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Pyramidal influences on ventral thalamic nuclei in the cat
254
Brain Research, 279 (1983) 254-257 Elsevier
Pyramidal influences on ventral thalamic nuclei in the cat ROSARIO GIUFFRIDA l, GUIDO LI VOLSI 1, MARIA ROSITA PANT(31 , VINCENCO PERCIAVALLE l and ANTONIO URBANO 2 tlnstitute of Human Physiology, University of Catania, Viale Andrea Doria, 6-95125 Catania and 22nd Institute of Human Physiology, University of Rome, Citt6 Universitaria, 00185 Rome (Italy)
(Accepted July 26th, 1983) Key words: pyramidal tract - - thalamus - - ventrobasal complex - - ventroanterior nucleus - ventrolateral nucleus - - ventromedial nucleus - - cats
In pericruciate cortex-ablated 'pyramidal cats', discharge changes in single neurons of ventral thalamic nuclei were studied, following stimulation of ipsilateral medullary (MPT) and contralateral cervical (CPT) pyramidal tract. It was seen that cells in ventrolateral nucleus, ventroanterior nucleus and ventromedial nucleus were not significantly (2.2%) modified by impulses coming from MPT and CPT. Conversely, a very high percentage (58.8%) of cells in ventrobasal complex (VB) responded to MPT stimulation (64.4% in ventroposterolateral nucleus, VPL, and 40.7% in ventroposteromedial nucleus, VPM), A considerable number (34.8%) of VPL cells responsive to MPT, were influenced by CPT, while none of the cells in VPM were. The most frequent effect observed in VB neurons, on MPT and CPT stimulation, was excitation followed by depression of discharge. Pyramidal tract (PT) collaterals to ventral thalamic nuclei have been electrophysiologically studied from discharge changes p r o d u c e d in single ventrobasal (VB) neurons upon activation of medullary PT (MPT), in cats with neuraxis intact 12, as well as from antidromic firing in PT neurons following stimulation of putative sites, stereotaxically d e t e r m i n e d , in ventroanterior ( V A ) , ventrolateral (VL) and ventroposterolateral (VPL) nuclei 4. It was seen that VB neurons were monosynaptically modified by MPT, and PT neurons were antidromically activated from V A , VL and VPL. A recent study by means of multiple fluorescent tracers has denied, however, a pyramidal collateral input to these nuclei I . The present experiments were u n d e r t a k e n to electrophysiologically reinvestigate this problem. With this objective, discharge changes p r o d u c e d in ventral thalamic neurons by pyramidal volleys backfired from M P T and cervical PT (CPT) were studied. Contamination of medial lemniscus (ML), and/or other ascending pathways, and trans-corticocerebrat reverberation of antidromic impulses could be excluded since brainstem transection, sparing the cerebral peduncles ( ' p y r a m i d a l cats') 11, and pericruciate cortex ablation were carried out. Preliminary accounts of the present results have (1(X)6-8993/83/$03.00 © 1983 Elsevier Science Publishers B.V.
