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Nucleus basalis and thalamic control of neocortical activity in the freely moving rat

Buzsaki, G, Bickford, RG, Ponomareff, G, Thal, LJ, Mandel, R, Gage, FH·1988·The Journal of Neuroscience
DOI 10.1523/jneurosci.08-11-04007.1988
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Abstract

EEG and single-unit techniques have been used to study the EEG correlates of cellular firing in the neocortex, n. reticularis (RT) and “specific” thalamic nuclei, and the cholinergic forebrain area (nucleus basalis, NB). Neuronal firing was related to the ongoing behavior of the rat. In addition, using a 16-channel neocortical recording/mapping system, we studied the effects of ibotenic acid lesion of NB, RT, and other thalamic nuclei on the patterns and spatial distribution of neocortical electrical activity. The majority of neurons in neocortex, NB, and RT increased their firing rates during walking, as compared to during immobility, with concurrent decrease of delta power in the neocortical EEG. During immobility, high-voltage spindles (HVS; greater than 1 mV) were occasionally recorded from the neocortex. Depth profiles of HVS and slow delta waves were different in the neocortex. Neocortical cells decreased their discharge frequency during the positive portion of delta waves recorded in layers V and VI. All cells in the neocortex and specific thalamic nuclei fired rhythmically and phase-locked to the spike component of HVS. RT neurons showed an opposite phase relationship and fired mainly during the wave component of HVS. Half of the NB neurons also showed phasic modulation with HVS. Circumscribed lesion of RT and extensive damage of other thalamic regions, including the intralaminar nuclei, suppressed HVS but had no effect on the neocortical EEG correlates of behavior. In sharp contrast, damage to the NB resulted in a dramatic increase of slow delta waves on the side of the lesion, mimicking the effect of scopolamine administration. We suggest that the NB plays a key role in neocortical arousal by directly activating the neocortex and by suppressing the rhythm generation in the RT-thalamocortical circuitry. We further suggest that the NB system may serve as a structural basis for the concept of the generalized ascending activation of Moruzzi and Magoun (1949).

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Crossref · 10.1523/jneurosci.08-11-04007.1988

