sustained fear to the 8-min clicker, in contrast to the lack of effect of the local infusion of a CRF antagonist into the CeA on phasic fear”

What the sources say

• Partly supported

  The section on intra-CeA infusion reports that the CRH antagonist did not block light-cued fear-potentiated startle, supporting the phasic-fear comparison. The intra-BNST results instead report attenuation of startle enhanced by infused CRH; they do not report sustained fear to an 8-minute clicker. Page numbers are unavailable in our copy. (LLM, conf=0.90)

  cites Lee and Davis, 1997 sourceExperimental — accuracy not yet measured

In the paper

“We also found that the BNSTL, but not the CeA, was involved in CRF-enhanced startle. For instance, excitotoxic BNSTL lesions, or local infusions of a CRF antagonist into the BNSTL, completely blocked CRF-enhanced startle, although similar lesions of the CeA, or infusions into the CeA, did not”

What the sources say

• Partly supported

  The chemical-lesion Results report that BNST lesions completely blocked CRH-enhanced startle, whereas CeA lesions did not. The intra-BNST infusion Results report a dose-dependent attenuation by the CRH antagonist—not complete blockade—and the intra-CeA infusion Results report no blockade. The paper identifies the targeted region as BNST, without establishing the more specific BNSTL designation in these passages (page numbers unavailable). (LLM, conf=0.87)

  cites Lee and Davis, 1997 sourceExperimental — accuracy not yet measured

In the paper

“using oral administration of the selective CRF-R1 antagonist GSK876008 (Di Fabio et al, 2008), at doses that dose dependently (linear) disrupt CRF-enhanced startle, we also observed a non-monotonic disruption of light-enhanced startle but no disruption of fear-potentiated startle in the same animals at the same doses”

What the sources say

• ?Not checked — no full text of the sourcecites Di Fabio et al, 2008 source
• Supported

  The Abstract reports a linear dose-response disruption of CRF-enhanced startle, a U-shaped disruption of light-enhanced startle, and no disruption of fear-potentiated startle. Materials and Methods (General Design and Experimental Sequence) confirms that the antagonist was given orally and that each rat in the primary study received the same dose across the three tests. Page numbers are not provided in our copy. (LLM, conf=0.94)

  cites Walker et al, 2009 source

In the paper

“excitotoxic lesions of the BNST, but not the CeA, blocked CRF-enhanced startle”

What the sources say

• Supported

  The section on chemical lesions of the hippocampus, BNST, and amygdala complex reports that NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas ibotenic acid lesions of the CeA did not. The passage describes the lesion types and outcome attributed to this source; no page number is provided in our copy. (LLM, conf=0.95)

  cites Lee and Davis (1997) source

In the paper

“our account cannot easily explain why neurotoxic lesions of the CeA block context conditioning in some studies (Goosens and Maren, 2001) but not in others (Koo et al, 2004), assuming the later lesions fully destroyed cells in the CeAL.”

What the sources say

• Partly supported

  The Results report that rats with neurotoxic central-amygdala lesions froze significantly less to the context than controls, supporting an impairment in context conditioning. The paper describes the effect as a deficit or attenuation, not a complete block. The comparison with other studies and the assumption about their lesion extent are not attributed to Goosens and Maren. (LLM, conf=0.82)

  cites Goosens and Maren, 2001 sourceExperimental — accuracy not yet measured
• Partly supported

  The Conditioned freezing results report that rats with neurotoxic CeA lesions did not differ significantly from controls in context freezing, supporting the finding attributed to Koo et al. The Histology section says the lesions included most of the lateral CeA, not that they fully destroyed its cells; the Discussion also notes spared neurons. The citing authors’ stated assumption of complete destruction is therefore not established by this source. (LLM, conf=0.86)

  cites Koo et al, 2004 sourceExperimental — accuracy not yet measured

In the paper

“this could explain why electrolytic lesions of the CeA blocked context conditioning (Koo et al, 2004), which depends on the BNST (Sullivan et al, 2004) and CRF, because electrolytic lesions of the CeA would have prevented the context-induced release of CRF to the BNST from the CeAL (Figure 7).”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites Koo et al, 2004 source
• ?Not checked — no full text of the sourcecites Sullivan et al, 2004 source

In the paper

“previous studies have shown that chronic corticosterone administration upregulates the CRF mRNA level in CeAL and BNSTL neurons (Liu et al, 2004; Makino et al, 1994a, b; Shepard et al, 2000; Swanson and Simmons, 1989; Watts and Sanchez-Watts, 1995) and interacts synergistically with CRF to increase startle amplitude (Lee et al, 1994).”

What the sources say

• ?Could not verify

  The Introduction describes BDNF and contextual fear learning; the Discussion mentions a glucocorticoid receptor agonist in relation to spatial-memory retrieval. Neither passage addresses whether chronic corticosterone upregulates CRF mRNA in CeAL or BNSTL neurons (searched: chronic corticosterone, CRF mRNA, CeAL, BNSTL). The startle-amplitude clause is attributed to Lee et al. (1994), not to this paper. Page numbers are unavailable in our copy. (LLM, conf=0.76)

  cites Liu et al, 2004 sourceExperimental — accuracy not yet measured
• Partly supported

  The Abstract reports that sustained corticosterone treatment elevated CRH mRNA in the central nucleus of the amygdala, supporting the core finding. The Methods specify measurements in the central amygdala and hypothalamic PVN, not the lateral central-amygdala subdivision or lateral bed nucleus of the stria terminalis. The startle-amplitude finding is attached to Lee et al. (1994), not to this source. (LLM, conf=0.90)

  cites Makino et al, 1994a, b sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Shepard et al, 2000 source

In the paper

“Anxiogenic effects were also found after chronic inhibition of GABA synthesis in the BNST, and these effects were reversible by local infusion of muscimol into the BNST (Sajdyk et al, 2008).”