been given previously 5. Twenty-one cats, weighing between 2.5 and 4 kg, were used. Brainstem transection sparing the cerebral peduncles was p e r f o r m e d , by means of coagulation, under gaseous anesthesia (40% 0 2, 60% N O 2, s u p p l e m e n t e d with 1-1.5% halothane). Coagulating lesions (500 kHz, 60 m A for 50 s) were m a d e in frontal plane 3.0 (cf. atlas of Jasper and A i m o n e - M a r san8), along the vertical axis, every 4 mm between planes H + 2 and - - 6 , and 1.5 mm between planes L 1.0 and 7.5 through n i c k e l - c h r o m e wires insulated up to 6 mm from the tips. The pericruciate cortex, including parts of coronal and ectosylvian gyri, was ablated by means of suction, to a depth of about 5 mm, on the side of the thalamic recordings. The rectal t e m p e r a t u r e was maintained at 37-38 °C with a heating pad. The heart rate was monitored. The recordings began 2-3 h after decerebration. Extracellular unitary spikes were recorded with tungsten microelectrodes having 4-8 Mr2 resistance. The thalamic regions explored were enclosed between planes Fr 7.0-12.0, L 1.0--9.0 and H + 6.0 to --2.08. The recording electrodes were stereotaxically inserted along the vertical axis, the indifferent electrode being a screw positioned in the skull. Action potentials arising from cells somata were those
255 which appeared initially negative-positive and then, as the electrode advanced, positive-negative with a clear inflexion on the ascending limb of the positive phaseT; their duration was above 0.8 ms. At the end of each electrode penetration, a small electrolytic reference lesion was performed by applying a 15/~A cathodal current for 15 s. Ipsilateral MPT and contralateral CPT (C1-C2) were activated with monopolar nickel-chrome electrodes (0.5-1 Mr2 resistance), insulated up to 60-80/~m from the tips. The indifferent electrode (Ag-AgC1) was positioned at face or neck muscles. MPT stimulation was carried out at the level of the lower medulla (P 11.5, L 0.9 and H --10.3; cf. atlas of Verhaart13), with 1-5 cathodal shocks (0.05-0.2 ms, 100-700 Hz, 100 ktA) delivered at intervals of 1-3 s. Stimuli delivered to CPT were similar to those delivered to MPT. Electrode position in MPT and CPT was checked from motor effects elicited in limbs (contralateral and ipsilateral, respectively) with 50 ms trains of 300 Hz pulses (80 #A) z. After completion of observations, the stimulating sites were marked and the animals were perfused with fixative under deep barbiturate anesthesia. Reconstructions of electrode penetrations were made on frontal sections of 50--60 a m thickness, stained according to Kliiver-Barrera's technique 9. Quantitative analysis of unitary discharges was done as reported elsewhere 6. Normally, 60 responses were converted into post-stimulus time histograms and cumulative frequency distributions. Excitatory and inhibitory responses were sequences of at least 3 bins, which showed frequency values of more then twice standard deviation (S.D.) above or below the
mean value during spontaneous activity. Solitary bins between these sequences were not considered. Latency was the time interval between the last shock of the stimulating train and the first bin of the sequence, and duration was the distance between the first and the last bin (0.1 and 2 ms bins). Response intensity (r) was calculated from the ratio of the number of the spikes recorded in an equal time interval during evoked (E) and spontaneous (S) sequences (r = E/S for excitations and S/E for inhibitions), using the method described by Neafsey et a1.10. Table I lists the number of cells recorded in different ventral thalamic nuclei, and the number and percentage (between brackets) of cells which were transynaptically influenced, in each nucleus, from stimulations of MPT and/or CPT. Of the 764 cells recorded in VA, VL and VM, 17 cells (2.2%) responded to MPT and no cell to CPT. On the contrary, 134/228 (58.8%) of the VB cells were influenced from MPT (64.4% and 40.7% of the examined cells in VPL and VPM, respectively). None of the VPM cells responsive to MPT displayed discharge changes following CPT stimulation, versus 39 cells (34.8%) in VPL that responded to MPT and CPT. Responses to only CPT were observed in 4 VPL cells. VA, VL and VM cells responded to MPT stimulation (4-5 shock, 200-300 Hz, 100/~A) with simple excitation (r, 6.5-11.2; duration, 6--15 ms), excitation followed by a period of depression (r, 7.7-15.3; duration; 28-75 ms), or pure inhibition (r, 6.1 and 16.5; duration, 78 and 125 ms). Excitation had a latency between 4 and 11 ms and early inhibition between 5 and 10 ms. The most frequent pattern of response observed in
TABLE I Number o f cells examined in different ventral thalamic nuclei, and number and incidence (percentage in parentheses), in each nucleus, o f cells influenced from medullary (MPT) and cervical pyramidal tract (CPT) stimulation.
Abbreviations: VA, ventroanterior nucleus; VL, ventrolateral nucleus; VM, ventromedial nucleus; VPL, ventroposterolateral nucleus; VPM, ventroposteromedial nucleus. VA (n = 257)
VL (n = 410)
VM (n = 97)
VPL (n = 174)
VPM (n = 54)
MPT + CPT
4 (1.6%) 0
12 (2.9%) 0
1 (1%) 0
22 (40.7%) 0
CPT
0
0
0
73 (41.9%) 39 (22.4%) 4
MPT
(2.3%)
0
256 MPT
CPT
2o!
