Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function

In the paper

“Further, whereas scaling up is completely dependent on the scaffold protein PSD-95, scaling down can be supported by either PSD-95 or PSD-93 (Sun and Turrigiano 2011).”

What the sources say

• Disputed

  The Discussion states the reverse: scaling down is critically dependent on PSD-95, while scaling up can be supported by either PSD-95 or PSD-93 in young neurons. The Results section ‘PSD-95 is necessary for scaling down’ likewise says PSD-93 cannot compensate for loss of PSD-95 during scaling down. The paper adds that scaling up becomes dependent on PSD-95 in older neurons. (LLM, conf=0.90)

  Checked by a reasoning model — may be wrong.

  cites Sun and Turrigiano 2011 sourceExperimental — accuracy not yet measured

In the paper

“It is worth noting, however, that postsynaptic knockdown of GluA2 is able to completely block synaptic scaling (Gainey et al. 2009), suggesting that if there is a presynaptic change in transmitter packaging it is not sufficient to enhance mini amplitude on its own.”

What the sources say

• Supported

  The Results section (‘GluR2 knockdown blocks synaptic scaling, but does not block LTP’) reports that TTX increased mEPSC amplitude in control neurons but not in GluR2-knockdown neurons. The Discussion explicitly says the knockdown completely blocked synaptic scaling. The statement about presynaptic transmitter packaging is the citing authors’ inference, not a separate finding attributed to this source. (LLM, conf=0.94)

  cites Gainey et al. 2009 source

In the paper

“Given that the postsynaptic and presynaptic responses to activity deprivation can occur independently (Wierenga et al. 2005(Wierenga et al. , 2006)), it is likely that they represent distinct forms of plasticity induced by distinct signaling pathways.”

What the sources say

• Supported

  The Discussion states that increased postsynaptic receptor accumulation can occur without measurable changes in presynaptic function and describes the changes as separable, independent homeostatic mechanisms. The statement about distinct signaling pathways is the citing authors’ inference, not the part directly attributed to this source. (LLM, conf=0.93)

  cites Wierenga et al. 2005 source
• ?Not checked — no full text of the sourcecites Wierenga et al. 2006 source

In the paper

“Like scaling up, scaling down in response to elevated network activity is a cell-autonomous function of postsynaptic firing, and involves enhanced calcium influx (Fig. 2), gene transcription, the CaMKK/CaMKIV signaling pathway, and targets the GluA2 subunit (Goold and Nicoll 2010).”

What the sources say

• Partly supported

  The Discussion reports that cell-autonomous excitation drives calcium-dependent synaptic depression through CaMKK/CaMK4. It also limits the transcription and GluA2 requirements to AMPAR depression: NMDAR depression does not require them. The citing sentence omits that distinction when describing scaling down generally. (LLM, conf=0.85)

  cites Goold and Nicoll 2010 sourceExperimental — accuracy not yet measured

In the paper

“Lowering presynaptic firing with an inwardly rectifying K ir channel was observed to selectively enhance the accumulation of GluA1 at postsynaptic sites, suggesting the existence of a synapse-specific form of homeostatic compensation to reduced receptor activation (Hou et al. 2008).”

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 Hou et al. 2008 source

In the paper

“Interestingly, synaptic scaling protocols homeostatically regulate both the NMDA and the AMPA component of glutamatergic synaptic currents, and the change in AMPA and NMDA currents are proportional at individual synapses (Watt et al. 2000;Perez-Otano and Ehlers 2005).”

