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Monosynaptic excitation of principal cells in the lateral geniculate nucleus by corticofugal fibers
454
Brain Research, 234 (1982) 454-458 Elsevier Biomedical Press
Monosynaptic excitation of principal cells in the lateral geniculate nucleus by corticofugal fibers
G. AHLSEN, K. GRANT* and S. LINDSTROM Department of Physiology, University of Giiteborg, Giiteborg (Sweden) (Accepted November 19th, 1981) Key words: lateral geniculate nucleus - - principal cell - - cortico-geniculate fibers - - monosynaptic excitation
Electrical stimulation of the primary visual cortex evoked long latency EPSPs in X and Y principal cells of the cat's lateral genie,ulate nucleus. An extrapolation procedure:was used to reveal that these EPSPs were mediated monosynaptically to principal cells by slowly conducting corticogeniculate fibers. A similar type of excitation was observed in intrageniculate interneurons.
It has been demonstrated in a large number of anatomical studies that the lateral geniculate nucleus receives a prominent projection from the visual cortexrL The pathway is retinotopically organized 15 and originates from pyramidal cells in the VIth layer of the cortex 4. After lesions in area 17, degenerating terminals are found on thin dendrites which may belong to either principal cells or local interneurons. There is evidence that intrageniculate interneurons are activated by electrical stimulation of the visual cortex s, while principal cells are usually inhibited by such stimuli, presumably due to the concomitant activation of a recurrent inhibitory pathway 1,11. The recent reports that binocular facilitation of principal cells is eliminated by cortex cooling (ref. 13) and that intracortical glutamate injections may excite principal cells 14 implies, however, that also these cells m a y receive excitation by the cortico-geniculate route. In the present study intracellular recordings from principal cells have been used to test this possibility. The experiments were performed on cats kept under light sodium pentobarbital anesthesia (Nembutal, Abbott, 25-30 mg/kg). The animals were paralyzed with succinylcholine chloride (Celucurin, Vitrum, 15 mg/kg/h) and respirated artificially. Atropine and Neosynephrine (Winthrop Laboratories) were applied topically to dilate the pupils and retract the nictitating membranes, and the eyes were focused through appropriate contact lenses onto a tangent screen placed 1.5 m in front o f the animals. * Present address: Unit6 de Recherches Neurobiologiques (U6), INSERM, 280 Boul. Sainte-Marguerite, 13009 Marseille, France. 0006-8993/82/0000-0000/$02.75 © Elsevier Biomedical Press
455 Different patterns of light stimuli could be projected onto this screen with a hand-held slide projector. Seven fine tungsten electrodes were inserted 3--4 mm into the visual cortex in a row at the border between areas 17 and 18. These electrodes were used for stimulation and to record evoked potentials. An additional concentric stimulation electrode was placed in the optic tract and in some experiments also in the optic radiation 5-8 mm from the lateral geniculate body. Glass micropipettes filled with 3 M potassium acetate were used to record extra- and intracellularly from principal cells. Recorded cells were classified as principal cells if they had typical concentric receptive fields 7, were excited monosynaptically from the optic tract and antidromically from the visual cortex. Fifty-eight principal cells were studied with respect to synaptic effects evoked by electrical stimulation of the visual cortex. Intracellular recordings were obtained from 33 cells, the remaining cells were studied only with an extracellular electrode position. The demonstration of direct corticofugal effects to the principal cells was complicated by the fact that cortex stimulation also evoked an antidromic spike and a recurrent IPSP in the cells 11. An illustrative example is shown in Fig. IA-C. The records in A were taken at threshold strength for antidromic activation of the cell. The prominent hyperpolarization in most traces is the postspike afterhyperpolarization, caused by the soma invasion of the spike. A small recurrent IPSP was evoked already at this intensity, as shown by the small hyperpolarization