16 F-'l Ex In
o)
~ a Z 4
0 8
12
16
20
24
Latency
.
! 4
, 8
.
, ., ' - ' ~ . 12 16
, 20
'
,_ 24
(rnsec)
Fig. 1. Histograms showing distributions of excitation, pure or followed by discharge depression, and inhibition, displayed by VB cells, following medullary (MPT) and cervical pyramidal tract (CPT) stimulation. Abbreviations: Ex, excited cells; In, inhibited cells. VB cells following stimulation of MPT (52.9%) and CPT (51.2%) was excitation (r, 12.3-28.5; duration, 7-21 ms) followed by discharge depression (r, 8.3-15.6; duration, 15-85 ms). In the remaining cases stimulation of MPT and CPT produced pure excitation or inhibition, or inhibition followed by excitatory rebound. Latency of excitation and inhibition, pure or followed by opposite change of discharge, is illustrated by the diagrams of Fig. 1. Following MPT stimulation, 71% of VB cells displayed excitation with latencies above 5-6 ms. The modal value of latency was 4-5 ms (mean value, 9.1 ms + 4.49 S.D.), while inhibition had a modal value of 8--9 ms (mean value, 10.1 ms + 3.85 S.D.). Responses to activation of CPT displayed latencies slightly higher (excitation, 9.7 ms +_ 2.86 S.D.; inhibition, 11.4 ms +
3.88 S.D.).
From a functional point of view, this finding, which agrees with histological results from Catsman-Berrevoets and Kuypersl, indicates that these ventral thalamic nuclei do not significantly receive 'efferent copy' of the motor c o m m a n d transmitted by pyramidal axons to their ultimate terminations. Pyramidal influences over sensory transmission in the thalamus 12 could be, instead, effective, as resulting from the high number (138/228) of VB cells modified by MPT and/or CPT stimulation in this study. None of the VPM cells were influenced by CPT, while many of the VPL cells (39/174) were modified by MPT as well CPT. Conceivably, corticospinal neurons could modulate the activity of VB cells which transmit spinal signals to the cerebral cortex, and corticobulbar neurons could influence the discharge of VB cells which relay sensory impulses of supraspinal origin. The effects of pyramidal stimulation upon VB cells, described in this study, were exerted in 71% of the cases at latencies above 5-6 ms, the majority of cells being excited and/or inhibited at latencies longer than 8 ms (see Fig. 1). The distance from stimulating sites within MPT to recording loci in VB was about 20-22 ram. Previous studies have demonstrated that a conspicuous (38%) contingent of PT fibers are unmyelinated3. However, the difference in the latency of excitatory responses induced in VB cells from MPT and CPT (distance between stimulating sites: 10-12 mm), was too low (0.6 ms) to involve unmyelinated PT fibers. Thus, the pyramidal influences on VB would be mediated by other thalamic or extrathalamic structures, and/or by internuncial cells in VB itself, The histological observations of CatsmanBerrevoets and Kuyperst would lead on the first hypothesis.
This electrophysiological study in 'pyramidal preparations' shows that a very low number (2.2%) of VA, VL and VM cells were influenced by impulses transmitted through pyramidal axon collaterals.
Financial support was obtained from the Consiqlio Nazionale delle Ricerche.