What the sources say

• Supported

  The Abstract reports that long-lasting changes in activity scaled AMPA and NMDA currents up and down proportionally. It also says their ratio at different synapses onto the same neuron was preserved after scaling. The findings concern neocortical synapses expressing both receptor types. (LLM, conf=0.93)

  cites Watt et al. 2000 source
• ?Not checked — no full text of the sourcecites Perez-Otano and Ehlers 2005 source

In the paper

“Interestingly, the same manipulation (activity blockade using TTX or AMPAR antagonists) that only affects mini amplitude in young cultures (Turrigiano et al. 1998;Wierenga et al. 2005) can also induce changes in mini frequency and in presynaptic release probability in older neuronal cultures (Wierenga et al. 2006), through a process that involves postsynaptic hyperpolarization and a drop in”

What the sources say

• ?Not checked — no full text of the sourcecites Turrigiano et al. 1998 source
• 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 Wierenga et al. 2005 source
• ?Not checked — no full text of the sourcecites Wierenga et al. 2006 source

In the paper

“Additionally, there is evidence that the neurotrophin brain-derived neurotrophic factor (BDNF) (Rutherford et al. 1998), the immediate early gene Arc (Shepherd et al. 2006), the cytokine TNFa (Stellwagen and Malenka 2006;Steinmetz and Turrigiano, 2010), the immune molecule MHC1 (Goddard et al. 2007), b3 integrins (Cingolani et al. 2008), the AMPAR binding protein PICK1 (Anggono et al. 2011), and”

What the sources say

• ?Not checked — no full text of the sourcecites Rutherford et al. 1998 source
• Supported

  The cited paper supports the Arc portion of the multi-citation claim. In “Arc/Arg3.1 Regulates Homeostatic Synaptic Scaling of AMPARs” (page unavailable), cultured wild-type hippocampal neurons showed activity-dependent changes in surface AMPA receptors, while Arc/Arg3.1 knockout neurons lacked those changes. The other molecules are attributed to other citations, not to this paper. (LLM, conf=0.94)

  cites Shepherd et al. 2006 source
• ?Not matched

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

  cites Stellwagen and Malenka 2006;Steinmetz and Turrigiano, 2010

In the paper

“Interestingly, chronic hyperpolarization of an entire neuron by expression of an inwardly rectifying K channel (K ir ) does not induce postsynaptic scaling (Burrone et al. 2002;Hou et al. 2008), suggesting that chronic global hyperpolarization of neuronal dendrites and somata overrides the signals that induce scaling up in response to a drop in firing.”

What the sources say

• ?Not checked — no full text of the sourcecites Burrone et al. 2002 source
• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites Hou et al. 2008 sourceExperimental — accuracy not yet measured

In the paper

“A number of reports have suggested that activity-dependent BDNF release is critical for scaling of inhibitory synapses onto pyramidal neurons as well as the homeostatic regulation of excitatory synapses onto inhibitory neurons (Rutherford et al. 1997(Rutherford et al. , 1998;;Copi et al. 2005;Swanwick et al. 2006).”

What the sources say

• Partly supported

  The Discussion reports that activity blockade reduces inhibition onto cortical pyramidal neurons and that exogenous BDNF prevents this reduction, supporting the inhibitory part of the claim. It infers reduced endogenous BDNF production rather than directly demonstrating activity-dependent release, and it does not establish homeostatic regulation of excitatory synapses onto inhibitory neurons; the excitatory currents it mentions are onto pyramidal neurons. (LLM, conf=0.88)

  cites Rutherford et al. 1997 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Rutherford et al. 1998 source
• ?Not checked — no full text of the sourcecites Copi et al. 2005 source

In the paper

“TNFa signaling was not necessary for the induction of early (6 h) scaling, but became essential for maintenance of scaling during prolonged (.24 h) activity blockade.”