What the sources say

• Supported

  The Social Interaction section reports that chronic L-AG infusion into the BNST reduced social interaction in rats and that local muscimol injections reversed this effect in a dose-dependent manner. The Discussion also states that muscimol attenuated L-AG-induced anxiety responses in two experiments. (LLM, conf=0.94)

  cites Sajdyk et al, 2008 source

In the paper

“Inhibition of GABA synthesis in the BNST produced an anxiogenic effect in the plus-maze and social interaction test, another measure of sustained fear in which rats exposed to novel places under high illumination tend not to interact with each other; this effect was reversed by local infusion of muscimol in the BNST (Sajdyk et al, 2008).”

What the sources say

• Partly supported

  The Elevated Plus-Maze, Social Interaction, and Discussion sections report anxiety-like effects after GABA-synthesis inhibition in the BNST; the Social Interaction results report reversal by local muscimol. However, the Social Interaction methods say testing occurred under low light in familiar conditions, not in novel places under high illumination. The paper describes the test as measuring anxiety-like behavior, not specifically sustained fear. (LLM, conf=0.90)

  cites Sajdyk et al, 2008 sourceExperimental — accuracy not yet measured

In the paper

“CRF-enhanced startle was much lower in progesterone-injected rats than in vehicle-injected rats and this effect seemed to be because of its major metabolite, allopregnanolone (Toufexis et al, 2004).”

What the sources say

• Supported

  Experiment 2 reports significantly lower CRF-enhanced startle in ovariectomized rats given acute progesterone than in controls. Experiment 5 reports that allopregnanolone (THP) also reduced CRF-enhanced startle, and the Discussion says THP may make the major contribution to progesterone’s effect. The claim’s tentative wording reflects that uncertainty. (LLM, conf=0.94)

  cites Toufexis et al, 2004 source

In the paper

“startle is exaggerated in panic disorder when tested in a threatening context (Grillon et al, 1994a), but not at baseline without obvious stressors (Amrhein et al, 2005; Ludewig et al, 2002; McTeague et al, 2009).”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon et al, 1994a source
• ?Not checked — no full text of the sourcecites Amrhein et al, 2005 source
• Supported

  The Ludewig et al. citation is attached to the baseline finding, not the threatening-context finding. In STARTLE REACTIVITY, patients and controls had equal startle magnitude in block 1; the DISCUSSION says the study used only safety conditions and found no difference in startle reactivity. (LLM, conf=0.94)

  cites Ludewig et al, 2002 source

In the paper

“Various vulnerability factors have been associated with risk for mood and anxiety disorders, including a parental history of anxiety disorders (Merikangas et al, 1999), early life stress (Nemeroff, 2004), and being female (Kessler et al, 1994).”

What the sources say

• Supported

  The citation to Merikangas et al. (1999) is attached specifically to parental history of anxiety disorders, not to early life stress or female sex. The paper’s Discussion reports that parental anxiety disorders were directly associated with anxiety disorders in offspring; the section on parental and child anxiety disorders also reports increasing rates as the number of affected parents rises. Page numbers were not provided in our copy. (LLM, conf=0.94)

  cites Merikangas et al, 1999 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Nemeroff, 2004
• ?Not checked — no full text of the sourcecites Kessler et al, 1994 source

In the paper

“Symptom severity was strongly associated with both self-reported danger and the skin conductance response to startle stimuli under distal threat. Symptom severity was also associated with eyeblink startle magnitude under intermediate threat. None of the self-reported or physiological measures were associated with symptom severity under proximal threat.”

What the sources say

• Partly supported

  The Discussion reports greater skin conductance responses under low threat and greater eyeblink responses under medium threat; it also says subjective fear under low threat predicted symptom severity. But the Abstract Results and Discussion report that skin conductance under high threat predicted symptom severity, contrary to the claim that no measure was associated under proximal threat. The paper uses low, medium, and high threat rather than the citing sentence’s distal, intermediate, and proximal labels. (LLM, conf=0.88)

  cites Pole et al, 2009 sourceExperimental — accuracy not yet measured

In the paper

“Exposure to bright light for 5–20 min led to a significant increase in acoustic startle amplitude going from the dark to the light (light-enhanced startle) compared with startle amplitude when the rats remained in the dark.”

In the paper

“However, airpuffs do not generate sustained contextual anxiety when administered unpredictably (Figure 2, right panel), suggesting that unpredictability per se does not elicit anxiety (Staub et al, 1971), but see (Herry et al, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Staub et al, 1971 source

In the paper

“Thus, after pairing a context with a shock in rats, the rats will show a fear reaction in that context but not in a novel one, ruling out sensitization to shock.”

In the paper

“Figure 6 shows that this procedure produced fear-potentiated startle throughout the duration of the clicker compared with little or no potentiation before or after the clicker, so that fear was sustained across the 8-min period when the clicker was on.”