l Catsman-Berrevoets, C. E. and Kuypers, H. G. J, M., A search for corticospinal collaterals to thalamus and mesencephalon by means of multiple retrograde and fluorescent tracers in cat and rat, Brain Research, 218 (1981) 15-33. 2 Cioni, M., Perciavalle, V., Santangelo, F., Sapienza, S. and Urbano, A., Motor responses to microstimulation of the medullary pyramidal tract in the cat, Exp. Neurol., 61 (1978) 664-679. 3 De Meyer, W. and Russel, J., The number of axons in the right and left medullary pyramids of macaca rhesus and the
ratio of axons to myelin sheaths, Acta morph, neerl, scand., 2 (1958) 134-139. 4 Endo, K,, Araki, T. and Yagi, N., The distribution of pattern of axon branching of pyramidal tract cells, Brain Research, 57 (1973) 484-491. 5 Giuffrida, R., Li Volsi, G., Pant6, M. R., Perciavalle, V. and Urbano, A., Pyramidal tract influences on single neurons of ventral thalamic nuclei in the cat, Proc. XXVIII int. Congr. Physiol. Sci., Budapest, 1980, com. n. 1552. 6 Giuffrida, R., Li Volsi, G., Perciavalle, V., Santangelo, F.
257
7
8
9
10
and Urbano, A., Influences of precerebellar systems triggering movement on single cells of the interpositus nucleus of the cat, Neuroscience, 6 (1981) 1625-1631. Hubel, D. H., Single unit activity in lateral geniculate body and optic tract of unrestrained cats, J. Physiol. (Lond.), 150 (1960) 91-104. Jasper, H. H. J. and Aimone-Marsan, C., A StereotaxicAtlas of the Diencephalon of the Cat, The National Research Council of Canada, Ottawa, 1954. Kliiver, H. and Barrera, E., A method for combined staining of cells and fibres in the nervous system, J. Neuropathol. exp. Neurol., 12 (1953) 400--403. Neafsey, E. J., Hull, C. D. and Buchwald, N. A., Prepara-
tion for movement in the cat. I. Unit activity in the cerebral cortex, Electroenceph. clin. Neurophysiol., 44 (1978) 706--713. 11 Preston, J. B. and Whitlock, D. G., Precentral facilitation and inhibition of spinal motoneurons, J. Neurophysiol., 23 (1960) 154-170. 12 Tsumoto, T., Nakamura, S. and Iwama, K., Pyramidal tract control over cutaneous and kinestetic sensory transmission in the cat thalamus, Exp. Brain Res., 22 (1975) 281-294. 13 Verhaart, W. J. C., A Stereotactic Atlas of the Brain Stem of the Cat, Van Gorcum, Assen, 1964.
Brain Research, 279 (1983) 254-257 Elsevier
Pyramidal influences on ventral thalamic nuclei in the cat ROSARIO GIUFFRIDA l, GUIDO LI VOLSI 1, MARIA ROSITA PANT(31 , VINCENCO PERCIAVALLE l and ANTONIO URBANO 2 tlnstitute of Human Physiology, University of Catania, Viale Andrea Doria, 6-95125 Catania and 22nd Institute of Human Physiology, University of Rome, Citt6 Universitaria, 00185 Rome (Italy)
(Accepted July 26th, 1983) Key words: pyramidal tract - - thalamus - - ventrobasal complex - - ventroanterior nucleus - ventrolateral nucleus - - ventromedial nucleus - - cats
In pericruciate cortex-ablated 'pyramidal cats', discharge changes in single neurons of ventral thalamic nuclei were studied, following stimulation of ipsilateral medullary (MPT) and contralateral cervical (CPT) pyramidal tract. It was seen that cells in ventrolateral nucleus, ventroanterior nucleus and ventromedial nucleus were not significantly (2.2%) modified by impulses coming from MPT and CPT. Conversely, a very high percentage (58.8%) of cells in ventrobasal complex (VB) responded to MPT stimulation (64.4% in ventroposterolateral nucleus, VPL, and 40.7% in ventroposteromedial nucleus, VPM), A considerable number (34.8%) of VPL cells responsive to MPT, were influenced by CPT, while none of the cells in VPM were. The most frequent effect observed in VB neurons, on MPT and CPT stimulation, was excitation followed by depression of discharge. Pyramidal tract (PT) collaterals to ventral thalamic nuclei have been electrophysiologically studied from discharge changes p r o d u c e d in single ventrobasal (VB) neurons upon activation of medullary PT (MPT), in cats with neuraxis intact 12, as well as from antidromic firing in PT neurons following stimulation of putative sites, stereotaxically d e t e r m i n e d , in ventroanterior ( V A ) , ventrolateral (VL) and ventroposterolateral (VPL) nuclei 4. It was seen that VB neurons were monosynaptically modified by MPT, and PT neurons were antidromically activated from V A , VL and VPL. A recent study by means of multiple fluorescent tracers has denied, however, a pyramidal collateral input to these nuclei I . The present experiments were u n d e r t a k e n to electrophysiologically reinvestigate this problem. With this objective, discharge changes p r o d u c e d in ventral thalamic neurons by pyramidal volleys backfired from M P T and cervical PT (CPT) were studied. Contamination of medial lemniscus (ML), and/or other ascending pathways, and trans-corticocerebrat reverberation of antidromic impulses could be excluded since brainstem transection, sparing the cerebral peduncles ( ' p y r a m i d a l cats') 11, and pericruciate cortex ablation were carried out. Preliminary accounts of the present results have (1(X)6-8993/83/$03.00 © 1983 Elsevier Science Publishers B.V.