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Figures

Image 1
CC-BY-NC-SA · From the PDF
Image 2
CC-BY-NC-SA · From the PDF
Figure 3 Spectral power in the delta band (1-4 Hz) during run-drinkstill transitions. Bipolar recording at location 6 of Figure 1 (n = 12 rats). Note monotonic increase in power from run to still. Note also that scopolamine-induced power increase is disproportionally greater during sitting still than during running. The 2 doses of scopolamine were tested in the same animals. Vertical bars, SEM. Arbitrary units.
Figure 3 Spectral power in the delta band (1-4 Hz) during run-drinkstill transitions. Bipolar recording at location 6 of Figure 1 (n = 12 rats). Note monotonic increase in power from run to still. Note also that scopolamine-induced power increase is disproportionally greater during sitting still than during running. The 2 doses of scopolamine were tested in the same animals. Vertical bars, SEM. Arbitrary units.CC-BY-NC-SA · From the PDF
Figure 4 Neocortically triggered HVSs. Dots indicate single-pulse (0.1 msec) stimulation of the neocortex (location 2 in Fig. 1). Note the frequent occurrence of induced HVS during sitting still (STILL) and its absence during slow-wave sleep (SWS) and movement (MOVE). The graphs on the right are based on 30 stimulations each. The sensitivity of the movement sensor was doubled during still behavior. Calibrations, 5 sec, 1 mV.
Figure 4 Neocortically triggered HVSs. Dots indicate single-pulse (0.1 msec) stimulation of the neocortex (location 2 in Fig. 1). Note the frequent occurrence of induced HVS during sitting still (STILL) and its absence during slow-wave sleep (SWS) and movement (MOVE). The graphs on the right are based on 30 stimulations each. The sensitivity of the movement sensor was doubled during still behavior. Calibrations, 5 sec, 1 mV.CC-BY-NC-SA · From the PDF
Figure 5 Depth profiles of HVS and delta waves. a, Amplitude distribution of the spike (interrupted line, black dots) and wave (dotted line, circles) components of HS as a function of depth. Samples of averaged HVSs (n = 30) at various depth levels are shown in c. b, Laminar distribution of th n ( ( s ( e ( y dividing the values obtained from the roving microelectrode by the values obtained from a cortical screw electrode and multiplying the ratio by the grand average. Note different depth profiles of HVS and delta waves.
Figure 5 Depth profiles of HVS and delta waves. a, Amplitude distribution of the spike (interrupted line, black dots) and wave (dotted line, circles) components of HS as a function of depth. Samples of averaged HVSs (n = 30) at various depth levels are shown in c. b, Laminar distribution of th n ( ( s ( e ( y dividing the values obtained from the roving microelectrode by the values obtained from a cortical screw electrode and multiplying the ratio by the grand average. Note different depth profiles of HVS and delta waves.CC-BY-NC-SA · From the PDF
Image 6
CC-BY-NC-SA · From the PDF
Image 7
CC-BY-NC-SA · From the PDF
Figure 8 Neuronal activity of the thalamus during HVS. a-c, RT cell. a, Rhythmic firing (6 Hz) while sitting still in the absence of HVS. b, HVS evoked by single-pulse stimulation of the ipsilateral neocortex (arrow), c, Faster sweep speed. Note repetitive discharge. d, Unit in n. ventralis lateralis (VL). Note single and burst discharges during the spike component of HVS. e, Perievent histograms (n = 50) of 4 cells recorded in the same track (f) and averaged HVS recorded from the neocortical surface (s). Note opposite phase relationships of RT and VL cells in relation to HVS. Symbols in f indicate the locations of the units shown in a-e. g, A small lesion (arrow) indicates the tip of the microelectrode in RT. Calibrations: 2 mV (field); 0.2 mV (a–c); 1 mV (d, unit); 0.4 sec (a, b, d); 10 msec (c).
Figure 8 Neuronal activity of the thalamus during HVS. a-c, RT cell. a, Rhythmic firing (6 Hz) while sitting still in the absence of HVS. b, HVS evoked by single-pulse stimulation of the ipsilateral neocortex (arrow), c, Faster sweep speed. Note repetitive discharge. d, Unit in n. ventralis lateralis (VL). Note single and burst discharges during the spike component of HVS. e, Perievent histograms (n = 50) of 4 cells recorded in the same track (f) and averaged HVS recorded from the neocortical surface (s). Note opposite phase relationships of RT and VL cells in relation to HVS. Symbols in f indicate the locations of the units shown in a-e. g, A small lesion (arrow) indicates the tip of the microelectrode in RT. Calibrations: 2 mV (field); 0.2 mV (a–c); 1 mV (d, unit); 0.4 sec (a, b, d); 10 msec (c).CC-BY-NC-SA · From the PDF
Image 9
CC-BY-NC-SA · From the PDF
Effect of thalamic lesion on neocortical EEG. a, Nissl stain. b, AChE stain. The lesion damaged most of the ventrolateral nucleus (vl) and laterodorsal nucleus (ld), intralaminar nuclei il), and part of the n. ventralis posterolateralis (vpl). c, Contour map of power distribution of slow activity (1-4 Hz) during immobility. Note symmetry of delta wave distribution. AU indicate increasing power; HVSs were attenuated on the side of the lesion (not shown). Figure 10.