In the paper

“Their first choice was overwhelmingly the no shock context. However, when they were forced to choose between the predictable and unpredictable contexts, most subjects (80%) avoided the unpredictable context (Grillon et al, 2006a).”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon et al, 2006a source

In the paper

“Although fear-potentiated startle to the cue was retained at the 1-week test, baseline startle amplitude in the absence of the cue was greater in the unpaired group compared with that in the paired group and lowest in the group that received no shocks (Figure 1).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Grillon and Davis, 1997

In the paper

“there was no pre- to post-conditioning increase in baseline startle (ie, in the absence of the clicker), indicating that the startle baseline, against which startle to the clicker was measured, was not influenced by contextual fear”

In the paper

“Replicating the pattern of responses seen in conditioning studies, subjects showed a large startle potentiation during the threat cue in the predictable condition. They also showed a linear increase in startle reactivity during the inter-trial interval that reflected the progressive increase in reactivity (ie, anxiety) from the no shock to the predictable shock to the unpredictable shock condition”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon et al, 2004 source

In the paper

“oral administration of the CRF-R1 antagonist dose dependently blocked fear-potentiated startle to an 8-min CS presentation, but did not disrupt fear-potentiated startle to 3.7-s CS presentations, and even enhanced it in some animals.”

In the paper

“Infusions into the BLA blocked both components and, in this study, infusions into the CeA blocked neither.”

In the paper

“BNST infusions decreased the late component of fear-potentiated startle (ie, minutes 5–8 of the CS) but actually increased the early component (ie, minutes 1–5).”

In the paper

“The CRF1 antagonist also had no effect on phasic startle increases (ie, to a 3.7-s clicker CS presentation) in rats trained using the sustained fear conditioning paradigm, confirming that it is the duration of the fear response during testing that confers sensitivity to CRF-R1 blockade, and not the nature of the training.”

In the paper

“Infusion into the caudal BLA was the most effective (Figure 8), consistent with caudal BLA projections to the BNST”

What the sources say

• ?Not checked — no full text of the sourcecites Dong et al, 2001 source
• ?Not checked — no full text of the sourcecites McDonald, 1991 source
• ?Not checked — no full text of the sourcecites Weller and Smith, 1982 source

In the paper

“light-enhanced startle was not blocked by local infusion of the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptor antagonist NBQX into the CeA, but was blocked by local infusions into the BNST.”

In the paper

“although fear-potentiated startle to the explicit CS was not disrupted by any dose of a CRF1 antagonist, the pre- to post-conditioning startle increases were disrupted at doses of between 3 and 30 mg/kg.”

In the paper

“fear-potentiated startle to a 3.7-s visual CS in other rats was not occluded by i.c.v. CRF infusions, although these infusions caused a much bigger increase in ‘baseline’ startle”

In the paper

“However, this effect was not observed at doses of 60 mg/kg (Figure 13)—a non-monotonic dose–response curve similar to that previously observed with light-enhanced startle”

In the paper

“although both groups showed a significant increase in startle amplitude after CRF infusions, lactating females showed significantly less CRF-enhanced startle compared with cycling females (Walker et al, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites Walker et al, 2003 source

In the paper

“In castrated males, the mean level of light-enhanced startle was comparable with that observed in females and this effect could be reversed with testosterone.”

In the paper

“in our original study we found that in rats, diazepam did not block the acquisition of fear-potentiated startle, only its expression.”

In the paper

“Light-enhanced startle was statistically significant in both female groups but statistically absent in intact male rats.”

In the paper

“The state of anxiety has been linked to the potential (pre-encounter) or distal (post-encounter) presence of a predator, whereas fear is evoked by the clear and imminent threat (circa strike).”

In the paper

“In contrast, sustained fear is measured using a more diffuse cue, or cues, arranged so that the subject does not know when during the aversive event will occur. This elicits a state of fear that can last for a much longer period of time and often decays more slowly after the fearful signal is removed (de Jongh et al, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites de Jongh et al, 2003 source

In the paper

“Finally, as learning is minimized during verbal threat, such procedures can be used in repeated designs. A recent study showed no reduction of fear-potentiated startle when a verbal threat procedure was repeated either four times in a single day or once per day for 4 days (Klumpers et al, 2008).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Klumpers et al, 2008

In the paper

“Fear-potentiated startle is closely time-locked to the CS; hence, it is generally maximal during testing at the time after the CS onset when the shock occurred in training (Davis et al, 1989).”

What the sources say

• ?Not checked — no full text of the sourcecites Davis et al, 1989 source

In the paper

“It is blocked by the benzodiazepine diazepam (Baas et al, 2002) and is increased in PTSD (Grillon et al, 1998b).”

What the sources say

• ?Not checked — no full text of the sourcecites Baas et al, 2002 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Grillon et al, 1998b

In the paper

“Moreover, in both rats and humans, sustained fear appears to be more sensitive to clinically effective anti-anxiety drugs or treatments, perhaps as a result of the different neural substrates of each.”

In the paper

“The eyeblink component of the startle reflex in humans shows many of the same characteristics seen in the whole-body startle response in rodents. In particular, both are increased by anticipation of aversive stimuli and during the processing of negatively valenced information (Brown et al, 1951; Lang et al, 2000).”