been given previously 5. Twenty-one cats, weighing between 2.5 and 4 kg, were used. Brainstem transection sparing the cerebral peduncles was p e r f o r m e d , by means of coagulation, under gaseous anesthesia (40% 0 2, 60% N O 2, s u p p l e m e n t e d with 1-1.5% halothane). Coagulating lesions (500 kHz, 60 m A for 50 s) were m a d e in frontal plane 3.0 (cf. atlas of Jasper and A i m o n e - M a r san8), along the vertical axis, every 4 mm between planes H + 2 and - - 6 , and 1.5 mm between planes L 1.0 and 7.5 through n i c k e l - c h r o m e wires insulated up to 6 mm from the tips. The pericruciate cortex, including parts of coronal and ectosylvian gyri, was ablated by means of suction, to a depth of about 5 mm, on the side of the thalamic recordings. The rectal t e m p e r a t u r e was maintained at 37-38 °C with a heating pad. The heart rate was monitored. The recordings began 2-3 h after decerebration. Extracellular unitary spikes were recorded with tungsten microelectrodes having 4-8 Mr2 resistance. The thalamic regions explored were enclosed between planes Fr 7.0-12.0, L 1.0--9.0 and H + 6.0 to --2.08. The recording electrodes were stereotaxically inserted along the vertical axis, the indifferent electrode being a screw positioned in the skull. Action potentials arising from cells somata were those
255 which appeared initially negative-positive and then, as the electrode advanced, positive-negative with a clear inflexion on the ascending limb of the positive phaseT; their duration was above 0.8 ms. At the end of each electrode penetration, a small electrolytic reference lesion was performed by applying a 15/~A cathodal current for 15 s. Ipsilateral MPT and contralateral CPT (C1-C2) were activated with monopolar nickel-chrome electrodes (0.5-1 Mr2 resistance), insulated up to 60-80/~m from the tips. The indifferent electrode (Ag-AgC1) was positioned at face or neck muscles. MPT stimulation was carried out at the level of the lower medulla (P 11.5, L 0.9 and H --10.3; cf. atlas of Verhaart13), with 1-5 cathodal shocks (0.05-0.2 ms, 100-700 Hz, 100 ktA) delivered at intervals of 1-3 s. Stimuli delivered to CPT were similar to those delivered to MPT. Electrode position in MPT and CPT was checked from motor effects elicited in limbs (contralateral and ipsilateral, respectively) with 50 ms trains of 300 Hz pulses (80 #A) z. After completion of observations, the stimulating sites were marked and the animals were perfused with fixative under deep barbiturate anesthesia. Reconstructions of electrode penetrations were made on frontal sections of 50--60 a m thickness, stained according to Kliiver-Barrera's technique 9. Quantitative analysis of unitary discharges was done as reported elsewhere 6. Normally, 60 responses were converted into post-stimulus time histograms and cumulative frequency distributions. Excitatory and inhibitory responses were sequences of at least 3 bins, which showed frequency values of more then twice standard deviation (S.D.) above or below the