Effect of thalamic lesion on neocortical EEG. a, Nissl stain. b, AChE stain. The lesion damaged most of the ventrolateral nucleus (vl) and laterodorsal nucleus (ld), intralaminar nuclei il), and part of the n. ventralis posterolateralis (vpl). c, Contour map of power distribution of slow activity (1-4 Hz) during immobility. Note symmetry of delta wave distribution. AU indicate increasing power; HVSs were attenuated on the side of the lesion (not shown). Figure 10.CC-BY-NC-SA · From the PDF
Figure 11 Ibotenic acid-induced lesion in n. reticularis thalami (RT). The ventral borders of RT are marked by arrows. Note gliosis (a) and absence of AChE-positive fibers (c) on the lesioned side. b, d, Intact side. VL, n. ventralis lateralis; AV, n. ventralis anterior.
Figure 11 Ibotenic acid-induced lesion in n. reticularis thalami (RT). The ventral borders of RT are marked by arrows. Note gliosis (a) and absence of AChE-positive fibers (c) on the lesioned side. b, d, Intact side. VL, n. ventralis lateralis; AV, n. ventralis anterior.CC-BY-NC-SA · From the PDF
N.RETICULARIS THALAMI LESION (RIGHT)
N.RETICULARIS THALAMI LESION (RIGHT)CC-BY-NC-SA · From the PDF
Figure 13 Ibotenic acid-induced lesion in the peripallidal region of NB. Left, Lesioned (right) side; right, intact sides. a-d, AChE-stained sections. Note decrease in the density of AChE-positive fibers in the injected NB and ipsilateral parietal cortex. Arrow in c indicates cannula track. e, f, CATimmunostained sections. Note reduced number of CAT-positive cells in the damaged NB. Calibration, 0.5 mm.
Figure 13 Ibotenic acid-induced lesion in the peripallidal region of NB. Left, Lesioned (right) side; right, intact sides. a-d, AChE-stained sections. Note decrease in the density of AChE-positive fibers in the injected NB and ipsilateral parietal cortex. Arrow in c indicates cannula track. e, f, CATimmunostained sections. Note reduced number of CAT-positive cells in the damaged NB. Calibration, 0.5 mm.CC-BY-NC-SA · From the PDF
Figure 14 Contour maps of delta power (1–4 Hz) recorded during immobility. Note focal power increase on the side of NB lesion (lower left). Note also that scopolamine reduced the asymmetry between the damaged and intact hemispheres (lower right). Units of the color scale are arbitrary.
Figure 14 Contour maps of delta power (1–4 Hz) recorded during immobility. Note focal power increase on the side of NB lesion (lower left). Note also that scopolamine reduced the asymmetry between the damaged and intact hemispheres (lower right). Units of the color scale are arbitrary.CC-BY-NC-SA · From the PDF
Figure 15 Asymmetry ratios of delta power (1–4 Hz) during different behaviors before and after NB lesion. Note that scopolamine (scop) reduced the interhemispheric differences during immobility (still). Figure 15. Asymmetry ratios of delta power (1–4 Hz) during different behaviors before and after NB lesion. Note that scopolamine (scop) reduced the interhemispheric differences during immobility (still).
Figure 15 Asymmetry ratios of delta power (1–4 Hz) during different behaviors before and after NB lesion. Note that scopolamine (scop) reduced the interhemispheric differences during immobility (still). Figure 15. Asymmetry ratios of delta power (1–4 Hz) during different behaviors before and after NB lesion. Note that scopolamine (scop) reduced the interhemispheric differences during immobility (still).CC-BY-NC-SA · From the PDF
Figure 16 Schematic circuitries of the hypothesized mechanisms of neocortical activation (desynchronization) (top) and HVS (bottom). Pathways and structures playing a dominant role in the respective electrical patterns are indicated by heavy lines and shading. Arrows, excitatory paths; bars, inhibitory paths. During activation, NB exerts an exiick ii i i i iceal rhythmic generator circuitry. When the RT-thalamocortical system is released from the suppressive effect of the NB (bottom), rhythmic activity of RT cells phasically inhibits thalamocortical cells and induces rhythmic rebound burst firing in these cells, resulting in rhythmic depolarization of cortical cells. NB, nucleus basalis; RT, n. reticularis thalami; spec.nn, "specific" nuclei of thalamus; IL, intralaminar thalamic nuclei; HVS, high-voltage spindle.
Figure 16 Schematic circuitries of the hypothesized mechanisms of neocortical activation (desynchronization) (top) and HVS (bottom). Pathways and structures playing a dominant role in the respective electrical patterns are indicated by heavy lines and shading. Arrows, excitatory paths; bars, inhibitory paths. During activation, NB exerts an exiick ii i i i iceal rhythmic generator circuitry. When the RT-thalamocortical system is released from the suppressive effect of the NB (bottom), rhythmic activity of RT cells phasically inhibits thalamocortical cells and induces rhythmic rebound burst firing in these cells, resulting in rhythmic depolarization of cortical cells. NB, nucleus basalis; RT, n. reticularis thalami; spec.nn, "specific" nuclei of thalamus; IL, intralaminar thalamic nuclei; HVS, high-voltage spindle.CC-BY-NC-SA · From the PDF
Image 17
CC-BY-NC-SA · From the PDF