What the sources say

• ?Not checked — no full text of the sourcecites Brown et al, 1951 source
• ?Not checked — no full text of the sourcecites Lang et al, 2000 source

In the paper

“In the laboratory, phasic fear can be measured using a short, discrete cue that is predictably paired with an aversive event. This elicits a state of fear highly time-locked to the fear-inducing stimulus that begins quickly and dissipates quickly once the fear stimulus is removed (Davis et al, 1989; de Jongh et al, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites Davis et al, 1989 source
• ?Not checked — no full text of the sourcecites de Jongh et al, 2003 source

In the paper

“In addition, the eyeblink component of the startle reflex has face validity for studying aversive states and anxiety disorders. For instance, the DSM-IV-R lists exaggerated startle as a criterion for posttraumatic stress disorder (PTSD).”

In the paper

“For example, as humans are endowed with a cognitive system that enables symbolic representation of aversive experience, the knowledge of future aversive events is sufficient to create a threatening context. Participation in an experiment in which subjects know that they will eventually receive shocks at a later time may be akin to the pre-encounter stage and may thus elicit mild anxiety.”

In the paper

“By analogy, fear and anxiety evoked experimentally in humans may be framed according to the same defensive distance continuum.”

In the paper

“In contrast to rodents, humans are diurnal and feel more vulnerable in the dark (Schaller et al, 2003), and darkness is sufficiently anxiogenic in humans to potentiate startle (Grillon et al, 1997b). Dark-enhanced startle is replicable across laboratories (Grillon et al, 1999), and can be observed in both adolescents (Grillon et al, 1999) and adults (Coplan et al, 1998; Grillon and Ameli, 1998b;”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon et al, 1997b source
• ?Not checked — no full text of the sourcecites Grillon et al, 1999 source

In the paper

“Fear-potentiated startle can also be used in mice (Falls et al, 1997) and rhesus monkeys (Winslow et al, 2002).”

What the sources say

• ?Not checked — no full text of the sourcecites Falls et al, 1997 source
• ?Not checked — no full text of the sourcecites Winslow et al, 2002 source

In the paper

“Pharmacological analyses of these defensive behaviors show that anxiety is sensitive to anxiolytic drugs, whereas fear is not (Blanchard et al, 1993).”

What the sources say

• ?Not checked — no full text of the sourcecites Blanchard et al, 1993 source

In the paper

“These results indicate that contextual anxiety is robust. However, it depends on a sufficiently aversive US.”

In the paper

“The benzodiazepine anxiolytic, chlordiazepozide, reduced this effect, but in control studies it did not reduce startle increases produced by the inhibitory glycine receptor antagonist strychnine”

What the sources say

• ?Not checked — no full text of the sourcecites Swerdlow et al, 1986 source
• ?Not checked — no full text of the sourcecites Kehne et al, 1981 source

In the paper

“phasic and sustained fear differ both in terms of their anatomy and their susceptibility to different pharmacological treatments.”

In the paper

“They showed that the central (CeA) and medial (MeA) nuclei of the amygdala and the bed nucleus of the stria terminalis (BNST) were connected by columns of cells located throughout the stria terminalis, the fiber tract that connects these amygdala nuclei with the BNST, and also in a ventrally located part of the basal forebrain.”

What the sources say

• ?Not checked — no full text of the sourcecites Alheid et al, 1998 source
• ?Not checked — no full text of the sourcecites Alheid and Heimer, 1988 source

In the paper

“electrolytic lesions of the CeA will not only block outputs of the CeA but also disconnect the BLA from the BNST and we believe many effects that have been found after electrolytic lesions of the CeA may result from this disconnection.”

In the paper

“CeAL neurons are a major source of BNSTL CRF. This was shown by Sakanaka et al (1986), who found that electrolytic CeA, but not BLA, lesions dramatically reduced BNSTL CRF immunoreactivity, nearly depleting it entirely from the dorsal BNSTL.”

What the sources say

• ?Not checked — no full text of the sourcecites Sakanaka et al, 1986 source

In the paper

“the CeA and the BNSTL are highly similar anatomically in terms of inputs, outputs, cell types, and neurochemical makeup, especially with respect to the high levels of several peptides found in both structures”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Alheid et al, 1995

In the paper

“Light-enhanced startle in rats, dark-enhanced startle in humans, context conditioning or verbal threats that involve unpredictable aversive events in rats and humans, long-duration cues paired with shocks in rats, or CRF infusion into the rat brain all produce longer, sustained states of fear.”

In the paper

“Instead, context conditioning serves as a model of hippocampal (and amygdala)-dependent fear conditioning, as opposed to phasic cue conditioning, which depends on the amygdala but not the hippocampus (Kim and Fanselow, 1992; Phillips and LeDoux, 1992).”

What the sources say

• ?Not checked — no full text of the sourcecites Kim and Fanselow, 1992 source
• ?Not checked — no full text of the sourcecites Phillips and LeDoux, 1992 source

In the paper

“The CeAL instead projects to the substantia innominata, perhaps to the CeAM, and quite prominently to the BNSTL”

What the sources say

• ?Not checked — no full text of the sourcecites Bourgeais et al, 2001 source
• ?Not checked — no full text of the sourcecites Dong et al, 2001 source
• ?Not checked — no full text of the sourcecites Petrovich and Swanson, 1997 source

In the paper

“In contrast to discrete cues that precisely signal the timing of US delivery, contextual cues are constant reminders of the US, but are less predictive of their occurrence; they leave the organisms in a sustained state of fearful apprehension.”

In the paper

“Together, these findings indicated that the effects of CRF on startle were directly mediated by CRF receptors in the brain, and did not involve activation of the CRF-regulated hypothalamic–pituitary–adrenal axis.”