in the trace with spike failure. This IPSP grew with increasing stimulus strength as revealed by the prolongation of the hyperpolarization (B). Note in these records the small depolarization on the early phase of the hyperpolarization (arrow). This depolarization increased in amplitude when the stimulus intensity was further increased (C). There was no corresponding extracellular potential (lower trace in C). Further, the depolarization increased in amplitude when the cell was artificially hyperpolarized by current injection and decreased with depolarization, more than could be accounted for by the potential effect on the concomitant IPSP and afterhyperpolarization. Thus, it is concluded that the depolarization was a true EPSP, evoked by the cortex stimulation. It should be pointed out that the small amplitude of this EPSP is partly artifactual and due to the shunting effect of the recurrent IPSP and the afterhyperpolarization. It was possible to demonstrate similar EPSPs in all tested principal cells provided proper stimulation parameters were used (cf. below). The material included both 'on-center' and 'off-center' cells, with excitation from either X or Y retinal ganglion cells2,e. The latencies of the IPSPs and EPSPs could be measured rather accurately by superimposing traces taken at different stimulus intensities and before and after the cell was polarized beyond the reversal potential for the IPSP (not illustrated). The IPSPs had latencies, measured from the onset of the stimulus shock artefact, between 1.9 and 2.7 ms (Fig. IE), as demonstrated before it. The latencies of the EPSPs in the same cells were almost 1 ms longer (range 2.6-4.0 ms). Despite the long latency the EPSPs appeared to be evoked by a monosynaptic pathway. There was little change in latency of the EPSPs with repetitive activation or with changes in the stimulus intensity, as is usually the case for di- or polysynaptic pathways.
456
A
E
Noof cells ~
Cx 0.5 mA
~
[] tPSP [] EPSP n=55
I0
B
Cx 1.0 mA ¢,, F-/ZT////////, I
2.0
--l__ 1 !
5.0
I
I
latency 4 0 ms
C Cx 2.0 mA
D
~
latent 50 ..L
EPSP IPSP
_
2.0-
ON 2.0 rnA
1.0ec.
0 ms
• -
5 ms
~-
OR
I' relative Cx distonce
Fig. 1. Monosynaptic EPSPs in pricipal cells after electrical stimtflation of the visual cortex. The records in A-D show intracellular responses in a principal cell evoked by stimulation of the cortex (Cx; A-C) and the optic radiation (OR; D). The pair of records show the same response at two different sweep speeds. A: threshold strength for antidromic spike, B: supramaximal for recurrent IPSP; C: supramaximal for EPSP (arrow). D: supramaximal for optic radiation response. Lower traces in C, D show extracellular recordings (e.c.). Voltage calibration in D refers to all traces, time calibrations to respective column. E: latency histogram for IPSPs and EPSPs evoked in a group of intracellularly recorded principal cells by cortex stimulation. F: extrapolation procedure to estimate 'local' latencies of the EPSPs and IPSPs, further details in the text. A monosynaptic linkage for the EPSP was demonstrated in 12 cells (9 Y-type, 3 X-type) by the extrapolation procedure illustrated in Fig. IF. Similar synaptic responses were evoked from the electrodes in the cortex and in the:optic radiation (Fig. 1C, D). The latencies of these synaptic potentials were then plotted against the conduction distance. Assuming a constant conduction velocity for the activating fibers, related points were joined by a straight line and the 'local' latency at the geniculate level estimated by extrapolation. The 'local' latency of the EPSPs and IPSPs will be equal to the intercept with the ordinate, minus 0.2 ms representing the spike initiating time at the stimulus sites a,11. Since the fibers have a complicated course in the optic radiation, the conduction distances could not be measured directly in these experiments. Instead, the relative distances were calculated from the latency difference of the antidromic spike in a number of cells. This procedure gave synaptic latencies between 0.3 and 0.8 ms for the EPSPs, which clearly demonstrates that the EPSPs were mediated by a monosynaptic pathway to the principal cells. The 'local' latency for the IPSPs was 1.1-1.8 ms, as would be expected for a disynaptic recurrent inhibitory pathway 11.