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Citations

Cites

Show all 5 references

Research works printed but not linked: 11

  1. Bickford, R. G. (1981) A combined EEG and evoked potential pro- cedure in clinical EEG (automated cerebral electrogram-ACE test). In Recent Advances in EEG and EMG Data Processing, N. Yamaguchi and K. Fujisaura, eds., pp. 2 17-235, Elsevier, Amsterdam.
  2. Bickford, R. G., and B. Allen (1986) A simple add-on personal com- puter procedure for color displays of electrophysiological data: Ad- vantage and pitfalls. In Topographic Mapping of Brain Electrical Ac- tivity, F. H. Duffy, ed., pp. 203-216, Butterworths, Boston.
  3. Buzs&i, G., R. G. Bickford, D. M. Armstrong, G. Ponomareff, K. Chen, R. Ruiz, L. J. Thal, and F. H. Gage (1988) EEG activity in the neocortex of freely moving young and aged rats. Neuroscience (in press).
  4. Colonnier, M. (198 1) The electron-microscopic analysis of the neu- ronal organization of the cerebral cortex. In The Organization ofthe Cerebral Cortex, F. 0. Schmitt, F. G. Worden, G. Adelman, and S. G. Dennis, eds., pp. 125-152, MIT Press, Cambridge, London.
  5. Gottesmann, C. (1967) Recherche sur psychophysiologie du sommeil chez la rat. Thesis, Doctor of Natural Science, Presse du Palais Royal, pp. 1-156.
  6. Peronnet, I., M. Sindou, A. Laviron, F. Quoex, and P. Germ (1981) Human cortical electrogenesis: Stratigraphy and spectral analysis. In Svnchronization ofEEG Activitv in Evilevsies, H. Petsche and M. A. B: Brazier, eds., pp. 235-261, Springer, Heidelberg.
  7. Purpura, D. P. (1969) Intemeuronal mechanisms in thalamically in- duced synchronizing and desynchronizing activities. In The Inter- neuron, V. E. Hall, ed., pp. 467-496, U. California Press, Berkeley, Los Angeles.
  8. Vanderwolf, C. H., and T. H. Robinson (1981) Reticulocortical ac- tivity and behavior: A critique of the arousal theory and a new syn- thesis. Behav. Brain Sci. 4: 459-5 14.
  9. Villablanca, J. (1974) Role of the thalamus in sleep control. In Basic Sleep Mechanisms, P. Petre-Quadeus and J. Schlag, eds., pp. 5 l-8 1, Academic, New York.
  10. Walker, A. E. (1938) The Primate Thalamus, U. Chicago Press, Chi- cago.
  11. Wikler, A. (1952) Pharmacologic dissociation on behavior and EEG sleep patterns in dogs: Morphine, N-allylnormotphine and atropine. Proc. Sot. Exp. Biol. Med. 79: 261-265.

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Metadata

Authors
Buzsaki, G., Bickford, R., Ponomareff, G., Thal, L., Mandel, R., & Gage, F.
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
1988-11-01
Volume
8
Issue
11
Pages
4007-4026
ISSN
  • 0270-6474
  • 1529-2401
DOI
10.1523/jneurosci.08-11-04007.1988
Cited by
848
References
5
Language
en
Licence
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 181 d)

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