In the paper

“The basolateral nucleus of the amygdala (BLA) also projects not only to the CeA but also to the BNSTL, particularly from the caudal part of the BLA (BLAc)”

What the sources say

• ?Not checked — no full text of the sourcecites Dong et al, 2001 source
• ?Not checked — no full text of the sourcecites McDonald, 1991 source
• ?Not checked — no full text of the sourcecites Weller and Smith, 1982 source

In the paper

“A cue paired with a US becomes the best predictor of the US. The cue overshadows the context, which then elicits little context conditioning (Rescorla and Wagner, 1972). In contrast, when the CS and US are not paired, the context becomes the only predictor of the US, although a poor one, leading to increased context conditioning (Odling-Smee, 1975a, b; Rescorla and Wagner, 1972).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Rescorla and Wagner, 1972
• ?Not checked — no full text of the sourcecites Odling-Smee, 1975a source
• ?Not checked — no full text of the sourcecites Odling-Smee, 1975b source

In the paper

“Thus, CRF-enhanced startle leads to a sustained increase in startle amplitude, is sensitive to benzodiazepines, and does not involve conditioning.”

In the paper

“They also showed that the CeA projected primarily to the lateral division of the BNST (BNSTL) and that the MeA projected primarily to the medial division of the BNST (BNSTM).”

What the sources say

• ?Not checked — no full text of the sourcecites Alheid et al, 1998 source
• ?Not checked — no full text of the sourcecites Alheid and Heimer, 1988 source

In the paper

“Fear-potentiated startle to a discrete cue predictably paired with an aversive cue or with a verbal threat is a measure of phasic fear.”

In the paper

“As this study was not designed with the specific intent to evaluate context conditioning, we did not include context discrimination controls that would be necessary to rule out the possibility that these increases were because of non-associative sensitization.”

In the paper

“PVT fibers appear to make contact onto CRF-containing neurons in the CeAL (Li and Kirouac, 2008), suggesting that they can directly modulate CRF transmission.”

What the sources say

• ?Not checked — no full text of the sourcecites Li and Kirouac, 2008 source

In the paper

“Bhatnagar and Dallman (1998) suggested that the PVT to the amygdala pathway is a key regulator of the hypothalamic-pituitary-adrenal response to stress.”

What the sources say

• ?Not checked — no full text of the sourcecites Bhatnagar and Dallman, 1998 source

In the paper

“we believe both effects involve the BLA, although we cannot say for certain whether the same or different BLA neurons are involved.”

In the paper

“the influence of startle on treatments that acted through different systems (ie, the CeA or BNST) would be additive, whereas the effects on startle of treatments that acted through the same system (ie, both CeA or both BNST) would occlude one another”

What the sources say

• ?Not checked — no full text of the sourcecites Walker and Davis, 2002b source

In the paper

“Sullivan et al (2004) reported that post-training electrolytic BNSTL lesions disrupt freezing, as well as corticosterone responses to a context CS, but do not affect these same responses to a brief auditory CS, whereas CeA lesions disrupt freezing to both.”

What the sources say

• ?Not checked — no full text of the sourcecites Sullivan et al, 2004 source

In the paper

“in the rat, the CeAM receives input from almost all other nuclei within the amygdala, whereas the CeAL receives virtually no amygdala input at all”

What the sources say

• ?Not checked — no full text of the sourcecites Jolkkonen and Pitkanen, 1998 source

In the paper

“we suspect that the transition from CeAM to BNSTL involvement may begin between 4 and 60 s after CS onset, although it may be several minutes before the response is fully dependent on the BNSTL.”

What the sources say

• ?Not checked — no full text of the sourcecites Davis et al, 1989 source
• ?Not checked — no full text of the sourcecites Walker and Davis, 1997a source

In the paper

“a more conservative interpretation may be that BNSTL lesions disrupt context-elicited freezing simply because context CSs are invariably long in duration, and so also are the responses they evoke.”

In the paper

“This suggests that at some level (quite possibly the BLA and perhaps elsewhere as well), these systems do interact and are thus not totally independent from each other”

In the paper

“Resstel et al (2008) reported that pre-test intra-BNST infusions cobalt chloride, which block neurotransmitter release but not action potential propagation, disrupted context-elicited freezing, and decreased heart rate and arterial blood pressure.”

What the sources say

• ?Not checked — no full text of the sourcecites Resstel et al, 2008 source

In the paper

“de Jongh et al (2003) reported that i.c.v. infusions of the CRF-R1/2 antagonist αhCRF9–41 had no effect on fear-potentiated startle to a 3.7-s light, but significantly disrupted light-enhanced startle at an intermediate (5 μg) but not at a higher dose (25 μg).”

What the sources say

• ?Not checked — no full text of the sourcecites de Jongh et al, 2003 source

In the paper

“the effects of CeA lesions may have been because of destruction of the CeAL, which we believe is particularly involved in sustained fear through projections to the BNST.”

In the paper

“The heaviest projections from the BLA to the CeA are to the CeAM, which in turn projects to the hypothalamus and brainstem to mediate phasic fear responses.”

In the paper

“It is therefore possible that glutamate selectively activates CeAM neurons that mediate short-duration fear responses, whereas CGRP, corticosterone, and/or other peptide receptors selectively influence CeAL neurons that mediate more sustained fear responses.”

In the paper

“Jasnow et al (2004) found that social defeat behavior in Syrian hamsters was reduced by pre-defeat unilateral electrolytic CeA lesions or by pre-test unilateral intra-BNSTL infusion of the CRF antagonist, D-Phe CRF12–41.”