mean value during spontaneous activity. Solitary bins between these sequences were not considered. Latency was the time interval between the last shock of the stimulating train and the first bin of the sequence, and duration was the distance between the first and the last bin (0.1 and 2 ms bins). Response intensity (r) was calculated from the ratio of the number of the spikes recorded in an equal time interval during evoked (E) and spontaneous (S) sequences (r = E/S for excitations and S/E for inhibitions), using the method described by Neafsey et a1.10. Table I lists the number of cells recorded in different ventral thalamic nuclei, and the number and percentage (between brackets) of cells which were transynaptically influenced, in each nucleus, from stimulations of MPT and/or CPT. Of the 764 cells recorded in VA, VL and VM, 17 cells (2.2%) responded to MPT and no cell to CPT. On the contrary, 134/228 (58.8%) of the VB cells were influenced from MPT (64.4% and 40.7% of the examined cells in VPL and VPM, respectively). None of the VPM cells responsive to MPT displayed discharge changes following CPT stimulation, versus 39 cells (34.8%) in VPL that responded to MPT and CPT. Responses to only CPT were observed in 4 VPL cells. VA, VL and VM cells responded to MPT stimulation (4-5 shock, 200-300 Hz, 100/~A) with simple excitation (r, 6.5-11.2; duration, 6--15 ms), excitation followed by a period of depression (r, 7.7-15.3; duration; 28-75 ms), or pure inhibition (r, 6.1 and 16.5; duration, 78 and 125 ms). Excitation had a latency between 4 and 11 ms and early inhibition between 5 and 10 ms. The most frequent pattern of response observed in
TABLE I Number o f cells examined in different ventral thalamic nuclei, and number and incidence (percentage in parentheses), in each nucleus, o f cells influenced from medullary (MPT) and cervical pyramidal tract (CPT) stimulation.
Abbreviations: VA, ventroanterior nucleus; VL, ventrolateral nucleus; VM, ventromedial nucleus; VPL, ventroposterolateral nucleus; VPM, ventroposteromedial nucleus. VA (n = 257)
VL (n = 410)
VM (n = 97)
VPL (n = 174)
VPM (n = 54)
MPT + CPT
4 (1.6%) 0
12 (2.9%) 0
1 (1%) 0
22 (40.7%) 0
CPT
0
0
0
73 (41.9%) 39 (22.4%) 4
MPT
(2.3%)
0
256 MPT
CPT
2o!
16 F-'l Ex In
o)
~ a Z 4
0 8
12
16
20
24
Latency
.
! 4
, 8
.
, ., ' - ' ~ . 12 16
, 20
'
,_ 24
(rnsec)
Fig. 1. Histograms showing distributions of excitation, pure or followed by discharge depression, and inhibition, displayed by VB cells, following medullary (MPT) and cervical pyramidal tract (CPT) stimulation. Abbreviations: Ex, excited cells; In, inhibited cells. VB cells following stimulation of MPT (52.9%) and CPT (51.2%) was excitation (r, 12.3-28.5; duration, 7-21 ms) followed by discharge depression (r, 8.3-15.6; duration, 15-85 ms). In the remaining cases stimulation of MPT and CPT produced pure excitation or inhibition, or inhibition followed by excitatory rebound. Latency of excitation and inhibition, pure or followed by opposite change of discharge, is illustrated by the diagrams of Fig. 1. Following MPT stimulation, 71% of VB cells displayed excitation with latencies above 5-6 ms. The modal value of latency was 4-5 ms (mean value, 9.1 ms + 4.49 S.D.), while inhibition had a modal value of 8--9 ms (mean value, 10.1 ms + 3.85 S.D.). Responses to activation of CPT displayed latencies slightly higher (excitation, 9.7 ms +_ 2.86 S.D.; inhibition, 11.4 ms +