457 The conduction velocity of the mediating fibers was estimated from the same plots, assuming a conduction distance of 18 mm. This gave conduction velocities between 5.5 and 9 m/s for the excitatory fibers. This is in excellent agreement with the anatomical finding that only the very thinnest myelinated fibers degenerate after cortex lesions9. The IPSPs were mediated by fibers having a conduction velocity of 18--60 m/s, which corresponds to the conduction velocity of antidromically activated principal cells. In view of the recent suggestion that some principal cells have interneuronal characteristicsa, it is worth pointing out that none of the recorded principal cells received EPSPs or IPSPs which could be assigned to direct connexions between antidromically activated principal cells. The EPSPs were evoked with lowest threshcld from the cortex electrode with minimal threshold intensity for antidromic activation of the cell. Usually the threshold was about 1.5-2 times higher for the EPSP than for the antidromic spike or recurrent IPSP. The rigid electrode arrangement used in the present study is not well suited for detailed threshold estimates, since the electrode position can be far from optimal. However, the low threshold electrode and required current intensity for the EPSP and antidromic spike varied together in a predictable way with the position of the cell's receptive field. This would be expected from the known retinotopical organization of the connexions between the geniculate and the cortex. Thus, the relatively high thresholds in Fig. 1A-C are explained by the cell having its receptive field about 10° from the vertical meridian. This cell would be expected to terminate 2-3 mm from the area 17-18 border, where the stimulation electrodes were placed. Cells with receptive fields close to the midline had thresholds for antidromic activation below 50 #A and below 100/tA for the EPSP, which dearly demonstrates that the excitatory pathway was stimulated in the visual cortex. However, it should be clear from this discussion that it is not possible to differentiate between fibers originating or terminating in area 17 or 18 by this method of stimulation. The projecting fibers run in the white matter and there may also be collateral connexions between these areas. In the present preparation it was never possible to activate the principal cell synaptically by single cortex stimuli at any strength. However, repetitive activation with short trains of 2-3 stimuli evoked bursts of spikes, presumably through some type of local cortical recruitment response. Confirming earlier reports 3, it was found that also intrageniculate interneurons were excited by cortex stimulation. Eighteen such cells, classified by their lack of antidromic activation from the cortex, were found intermixed with principal cells in laminae A and A1. In contrast to the principal cells the intrageniculate interneurons fired synaptically on single cortex stimuli, with a latency of 2.8-4.5 ms. Presumably the excitation of the intetneurons and the EPSPs in the principal cells were mediated by the same neuronal pathway - - most likely the cortico-geniculate fiber system. From the work by Schmielau and Singer 13 and the present result, it can be inferred that the cortico-geniculate system is organized in such a way that both the central response and the surround inhibition of principal cells are enhanced by activity in this feed-back pathway. The centre response is increased by the direct excitatory route to principal cells and the surround by excitation of the
458 i n t t a g e n i c u l a t e interneurons. This a r r a n g e m e n t m a y help to i m p r o v e the c o n t r a s t sensitivity o f the visual inflow to the cortex. I f so, the cortico-geniculate system m a y be a c t i v a t e d b y i n t r a c o r t i c a l m e c h a n i s m s in situations where the i n d i v i d u a l attends to difficult visual d i s c r i m i n a t i o n tasks. Such a function m a y explain the w e a k effect on p r i n c i p a l cell firing which has been f o u n d in studies with cortical cooling10,13 - - the c o r t i c o g e n i c u l a t e p a t h w a y m a y be little active in anesthetized p r e p a r a t i o n s . This investigation was s u p p o r t e d b y M a g n u s Bergvalls Stiftelse a n d the Swedish M e d i c a l R e s e a r c h Council (Project no. 4767).