What the sources say

• ?Not checked — no full text of the sourcecites Jasnow et al (2004) source

In the paper

“This result could explain why electrolytic lesions of the CeA blocked CRF-enhanced startle because these lesions would effectively disconnect the BLA from the BNST, although other possibilities cannot be ruled out.”

In the paper

“Our current working hypothesis is that CRF terminals in the BNST act presynaptically on BLA terminals within BNSTL, where they promote glutamate release and, therefore, excitatory drive onto BNSTL neurons.”

In the paper

“The CeAL, activated perhaps by the BLA but also by the stress-sensitive PVT, and by cortical inputs, projects to and releases CRF that acts presynaptically on glutamate terminals from the caudal BLA”

In the paper

“Thus, the observed behavioral effects in these studies might have been attributable to an interruption of this pathway instead.”

In the paper

“Erb et al (2001) found that neither unilateral intra-CeA TTX infusions nor unilateral intra-BNSTL infusions of D-Phe CRF12–41 disrupted shock-induced reinstatement of extinguished cocaine-seeking behavior, but that the combination of both treatments, again on opposite sides of the brain, did.”

What the sources say

• ?Not checked — no full text of the sourcecites Erb et al (2001) source

In the paper

“Inhibitory feedback to the CeAM from either the CeAL or the BNST shuts down the CeAM, allowing a seamless transition from phasic to sustained fear.”

In the paper

“both stress (Albeck et al, 1997; Hatalski et al, 1998; Hsu et al, 1998; Kalin et al, 1994; Makino et al, 1999) and the stress-related hormone corticosterone increase CRF mRNA level in CeA neurons (Makino et al, 1994b; Shepard et al, 2000; Thompson et al, 2004; Watts and Sanchez-Watts, 1995).”

What the sources say

• ?Not checked — no full text of the sourcecites Albeck et al, 1997 source
• ?Not checked — no full text of the sourcecites Hatalski et al, 1998 source
• ?Not checked — no full text of the sourcecites Hsu et al, 1998 source

In the paper

“They have found that [K+]-evoked glutamate release was persistently elevated in rats undergoing chronic immobilization stress (2 h/day for 15 days) and that this increase was normalized by intra-BNST infusions of the CRF-R1 antagonist NBI-27914.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Forray et al, 2005

In the paper

“Lactation is associated with high progesterone levels, and anxiolytic effects are seen during lactation, probably because progesterone and its GABAA receptor modulating metabolites (most notably allopregnanolone) increase GABA transmission (c.f., Lambert et al, 2001; Lan and Gee, 1994) (eg, Akwa et al, 1999; Bitran et al, 1995, 1999; Brot et al, 1997).”

What the sources say

• ?Not checked — no full text of the sourcecites Lambert et al, 2001 source
• ?Not checked — no full text of the sourcecites Lan and Gee, 1994 source
• ?Not checked — no full text of the sourcecites Akwa et al, 1999 source

In the paper

“Figure 14 summarizes our working model of phasic vs sustained fear focusing on the BLA, CeA, and BNSTL and how CRF-containing projections from the CeAL to the BNSTL are involved in sustained fear.”

In the paper

“Although the results of both studies are consistent with the conclusions that were drawn, they are not definitive insofar as only a partial implementation of the crossed-lesion design was used.”

In the paper

“One possibility is that the CeAM neurons thought to mediate short-duration fear responses through direct projections to the brainstem are AMPA-responsive, whereas the CeAL neurons that may mediate longer duration fear responses indirectly by way of projections to the BNSTL are not.”

In the paper

“diazepam was found in humans to disrupt acquisition of cued fear-potentiated startle conditioning when given before training, but not when given before a performance test that assessed the expression of an acquired conditioned fear response (Scaife, 2005; Scaife et al, 2005).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Scaife, 2005
• ?Not checked — no full text of the sourcecites Scaife et al, 2005 source

In the paper

“Initial studies found that diazepam (Bitsios et al, 1999) and alprazolam (Riba et al, 2001) decreased fear-potentiated startle during a verbal threat procedure in which short-duration threat cues predicted a shock, but these findings were not confirmed in several studies using various benzodiazepines (Baas et al, 2002; Grillon et al, 2006b; Riba et al, 1999; Scaife et al, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Bitsios et al, 1999 source
• ?Not checked — no full text of the sourcecites Riba et al, 2001 source
• ?Not checked — no full text of the sourcecites Baas et al, 2002 source

In the paper

“it has been argued that the positive effect of benzodiazepines on fear-potentiated startle (Bitsios et al, 1999; Riba et al, 2001) did not reflect genuine reductions in fear but was artifactual, secondary to reduced baseline startle reactivity (Grillon and Baas, 2002; Walker and Davis, 2002b).”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon and Baas, 2002 source
• ?Not checked — no full text of the sourcecites Walker and Davis, 2002b source

In the paper

“The attenuating effect of benzodiazepines on startle is not surprising, given that these drugs have muscle relaxant and sedative properties (File, 1982).”

What the sources say

• ?Not checked — no full text of the sourcecites File, 1982 source

In the paper

“These latter processes can be disrupted by benzodiazepines (Dickinson-Anson and McGaugh, 1997; Harris and Westbrook, 2001; Jensen et al, 1979; Pain et al, 2002), raising the possibility that benzodiazepines reduce fear conditioning because of their amnestic effects, rather than their anxiolytic properties when given before training.”