What the sources say

• Supported

  The Results section reports that blocking TNFα signaling for 6 hours did not prevent early scaling, whereas 24 hours of blockade prevented scaling and reversed scaling that had already been induced. The Discussion interprets this as a requirement for TNFα signaling to maintain synapses’ ability to express or maintain scaling during prolonged activity blockade. (LLM, conf=0.92)

  cites Steinmetz and Turrigiano 2010 source

In the paper

“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”

What the sources say

• ?Not checked — no full text of the sourcecites Beattie et al. 2002 source
• Partly supported

  The culture electrophysiology methods (page not provided) say TNFα was applied 15–25 minutes before recording, and the Figure 5 caption reports a significant increase in mEPSC amplitude in TNFα-treated cultures. The passages do not support the separate claim about conditioned media from activity-blocked cultures. (LLM, conf=0.85)

  cites Stellwagen et al. 2005 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Stellwagen and Malenka 2006 source

In the paper

“Synapses onto the same dendrite tended to have similar P r , and there was an inverse relationship between synapse number and P r onto individual dendrites, suggesting that this regulation happens in a”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites Branco et al. 2008 sourceExperimental — accuracy not yet measured

In the paper

“In apparent conflict with this model, a positive correlation between P r and synaptic strength at cortical synapses has been reported (Hardingham et al. 2010;Kay et al. 2011), but because in these studies synaptic strength was measured at unitary connections, it remains an open possibility that such an inverse correlation exists at the level of summed dendritic input.”

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 Hardingham et al. 2010 source
• ?Could not verify

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

  cites Kay et al. 2011 sourceExperimental — accuracy not yet measured

In the paper

“This quasi-local (dendrite-wide) form of presynaptic homeostasis has been suggested to prevent synaptic saturation owing to strong depolarization from summed inputs onto a dendrite, by reducing P r when postsynaptic activation rises too high (Branco et al. 2008).”

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 Branco et al. 2008 source

In the paper

“BDNF was the first such secreted factor suggested to play a role in homeostatic plasticity (Rutherford et al. 1997(Rutherford et al. , 1998)).”

What the sources say

• Partly supported

  The Discussion (page not specified in our copy) says BDNF regulates inhibition in cortical cultures and may help reduce inhibition when activity falls too low, supporting a role in homeostatic plasticity. The paper does not establish the historical claim that BDNF was the first secreted factor suggested to have that role. (LLM, conf=0.84)

  cites Rutherford et al. 1997 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Rutherford et al. 1998 source

In the paper

“Unlike TTX treatment, acute TNFa application does not scale up mini amplitude and adding TNFa to prescaled synapses actually reduces synaptic strength, indicating that scaling and TNFa are neither additive nor simply occlusive (Steinmetz and Turrigiano 2010).”

What the sources say

• Supported

  The Results section, “Synaptic scaling modulates but does not occlude the effect of TNFα application,” reports that TNFα increased mEPSC amplitude at control synapses but did not produce the multiplicative change characteristic of TTX-induced scaling. Applied after 24 hours of TTX, it reduced mEPSC amplitude rather than adding to or merely occluding the increase. The supplied copy gives no page number for these passages. (LLM, conf=0.91)

  cites Steinmetz and Turrigiano 2010 source

In the paper

“In contrast, dark rearing increases the abundance of GluA2-lacking receptors and requires GluA1 phosphorylation, suggesting that these two modes of deprivation may induce different forms of compensatory synaptic plasticity (Goel and Lee 2007;Goel et al. 2011).”

What the sources say

• Partly supported

  The Results section (page unavailable) reports that two days of dark rearing increased AMPA receptor-mediated mEPSC amplitude in mouse visual cortex. The Discussion (page unavailable) says dark rearing increased GluR1 (GluA1) phosphorylation, but our copy does not establish that phosphorylation is required or that GluA2-lacking receptors become more abundant. (LLM, conf=0.83)

  cites Goel and Lee 2007 sourceExperimental — accuracy not yet measured
• Partly supported

  The Results report that two days of dark exposure increased functional calcium-permeable AMPA receptors, consistent with more GluA2-lacking receptors; the Discussion says deprivation-induced synaptic changes require GluA1 phosphorylation. But the Methods specify that mice were raised under normal lighting until postnatal day 21, then exposed to darkness for two days. The paper does not establish these effects for dark rearing from birth. (LLM, conf=0.83)

  cites Goel et al. 2011 sourceExperimental — accuracy not yet measured

In the paper

“Interestingly, binocularly driven neurons maintained a similar average level of combined responsiveness to the two eyes, suggesting that the drop in deprived eye responsiveness was compensated by an increase in nondeprived eye responsiveness (Mrsic-Flogel et al. 2007); a very similar response homeostasis following visual deprivation has been reported at retinotectal synapses (Chandrasekaran et al.”