1 Burke, W. and Sefton, A. J., Inhibitory mechanisms in lateral geniculate nucleus of rat, J. PhysioL (Lond.), 187 (1966) 231-246. 2 Cleland, B. G., Dubin, M. W. and Levick, W. R., Sustained and transient neurones in the cat's retina and lateral gcniculate nucleus, J. Physiol. (Lond.), 217 (1971) 473-496. 3 Dubin, M. W. and Cleland, B. G., Organization of visual inputs to interneurons of lateral geniculate nucleus of the cat, J. Neurophysiol., 40 (1977) 410--427. 4 Friedlander, M. J., Lin C.-S. and Sherman, S, M., Structure of physiologically identified X and Y cells in the cat's lateral geniculate nucleus, Science, 204 (1979) 1114-1117. 5 Gilbert, C. D. and Kelly, J. P., The projection of cells in different layers of the cat's visual cortex, J. comp. Neurol., 163 (1975) 81-106. 6 Hoffmann, K.-P., Stone, J. and Sherman, S. M., Relay of receptive field properties in dorsal lateral geniculate nucleus of the cat, J. Neurophysiol., 35 (1972) 518-53t. 7 Hubel, D. H. and Wiesel, T. N., Integrative action in the cat's lateral geniculate body, J. Physiol. (Lond.), 155 (1961) 385-398. 8 Jankowska, E. and Roberts, W. J., Synaptic actions of single interneurones mediating reciprocal Ia inhibition of motoneurones, J. PhysioL (Lond.), 222 (1972) 623-64Z 9 Jones, E. G, and Powell, T. P. S., An electron microscopic study of the mode of termination of cortico-thalamic fibres within the sensory relay nuclei of the thalamus, Proc. Roy. Soc. B, 172 (1969) 173-185. 10 Kalil, R. E. and Chase, R., Corticofugal influence on activity of lateral geniculate neurons in the cat, J. Neurophysiol., 33 (1970) 459-474. 11 Lindstrtim, S., Synaptic organization of inhibitory pathways to principal cells in the lateral geniculate nucleus of the cat, Brain Research, 234 (1982) 447-453. 12 Macchi, G. and Rinvik, E., Thalamo-telencephalic circuits: a neuroanatomical survey. In A. R6mond (Ed.), Handbook of Electroencephalography and Clinical Neurophysiology, Vol. 2, Part A, Elsevier, Amsterdam, 1976, pp. 86--133. 13 Schmielau, F. and Singer, W., The role of visual cortex for binocular interactions in the cat lateral geniculate nucleus, Brain Research, 120 (1977) 354-361. 14 Tsumoto, T., Creutzfeldt, O. D. and Leg6ndy, C. R., Functional organization of the corticofugal system from visual cortex to lateral geniculate nucleus in the cat (with an appendix on geniculocortical mono-synaptic connections), Exp. Brain Res., 32 (1978) 345-364. 15 Updyke, B. V., The patterns of projections of cortical areas 17, 18 and 19 onto the laminae of the dorsal lateral geniculate nucleus in the cat, J. comp. Neurol., 163 (1975) 377-396.
Brain Research, 234 (1982) 454-458 Elsevier Biomedical Press
Monosynaptic excitation of principal cells in the lateral geniculate nucleus by corticofugal fibers
G. AHLSEN, K. GRANT* and S. LINDSTROM Department of Physiology, University of Giiteborg, Giiteborg (Sweden) (Accepted November 19th, 1981) Key words: lateral geniculate nucleus - - principal cell - - cortico-geniculate fibers - - monosynaptic excitation
Electrical stimulation of the primary visual cortex evoked long latency EPSPs in X and Y principal cells of the cat's lateral genie,ulate nucleus. An extrapolation procedure:was used to reveal that these EPSPs were mediated monosynaptically to principal cells by slowly conducting corticogeniculate fibers. A similar type of excitation was observed in intrageniculate interneurons.