What the sources say

• ?Not checked — no full text of the sourcecites Dickinson-Anson and McGaugh, 1997 source
• ?Not checked — no full text of the sourcecites Harris and Westbrook, 2001 source
• ?Not checked — no full text of the sourcecites Jensen et al, 1979 source

In the paper

“most human studies use verbal threat to a specific cue, which examines the expression of fear responses, whereas animal studies rely on fear conditioning, a task that depends on learning and memory.”

In the paper

“another possibility is that startle in rats is much less sensitive to the sedative effects of benzodiazepines so that much higher doses can be used in rats than in humans, thus allowing anxiolytic effects in phasic fear to be measured.”

In the paper

“Overall, therefore, gonadal steroids appear to affect sustained but not phasic fear, providing further support for the idea that these different procedures produce qualitatively different forms of fear or anxiety-like behaviors.”

In the paper

“it is possible that rather than simply reflecting a nonspecific side effect, the reduction in startle baseline by diazepam in humans (Baas et al, 2002) and rodents (Guscott et al, 2000) might be caused by an anxiolytic effect on contextual anxiety.”

What the sources say

• ?Not checked — no full text of the sourcecites Baas et al, 2002 source
• ?Not checked — no full text of the sourcecites Guscott et al, 2000 source

In the paper

“This effect did not appear to be due to a disruption of memory consolidation because diazepam blocked conditioned fear when given before but not after training (Scaife et al, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Scaife et al, 2005 source

In the paper

“in several cases, lesions of the CeA did not block these anxiolytic effects of benzodiazepines, although the CeA lesions tended to have anxiolytic effects on their own (Kopchia et al, 1992; Yadin et al, 1991; Treit et al, 1993b).”

What the sources say

• ?Not checked — no full text of the sourcecites Kopchia et al, 1992 source
• ?Not checked — no full text of the sourcecites Yadin et al, 1991 source
• ?Not checked — no full text of the sourcecites Treit et al, 1993b source

In the paper

“Baas et al (2002) conducted four separate within- and between-subject studies and reported that neither diazepam nor oxazepam reduced fear-potentiated startle, although these drugs reduced baseline startle.”

What the sources say

• ?Not checked — no full text of the sourcecites Baas et al, 2002 source

In the paper

“This is in line with the clinical observation that specific phobias respond less well to treatments such as citalopram than other pathological anxiety states (Baldwin et al, 2005) and with preclinical evidence in rodents showing that the serotonergic system may not be critical for the expression of phasic fear-potentiated startle (Davis et al, 1988).”

What the sources say

• ?Not checked — no full text of the sourcecites Baldwin et al, 2005 source
• ?Not checked — no full text of the sourcecites Davis et al, 1988 source

In the paper

“participating in an experiment involving the future delivery of aversive stimuli can be considered analogous to the pre-encounter stage of the defensive distance model and can evoke mild and measurable anxiety (Bocker et al, 2004; Grillon et al, 1998c).”

What the sources say

• ?Not checked — no full text of the sourcecites Bocker et al, 2004 source
• ?Not checked — no full text of the sourcecites Grillon et al, 1998c source

In the paper

“Hierarchical models confirm the presence of a unique broad negative affectivity factor that cuts across most anxiety disorders (including depression), and of a separate and a unique fear factor that discriminates among anxiety disorders (Brown et al, 1998).”

What the sources say

• ?Not checked — no full text of the sourcecites Brown et al, 1998 source

In the paper

“although acute citalopram increased both fear and anxiety to predictable and unpredictable shock, respectively (Grillon et al, 2007)”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon et al, 2007 source

In the paper

“the broad vulnerability factor loads more heavily in GAD, panic disorder, and PTSD and less on disorders with circumscribed fear such as simple phobias, with social phobia being intermediate (Chantarujikapong et al, 2001; Craske and Waters, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Chantarujikapong et al, 2001 source
• ?Not checked — no full text of the sourcecites Craske and Waters, 2005 source

In the paper

“Anxiety disorders also differ from each other in the primary object or specificity of threat, ranging from diffuse (eg, in generalized anxiety disorder (GAD)) to circumscribed (eg, in specific phobias), the former leading to symptoms of chronic sustained anxiety and the latter prompting strong fear (Cuthbert et al, 2003; Lang et al, 2000).”

What the sources say

• ?Not checked — no full text of the sourcecites Cuthbert et al, 2003 source
• ?Not checked — no full text of the sourcecites Lang et al, 2000 source

In the paper

“It can be noted that it may help distinguish among fear- and anxiety-related anxiety disorders (Watson, 2005; Kruger et al, 1988) based on core underlying features and help discover vulnerability markers in individuals at high risk for these conditions.”

What the sources say

• ?Not checked — no full text of the sourcecites Watson, 2005 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Kruger et al, 1988

In the paper

“The distinction between phasic and sustained fear as operational definitions of fear and anxiety has implications in several areas of clinical research.”

In the paper

“Acute administration of citalopram in rats before training was reported to increase fear conditioning to a 20-s tone paired with footshock, whereas chronic administration had the opposite effect (Burghardt et al, 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Burghardt et al, 2004 source

In the paper

“The distinction between fear and anxiety states based on our model of potentiated startle may therefore provide a valuable tool when classifying anxiety states.”