What the sources say

• Supported

  The paper states that neurons with binocular input adjusted their eye-specific responses so the summed visual response remained roughly preserved. It also reports that after monocular deprivation, deprived-eye responses fell while nondeprived-eye responses rose (Results, page unavailable). (LLM, conf=0.93)

  cites Mrsic-Flogel et al. 2007 source

In the paper

“When one eye is deprived of patterned vision during the classical critical period (using lid suture) there is a change in the ability of the two eyes to drive neurons within the binocular portion of visual cortex: cortical neurons rapidly (within 2 or 3 days) lose responsiveness to the deprived eye, and then more slowly (over 4 -6 days) gain responsiveness to the nondeprived eye (Frenkel and Bear”

What the sources say

• ?Not checked — no full text of the sourcecites Frenkel and Bear 2004 source
• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites Mrsic-Flogel et al. 2007 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Kaneko et al. 2008 source

In the paper

“This possibility is raised by the finding that the same visual deprivation paradigm that scales minis up in younger mice produces nonmultiplicative changes in minis in older mice, suggesting that not all synapses are affected equally (Goel and Lee 2007); however, this could also reflect the simultaneous activation of synaptic scaling and Hebbian, synapse-specific mechanisms (see Turrigiano 2011”

What the sources say

• Supported

  The “Loss of multiplicative synaptic scaling in adult mice” section reports that two days of dark rearing increased mEPSC amplitude multiplicatively in P23 mice (Fig. 4a). The same section reports that the increase in P97 mice did not follow a global multiplicative mechanism (Fig. 4e). (LLM, conf=0.94)

  cites Goel and Lee 2007 source

In the paper

“Visual deprivation induced by optic nerve block scale ups mEPSC amplitude in vivo as in vitro, and results in insertion of GluA2-containing AMPAR (Desai et al. 2002;Maffei and Turrigiano 2008;Gainey et al. 2009).”

What the sources say

• ?Not checked — no full text of the sourcecites Desai et al. 2002 source
• Partly supported

  The Results section on experience-dependent plasticity at excitatory layer 2/3 synapses reports that visual deprivation by intraocular TTX injection increased AMPA mEPSC amplitude in rats. The paper does not establish an in vitro comparison or report insertion of GluA2-containing AMPARs, so those parts of the sentence are unsupported by this source. (LLM, conf=0.88)

  cites Maffei and Turrigiano 2008 sourceExperimental — accuracy not yet measured
• Supported

  The Results section reports that visual deprivation by intraocular TTX significantly increased mEPSC amplitude in visual cortical neurons. The Discussion states that scaling in vivo after monocular TTX injection increased accumulation of GluR2-containing AMPARs (now called GluA2-containing AMPARs), consistent with the claim. (LLM, conf=0.92)

  cites Gainey et al. 2009 source

In the paper

“In visual cortex the expression of synaptic scaling is developmentally regulated (Desai et al. 2002;Maffei et al. 2004Maffei et al. , 2006;;Maffei and Turrigiano 2008); synaptic scaling is expressed by pyramidal neurons in layer 4 early in postnatal development, but then turns off in layer 4 and begins to be expressed in layer 2/3 pyramidal neurons around the opening of the classical visual system”

What the sources say

• ?Not checked — no full text of the sourcecites Desai et al. 2002 source
• 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 Maffei and Turrigiano 2008 source
• Partly supported