It has been demonstrated in a large number of anatomical studies that the lateral geniculate nucleus receives a prominent projection from the visual cortexrL The pathway is retinotopically organized 15 and originates from pyramidal cells in the VIth layer of the cortex 4. After lesions in area 17, degenerating terminals are found on thin dendrites which may belong to either principal cells or local interneurons. There is evidence that intrageniculate interneurons are activated by electrical stimulation of the visual cortex s, while principal cells are usually inhibited by such stimuli, presumably due to the concomitant activation of a recurrent inhibitory pathway 1,11. The recent reports that binocular facilitation of principal cells is eliminated by cortex cooling (ref. 13) and that intracortical glutamate injections may excite principal cells 14 implies, however, that also these cells m a y receive excitation by the cortico-geniculate route. In the present study intracellular recordings from principal cells have been used to test this possibility. The experiments were performed on cats kept under light sodium pentobarbital anesthesia (Nembutal, Abbott, 25-30 mg/kg). The animals were paralyzed with succinylcholine chloride (Celucurin, Vitrum, 15 mg/kg/h) and respirated artificially. Atropine and Neosynephrine (Winthrop Laboratories) were applied topically to dilate the pupils and retract the nictitating membranes, and the eyes were focused through appropriate contact lenses onto a tangent screen placed 1.5 m in front o f the animals. * Present address: Unit6 de Recherches Neurobiologiques (U6), INSERM, 280 Boul. Sainte-Marguerite, 13009 Marseille, France. 0006-8993/82/0000-0000/$02.75 © Elsevier Biomedical Press
455 Different patterns of light stimuli could be projected onto this screen with a hand-held slide projector. Seven fine tungsten electrodes were inserted 3--4 mm into the visual cortex in a row at the border between areas 17 and 18. These electrodes were used for stimulation and to record evoked potentials. An additional concentric stimulation electrode was placed in the optic tract and in some experiments also in the optic radiation 5-8 mm from the lateral geniculate body. Glass micropipettes filled with 3 M potassium acetate were used to record extra- and intracellularly from principal cells. Recorded cells were classified as principal cells if they had typical concentric receptive fields 7, were excited monosynaptically from the optic tract and antidromically from the visual cortex. Fifty-eight principal cells were studied with respect to synaptic effects evoked by electrical stimulation of the visual cortex. Intracellular recordings were obtained from 33 cells, the remaining cells were studied only with an extracellular electrode position. The demonstration of direct corticofugal effects to the principal cells was complicated by the fact that cortex stimulation also evoked an antidromic spike and a recurrent IPSP in the cells 11. An illustrative example is shown in Fig. IA-C. The records in A were taken at threshold strength for antidromic activation of the cell. The prominent hyperpolarization in most traces is the postspike afterhyperpolarization, caused by the soma invasion of the spike. A small recurrent IPSP was evoked already at this intensity, as shown by the small hyperpolarization in the trace with spike failure. This IPSP grew with increasing stimulus strength as revealed by the prolongation of the hyperpolarization (B). Note in these records the small depolarization on the early phase of the hyperpolarization (arrow). This depolarization increased in amplitude when the stimulus intensity was further increased (C). There was no corresponding extracellular potential (lower trace in C). Further, the depolarization increased in amplitude when the cell was artificially hyperpolarized by current injection and decreased with depolarization, more than could be accounted for by the potential effect on the concomitant IPSP and afterhyperpolarization. Thus, it is concluded that the depolarization was a true EPSP, evoked by the cortex stimulation. It should be pointed out that the small amplitude of this EPSP is partly artifactual and due to the shunting effect of the recurrent IPSP and the afterhyperpolarization. It was possible to demonstrate similar EPSPs in all tested principal cells provided proper stimulation parameters were used (cf. below). The material included both 'on-center' and 'off-center' cells, with excitation from either X or Y retinal ganglion cells2,e. The latencies of the IPSPs and EPSPs could be measured rather accurately by superimposing traces taken at different stimulus intensities and before and after the cell was polarized beyond the reversal potential for the IPSP (not illustrated). The IPSPs had latencies, measured from the onset of the stimulus shock artefact, between 1.9 and 2.7 ms (Fig. IE), as demonstrated before it. The latencies of the EPSPs in the same cells were almost 1 ms longer (range 2.6-4.0 ms). Despite the long latency the EPSPs appeared to be evoked by a monosynaptic pathway. There was little change in latency of the EPSPs with repetitive activation or with changes in the stimulus intensity, as is usually the case for di- or polysynaptic pathways.
456
A
E
Noof cells ~
Cx 0.5 mA
~
[] tPSP [] EPSP n=55
I0
B
Cx 1.0 mA ¢,, F-/ZT////////, I
2.0
--l__ 1 !
5.0
I
I
latency 4 0 ms
C Cx 2.0 mA
D
~
latent 50 ..L
EPSP IPSP
_
2.0-
ON 2.0 rnA
1.0ec.