In the paper

“Buspirone is a mixed serotonergic agonist and dopamine D2 antagonist that has repeatedly been found to reduce the expression of fear-potentiated startle after acute administration (Kehne et al, 1988; Mansbach and Geyer, 1988), as well as light-enhanced startle (Walker and Davis, 1997a).”

What the sources say

• ?Not checked — no full text of the sourcecites Kehne et al, 1988 source
• ?Not checked — no full text of the sourcecites Mansbach and Geyer, 1988 source
• ?Not checked — no full text of the sourcecites Walker and Davis, 1997a source

In the paper

“Simple phobia, which is associated with fear to circumscribed objects or situations, is the archetype of a fear-related disorder.”

In the paper

“First, worry is essentially a cognitive avoidance strategy, which, some suggest, serves to reduce anticipatory anxiety (Borkovec and Inz, 1990).”

What the sources say

• ?Not checked — no full text of the sourcecites Borkovec and Inz, 1990 source

In the paper

“The finding that neuroticism had no effect during proximal threat is consistent with results indicating that individuals with or at-risk for an anxiety disorder had no increase in fearfulness to imminent danger.”

In the paper

“For example, although panic disorder and PTSD are distinguishable based on phenotypic studies (Kruger et al, 1988, Vollebergh et al, 2001), startle studies suggest that these two disorders share a common susceptibility to enhanced sustained fear to aversive contexts.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Kruger et al, 1988
• ?Not checked — no full text of the sourcecites Vollebergh et al, 2001 source

In the paper

“Men and women do not differ in their fear-potentiated startle to a threat cue, but women show enhanced sustained anxiety to unpredictable shocks (Grillon, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon, 2008 source

In the paper

“The patients were not medicated and were compared with healthy controls.”

In the paper

“These results confirm that although fearful responses to a nonspecific stressor do not differ between clinically anxious patients and controls, sustained contextual fear to unpredictable aversive stimuli distinguishes individuals with PTSD or panic disorder from controls and individuals with GAD.”

In the paper

“Panic disorder is similarly characterized by brief and intermittent unpredictable and uncontrollable aversive episodes (panic attacks) interspersed with high levels of anticipation anxiety of these aversive events, which in turn increases the likelihood of panic attacks.”

In the paper

“Taken together, the results obtained in anxious patients point to two dimensions of startle reactivity: one corresponding to high levels of phasic fear (eg, simple phobia) in the absence of heightened sustained fear and the other of heightened sustained fear (eg, PTSD, panic disorder) without elevated phasic fear.”

In the paper

“The fact that only high-risk females show elevated contextual anxiety suggests gender differences in sustained anxiety, which is consistent with basic findings in rodents.”

In the paper

“Worrisome thinking relies on verbally mediated processes (rumination) to shift the focus of attention away from the actual threat in order to reduce anxiety.”

In the paper

“GAD also differs from PTSD and panic disorder, in which the latter two conditions involve sudden attacks of increased arousal (paroxysm), whereas GAD involves chronically elevated anxiety in the face of no such paroxysm.”

In the paper

“Given that GAD is characterized by excessive and uncontrollable worry (Borkovec et al, 1991; Roemer et al, 2002)”

What the sources say

• ?Not checked — no full text of the sourcecites Borkovec et al, 1991
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Roemer et al, 2002

In the paper

“From this perspective, worry may not be equivalent with anticipatory anxiety, rather it is an attempt to cope with anxiety (Craske, 1999).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Craske, 1999

In the paper

“PTSD and panic disorder share common phenomenology, including the unpredictable and uncontrollable nature of the stress and enhanced anxiety sensitivity (Asmundson and Stapleton, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Asmundson and Stapleton, 2008 source

In the paper

“Neuroticism is a widely recognized risk factor for anxiety disorders (Bienvenu and Stein, 2003; Kendler et al, 2002).”

What the sources say

• ?Not checked — no full text of the sourcecites Bienvenu and Stein, 2003 source
• ?Not checked — no full text of the sourcecites Kendler et al, 2002 source

In the paper

“PTSD is precipitated by uncontrollable and unpredictable traumatic events, which result in intrusive recollections of the trauma with associated hyper-arousal and anxiety (American Psychiatric Association, 1994).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites American Psychiatric Association, 1994

In the paper

“study on physiological reactivity in GAD has found minimal evidence of hyper-arousal and some evidence of reduced arousal (Hoehn-Saric et al, 1989).”

What the sources say

• ?Not checked — no full text of the sourcecites Hoehn-Saric et al, 1989 source

In the paper

“Neuroticism was associated with elevated potentiation in conditions of intermediate distal threat, but not in the condition when threat was proximal or more distal.”

What the sources say

• ?Not checked — no full text of the sourcecites Waters et al, 2008 source

In the paper

“Vietnam veterans with PTSD showed normative levels of fear-potentiated startle to a CS that predicted a shock, but enhanced context conditioning when returning to an experimental room where they had previously received shocks (Grillon et al, 1998c).”

What the sources say

• ?Not checked — no full text of the sourcecites Grillon et al, 1998c source

In the paper

“neuroticism, a core personality dimension associated with a proneness to experience negative feelings (Costa and McCrae, 1992).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Costa and McCrae, 1992

In the paper

“These results were attributed to sexual dimorphism in the BNST (Allen and Gorski, 1990) and to the action of sex hormones on these structures (Toufexis, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Allen and Gorski, 1990 source
• ?Not checked — no full text of the sourcecites Toufexis, 2007 source