  The Discussion (page unavailable) reports scaling in layer 4 at P14–P16 but not P21–P23, with the opposite pattern in layer 2/3; it also says the authors’ data extend layer 2/3 plasticity through adulthood. Our copy does not establish that the switch coincides with the opening of the classical visual critical period, or identify the early layer 4 cells specifically as pyramidal neurons. (LLM, conf=0.82)

  cites Goel and Lee 2007 sourceExperimental — accuracy not yet measured

In the paper

“For example, reductions in glutamate receptor function, or chronic hyper-polarization of the muscle, lead to compensatory increases in transmitter release that restore evoked transmission to control levels (Paradis et al. 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites Paradis et al. 2001 source

In the paper

“When cortical or hippocampal neurons are induced to fire more than normal, over many hours firing returns to baseline levels, and similarly, if neuronal firing is reduced over time, neurons compensate and again firing is restored (Fig. 1A) (Turrigiano et al. 1998;Burrone et al. 2002).”

What the sources say

• ?Not checked — no full text of the sourcecites Turrigiano et al. 1998 source
• ?Not checked — no full text of the sourcecites Burrone et al. 2002 source

In the paper

“Thus, without forces that prevent the excitability of the postsynaptic neuron from changing in response to correlation-based plasticity mechanisms, their specificity breaks down and information can no longer be effectively stored through differences in synaptic strengths.”

In the paper

“On a functional level, neuronal networks likely use this complex set of regulatory mechanisms to achieve homeostasis over a wide range of temporal and spatial scales.”

In the paper

“More recently work at the mammalian and invertebrate NMJ has shown that perturbations in postsynaptic function can lead to compensatory changes in presynaptic release, and vice versa (Davis and Bezprozvanny 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites Davis and Bezprozvanny 2001 source

In the paper

“Although all of these phenomena are theoretically capable of serving a homeostatic function, for many of them such a function has not been directly shown.”

In the paper

“Thus, cell-autonomously induced synaptic scaling is fundamentally different from LTP and LTD: it operates over a longer temporal scale (hours), a wider spatial scale (global), and utilizes distinct trafficking steps and molecular machinery to enhance or reduce the synaptic accumulation of GluA2-containing AMPAR at most if not all synapses onto a neuron.”

In the paper

“The ability of synapses to undergo postsynaptic homeostatic regulation as a function of purely local changes in transmitter release and receptor activation thus remains controversial and may require either extreme presynaptic hyperpolarization (such as would be obtained with presynaptic expression of K ir ) or a situation in which spiking and transmitter release are both severely impaired (see”

In the paper

“On the other hand, theoretical work has suggested that quasi-local forms of homeostasis that act on groups of nearby synapses can serve a useful normalization function without severely disrupting Hebbian plasticity (Rabinowitch and Segev 2006a,b).”

What the sources say

• ?Not matched

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

  cites Rabinowitch and Segev 2006a,b

In the paper

“This suggests that a drop in somatic calcium influx will simultaneously enhance signaling in the pathways that scale synapses up and reduce signaling in the pathways that scale synapses down, and vice versa when firing rises.”

In the paper

“Such a postsynaptic scaling process has the attractive property of allowing neurons to stabilize activity without changing the relative strength of synaptic inputs, thus avoiding disrupting information storage or processing mechanisms that rely on differences in synaptic weights (Fig. 1B).”

In the paper

“The locus of change during homeostatic plasticity has important consequences for circuit function, because (for example) presynaptic changes in release probability will strongly affect short-term plasticity and thus the dynamics of information transfer across synapses, whereas a postsynaptic change in receptor accumulation can scale postsynaptic responsiveness without affecting the short-term”

What the sources say

• ?Not checked — no full text of the sourcecites Abbott and Nelson 2000 source

In the paper

“Selectively blocking firing by microperfusion of TTX to the soma of individual neurons scales up synaptic strengths to the same degree as blockade of network activity, whereas local block of synaptic transmission does not induce a local enhancement of receptor accumulation (Ibata et al. 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Ibata et al. 2008 source

In the paper

“In dissociated cortical cultures it has been shown that excitatory synapses onto excitatory pyramidal neurons are scaled up by activity blockade, whereas excitatory synapses onto GA-BAergic interneurons are not (Rutherford et al. 1998).”