0 ms
• -
5 ms
~-
OR
I' relative Cx distonce
Fig. 1. Monosynaptic EPSPs in pricipal cells after electrical stimtflation of the visual cortex. The records in A-D show intracellular responses in a principal cell evoked by stimulation of the cortex (Cx; A-C) and the optic radiation (OR; D). The pair of records show the same response at two different sweep speeds. A: threshold strength for antidromic spike, B: supramaximal for recurrent IPSP; C: supramaximal for EPSP (arrow). D: supramaximal for optic radiation response. Lower traces in C, D show extracellular recordings (e.c.). Voltage calibration in D refers to all traces, time calibrations to respective column. E: latency histogram for IPSPs and EPSPs evoked in a group of intracellularly recorded principal cells by cortex stimulation. F: extrapolation procedure to estimate 'local' latencies of the EPSPs and IPSPs, further details in the text. A monosynaptic linkage for the EPSP was demonstrated in 12 cells (9 Y-type, 3 X-type) by the extrapolation procedure illustrated in Fig. IF. Similar synaptic responses were evoked from the electrodes in the cortex and in the:optic radiation (Fig. 1C, D). The latencies of these synaptic potentials were then plotted against the conduction distance. Assuming a constant conduction velocity for the activating fibers, related points were joined by a straight line and the 'local' latency at the geniculate level estimated by extrapolation. The 'local' latency of the EPSPs and IPSPs will be equal to the intercept with the ordinate, minus 0.2 ms representing the spike initiating time at the stimulus sites a,11. Since the fibers have a complicated course in the optic radiation, the conduction distances could not be measured directly in these experiments. Instead, the relative distances were calculated from the latency difference of the antidromic spike in a number of cells. This procedure gave synaptic latencies between 0.3 and 0.8 ms for the EPSPs, which clearly demonstrates that the EPSPs were mediated by a monosynaptic pathway to the principal cells. The 'local' latency for the IPSPs was 1.1-1.8 ms, as would be expected for a disynaptic recurrent inhibitory pathway 11.
457 The conduction velocity of the mediating fibers was estimated from the same plots, assuming a conduction distance of 18 mm. This gave conduction velocities between 5.5 and 9 m/s for the excitatory fibers. This is in excellent agreement with the anatomical finding that only the very thinnest myelinated fibers degenerate after cortex lesions9. The IPSPs were mediated by fibers having a conduction velocity of 18--60 m/s, which corresponds to the conduction velocity of antidromically activated principal cells. In view of the recent suggestion that some principal cells have interneuronal characteristicsa, it is worth pointing out that none of the recorded principal cells received EPSPs or IPSPs which could be assigned to direct connexions between antidromically activated principal cells. The EPSPs were evoked with lowest threshcld from the cortex electrode with minimal threshold intensity for antidromic activation of the cell. Usually the threshold was about 1.5-2 times higher for the EPSP than for the antidromic spike or recurrent IPSP. The rigid electrode arrangement used in the present study is not well suited for detailed threshold estimates, since the electrode position can be far from optimal. However, the low threshold electrode and required current intensity for the EPSP and antidromic spike varied together in a predictable way with the position of the cell's receptive field. This would be expected from the known retinotopical organization of the connexions between the geniculate and the cortex. Thus, the relatively high thresholds in Fig. 1A-C are explained by the cell having its receptive field about 10° from the vertical meridian. This cell would be expected to terminate 2-3 mm from the area 17-18 border, where the stimulation electrodes were placed. Cells with receptive fields close to the midline had thresholds for antidromic activation below 50 #A and below 100/tA for the EPSP, which dearly demonstrates that the excitatory pathway was stimulated in the visual cortex. However, it should be clear from this discussion that it is not possible to differentiate between fibers originating or terminating in area 17 or 18 by this method of stimulation. The projecting fibers run in the white matter and there may also be collateral connexions between these areas. In the present preparation it was never possible to activate the principal cell synaptically by single cortex stimuli at any strength. However, repetitive activation with short trains of 2-3 stimuli evoked bursts of spikes, presumably through some type of local cortical recruitment response. Confirming earlier reports 3, it was found that also intrageniculate interneurons were excited by cortex stimulation. Eighteen such cells, classified by their lack of antidromic activation from the cortex, were found intermixed with principal cells in laminae A and A1. In contrast to the principal cells the intrageniculate interneurons fired synaptically on single cortex stimuli, with a latency of 2.8-4.5 ms. Presumably the excitation of the intetneurons and the EPSPs in the principal cells were mediated by the same neuronal pathway - - most likely the cortico-geniculate fiber system. From the work by Schmielau and Singer 13 and the present result, it can be inferred that the cortico-geniculate system is organized in such a way that both the central response and the surround inhibition of principal cells are enhanced by activity in this feed-back pathway. The centre response is increased by the direct excitatory route to principal cells and the surround by excitation of the
458 i n t t a g e n i c u l a t e interneurons. This a r r a n g e m e n t m a y help to i m p r o v e the c o n t r a s t sensitivity o f the visual inflow to the cortex. I f so, the cortico-geniculate system m a y be a c t i v a t e d b y i n t r a c o r t i c a l m e c h a n i s m s in situations where the i n d i v i d u a l attends to difficult visual d i s c r i m i n a t i o n tasks. Such a function m a y explain the w e a k effect on p r i n c i p a l cell firing which has been f o u n d in studies with cortical cooling10,13 - - the c o r t i c o g e n i c u l a t e p a t h w a y m a y be little active in anesthetized p r e p a r a t i o n s . This investigation was s u p p o r t e d b y M a g n u s Bergvalls Stiftelse a n d the Swedish M e d i c a l R e s e a r c h Council (Project no. 4767).