3.88 S.D.).
From a functional point of view, this finding, which agrees with histological results from Catsman-Berrevoets and Kuypersl, indicates that these ventral thalamic nuclei do not significantly receive 'efferent copy' of the motor c o m m a n d transmitted by pyramidal axons to their ultimate terminations. Pyramidal influences over sensory transmission in the thalamus 12 could be, instead, effective, as resulting from the high number (138/228) of VB cells modified by MPT and/or CPT stimulation in this study. None of the VPM cells were influenced by CPT, while many of the VPL cells (39/174) were modified by MPT as well CPT. Conceivably, corticospinal neurons could modulate the activity of VB cells which transmit spinal signals to the cerebral cortex, and corticobulbar neurons could influence the discharge of VB cells which relay sensory impulses of supraspinal origin. The effects of pyramidal stimulation upon VB cells, described in this study, were exerted in 71% of the cases at latencies above 5-6 ms, the majority of cells being excited and/or inhibited at latencies longer than 8 ms (see Fig. 1). The distance from stimulating sites within MPT to recording loci in VB was about 20-22 ram. Previous studies have demonstrated that a conspicuous (38%) contingent of PT fibers are unmyelinated3. However, the difference in the latency of excitatory responses induced in VB cells from MPT and CPT (distance between stimulating sites: 10-12 mm), was too low (0.6 ms) to involve unmyelinated PT fibers. Thus, the pyramidal influences on VB would be mediated by other thalamic or extrathalamic structures, and/or by internuncial cells in VB itself, The histological observations of CatsmanBerrevoets and Kuyperst would lead on the first hypothesis.
This electrophysiological study in 'pyramidal preparations' shows that a very low number (2.2%) of VA, VL and VM cells were influenced by impulses transmitted through pyramidal axon collaterals.
Financial support was obtained from the Consiqlio Nazionale delle Ricerche.
l Catsman-Berrevoets, C. E. and Kuypers, H. G. J, M., A search for corticospinal collaterals to thalamus and mesencephalon by means of multiple retrograde and fluorescent tracers in cat and rat, Brain Research, 218 (1981) 15-33. 2 Cioni, M., Perciavalle, V., Santangelo, F., Sapienza, S. and Urbano, A., Motor responses to microstimulation of the medullary pyramidal tract in the cat, Exp. Neurol., 61 (1978) 664-679. 3 De Meyer, W. and Russel, J., The number of axons in the right and left medullary pyramids of macaca rhesus and the
ratio of axons to myelin sheaths, Acta morph, neerl, scand., 2 (1958) 134-139. 4 Endo, K,, Araki, T. and Yagi, N., The distribution of pattern of axon branching of pyramidal tract cells, Brain Research, 57 (1973) 484-491. 5 Giuffrida, R., Li Volsi, G., Pant6, M. R., Perciavalle, V. and Urbano, A., Pyramidal tract influences on single neurons of ventral thalamic nuclei in the cat, Proc. XXVIII int. Congr. Physiol. Sci., Budapest, 1980, com. n. 1552. 6 Giuffrida, R., Li Volsi, G., Perciavalle, V., Santangelo, F.
257
7
8
9
10
and Urbano, A., Influences of precerebellar systems triggering movement on single cells of the interpositus nucleus of the cat, Neuroscience, 6 (1981) 1625-1631. Hubel, D. H., Single unit activity in lateral geniculate body and optic tract of unrestrained cats, J. Physiol. (Lond.), 150 (1960) 91-104. Jasper, H. H. J. and Aimone-Marsan, C., A StereotaxicAtlas of the Diencephalon of the Cat, The National Research Council of Canada, Ottawa, 1954. Kliiver, H. and Barrera, E., A method for combined staining of cells and fibres in the nervous system, J. Neuropathol. exp. Neurol., 12 (1953) 400--403. Neafsey, E. J., Hull, C. D. and Buchwald, N. A., Prepara-
tion for movement in the cat. I. Unit activity in the cerebral cortex, Electroenceph. clin. Neurophysiol., 44 (1978) 706--713. 11 Preston, J. B. and Whitlock, D. G., Precentral facilitation and inhibition of spinal motoneurons, J. Neurophysiol., 23 (1960) 154-170. 12 Tsumoto, T., Nakamura, S. and Iwama, K., Pyramidal tract control over cutaneous and kinestetic sensory transmission in the cat thalamus, Exp. Brain Res., 22 (1975) 281-294. 13 Verhaart, W. J. C., A Stereotactic Atlas of the Brain Stem of the Cat, Van Gorcum, Assen, 1964.