What the sources say

• ?Not checked — no full text of the sourcecites Rutherford et al. 1998 source

In the paper

“If this mechanism operates in vivo, it predicts an inverse relationship between P r and the summed synaptic strength onto a dendritic branch.”

In the paper

“This is consistent with evidence that chronic hyperpolarization of entire neurons (including dendrites) results in enhanced P r (Burrone et al. 2002), suggesting that P r can be bidirectionally regulated by changes in the amount of dendritic depolarization.”

What the sources say

• ?Not checked — no full text of the sourcecites Burrone et al. 2002 source

In the paper

“Blocking BDNF signaling mimics, and exogenous BDNF application prevents, the effects of activity blockade on excitatory minis, suggesting that in neocortical neurons activitydependent BDNF release could mediate synaptic scaling (Rutherford et al. 1998).”

What the sources say

• ?Not checked — no full text of the sourcecites Rutherford et al. 1998 source

In the paper

“BDNF is thought to be released as a function of pyramidal neuron activity, and activates Trk receptors on both pyramidal and interneurons (Lu 2003).”

What the sources say

• ?Not matched

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

  cites Lu 2003

In the paper

“It was recently proposed that prolonged activity blockade (with TTX) increases glial release of TNFa, which then acts on neurons to enhance AMPAR insertion and scale up mEPSC amplitude (Stellwagen and Malenka 2006).”

What the sources say

• ?Not checked — no full text of the sourcecites Stellwagen and Malenka 2006 source

In the paper

“These distinct plasticity rules at different classes of excitatory and inhibitory synapse are consistent with an overall homeostatic shift in the balance between excitation and inhibition, as the net effect of the changes induced by activity blockade are to enhance excitation and reduce inhibition, which will act to restore network excitability.”

In the paper

“Interestingly, not all excitatory neurons in cortical networks express synaptic scaling.In hippocampal networks CA1 neurons scale synapses up in response to activity blockade, whereas CA3 neurons do not (Kim and Tsien 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Kim and Tsien 2008 source

In the paper

“Interestingly, in visual cortical microcircuits the locus of homeostatic plasticity changes as the circuit matures.Early in postnatal development layer 4 (the first input layer to cortex, and the first layer to mature) responds homeostatically to brief (2 days) inactivation of the optic nerve with TTX (Desai et al. 2002;Maffei et al. 2004), whereas later (at the opening of the classical visual”

What the sources say

• ?Not checked — no full text of the sourcecites Desai et al. 2002 source
• ?Not checked — no full text of the sourcecites Maffei et al. 2004 source
• ?Not checked — no full text of the sourcecites Maffei et al. 2006 source

In the paper

“When sensory drive to primary visual cortex is lowered in vivo, connections from fast-spiking basket cells onto layer 4 pyramidal neurons are reduced in amplitude, whereas connections from another class of interneuron become sparser but stronger (Maffei et al. 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Maffei et al. 2004 source

In the paper

“Similarly, in visual cortex during the second and third postnatal weeks when synaptogenesis is high, there is an inverse relationship between the frequency and amplitude of mEPSCs onto pyramidal neurons, and this can be prevented by raising animals in the dark (Desai et al. 2002).”

What the sources say

• ?Not checked — no full text of the sourcecites Desai et al. 2002 source

In the paper

“Neurons and networks use a family of homeostatic synaptic plasticity mechanisms to stabilize firing rates in the face of developmental or learning-induced changes in drive, and this contributes to the ability of central neuronal networks to maintain stable function and enables networks to maintain the specificity of synaptic changes that encode information.”