1 Burke, W. and Sefton, A. J., Inhibitory mechanisms in lateral geniculate nucleus of rat, J. PhysioL (Lond.), 187 (1966) 231-246. 2 Cleland, B. G., Dubin, M. W. and Levick, W. R., Sustained and transient neurones in the cat's retina and lateral gcniculate nucleus, J. Physiol. (Lond.), 217 (1971) 473-496. 3 Dubin, M. W. and Cleland, B. G., Organization of visual inputs to interneurons of lateral geniculate nucleus of the cat, J. Neurophysiol., 40 (1977) 410--427. 4 Friedlander, M. J., Lin C.-S. and Sherman, S, M., Structure of physiologically identified X and Y cells in the cat's lateral geniculate nucleus, Science, 204 (1979) 1114-1117. 5 Gilbert, C. D. and Kelly, J. P., The projection of cells in different layers of the cat's visual cortex, J. comp. Neurol., 163 (1975) 81-106. 6 Hoffmann, K.-P., Stone, J. and Sherman, S. M., Relay of receptive field properties in dorsal lateral geniculate nucleus of the cat, J. Neurophysiol., 35 (1972) 518-53t. 7 Hubel, D. H. and Wiesel, T. N., Integrative action in the cat's lateral geniculate body, J. Physiol. (Lond.), 155 (1961) 385-398. 8 Jankowska, E. and Roberts, W. J., Synaptic actions of single interneurones mediating reciprocal Ia inhibition of motoneurones, J. PhysioL (Lond.), 222 (1972) 623-64Z 9 Jones, E. G, and Powell, T. P. S., An electron microscopic study of the mode of termination of cortico-thalamic fibres within the sensory relay nuclei of the thalamus, Proc. Roy. Soc. B, 172 (1969) 173-185. 10 Kalil, R. E. and Chase, R., Corticofugal influence on activity of lateral geniculate neurons in the cat, J. Neurophysiol., 33 (1970) 459-474. 11 Lindstrtim, S., Synaptic organization of inhibitory pathways to principal cells in the lateral geniculate nucleus of the cat, Brain Research, 234 (1982) 447-453. 12 Macchi, G. and Rinvik, E., Thalamo-telencephalic circuits: a neuroanatomical survey. In A. R6mond (Ed.), Handbook of Electroencephalography and Clinical Neurophysiology, Vol. 2, Part A, Elsevier, Amsterdam, 1976, pp. 86--133. 13 Schmielau, F. and Singer, W., The role of visual cortex for binocular interactions in the cat lateral geniculate nucleus, Brain Research, 120 (1977) 354-361. 14 Tsumoto, T., Creutzfeldt, O. D. and Leg6ndy, C. R., Functional organization of the corticofugal system from visual cortex to lateral geniculate nucleus in the cat (with an appendix on geniculocortical mono-synaptic connections), Exp. Brain Res., 32 (1978) 345-364. 15 Updyke, B. V., The patterns of projections of cortical areas 17, 18 and 19 onto the laminae of the dorsal lateral geniculate nucleus in the cat, J. comp. Neurol., 163 (1975) 377-396.