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At least 19 recordsLinked to original sources
PubMed1983

Pyramidal influences on ventral thalamic nuclei in the cat.

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.

Animals↗
PubMed1986

Topographical organization of frontal association cortex afferents originating in ventral thalamic nuclei in dog brain.

The frontal associatron cortex involves the prefrontal (PFC) and premotor (PMC) areas which are reached by projections originating in the ventral medial (VM), ventral anterior (VA) and ventral lateral (VL) thalamic nuclei. Afferents arising in particular thalamic nuclei cover various PFC-PMC regions. On the basis of afferents distribution three territories can be distinguished in this cortex. The first or ventral territory involving ventral and ventrolateral PFC (subgenual, subproreal and orbital, paraorbital areas) is reached only by VM afferents. In the second, dorsal PFC territory (proreal and medial precruciate areas) afferents originated in VM and VA thalamic nuclei terminate. The third cortical territory, involving the extreme caudal belt of the frontal association cortex (dorsal and posterior precruciatal region as well as the anterior composite area of the lateral presylvian wall), is reached by VM, VA and VL projections. The density of these projections increases in the caudal direction. VM and VA afferents are concentrated in the medial precruciate PFC-PMC area, whereas VL afferent in the dorsal PMC and fissural region.

Afferent Pathways↗
PubMed1985

Cortical and brain stem afferents to the ventral thalamic nuclei of the cat demonstrated by retrograde axonal transport of horseradish peroxidase.

After horseradish peroxidase (HRP) injections into various parts of the ventral thalamic nuclear group and its adjacent areas, the distribution of labeled neurons was compared in the cerebral cortex, basal ganglia, and the brain stem. The major differences in distribution patterns were as follows: Injections of HRP into the lateral or ventrolateral portions of the ventroanterior and ventrolateral nuclear complex of the thalamus (VA-VL) produced retrogradely labeled neurons consistently in area 4 gamma (lateral part of the anterior and posterior sigmoid gyri, lateral sigmoid gyrus and the lateral fundus of the cruciate sulcus), the medial division of posterior thalamic group (POm), suprageniculate nucleus (SG) and anterior pretectal nucleus ipsilaterally, and in the nucleus Z of the vestibular nuclear complex bilaterally. Injections into the medial or dorsomedial portion of the VA-VL resulted in labeled neurons within the areas 6a beta (medial part of the anterior sigmoid gyrus), 6a delta (anterior part of ventral bank of buried cruciate sulcus), 6 if. fu (posterior part of the bank), fundus of the presylvian sulcus (area 6a beta), medial part of the nucleus lateralis posterior of thalamus and nucleus centralis dorsalis ipsilaterally, and in the entopeduncular nucleus (EPN) and medial pretectal nucleus bilaterally. Only a few neurons were present in the contralateral area 6a delta. After HRP injections into the ventral medial nucleus (VM), major labeled neurons were observed in the gyrus proreus, area 6a beta (mainly in the medial bank of the presylvian sulcus), and EPN ipsilaterally, and in the medial pretectal nucleus and substantia nigra bilaterally. Following HRP injections into the centre médian nucleus (CM), major labeled neurons were found in the areas 4 gamma, 6a beta, and the orbital gyrus ipsilaterally, and in the EPN, rostral and rostrolateral parts of the thalamic reticular nucleus, locus ceruleus, nucleus reticularis pontis oralis et caudalis and nucleus prepositus hypoglossi bilaterally. The contralateral intercalatus nucleus also possessed labeled neurons. With HRP injections into the paracentral and centrolateral nuclei, labeled neurons were observed in the gyrus proreus and the cortical areas between the caudal presylvian sulcus and anterior rhinal sulcus ipsilaterally, and in the nuclei interstitialis and Darkschewitsch bilaterally. Minor differences in the distribution pattern were observed in the superior colliculus, periaqueductal gray, mesencephalic and medullary reticular formations, and vestibular nuclei in all cases of injections.

Afferent Pathways↗
PubMed1996

Distribution of AT4 receptors in the Macaca fascicularis brain.

Angiotensin IV (Val Tyr Ile His Pro Phe), administered centrally, increases memory retrieval and induces c-fos expression in the hippocampus and piriform cortex. Angiotensin IV binds to a high affinity site that is quite distinct in pharmacology and distribution from the angiotensin II AT1 and AT2 receptors and is known as the AT4 receptor. These observations suggest that the AT4 receptor may have multiple central effects. The present study uses in vitro receptor autoradiography, and employs [125I]angiotensin IV to map AT4 receptors in the macaca fascicularis brain. The distribution of the AT4 receptor is remarkable in that its distribution extends throughout several neural systems. Most striking is its localization in motor nuclei and motor associated regions. These include the ventral horn spinal motor neurons, all cranial motor nuclei including the oculomotor, abducens, facial and hypoglossal nuclei, and the dorsal motor nucleus of the vagus. Receptors are also present in the vestibular, reticular and inferior olivary nuclei, the granular layer of the cerebellum, and the Betz cells of the motor cortex. Moderate AT4 receptor density is seen in all cerebellar nuclei, ventral thalamic nuclei and the substantia nigra pars compacta, with lower receptor density observed in the caudate nucleus and putamen. Abundant AT4 receptors are also found in areas associated with cholinergic nuclei and their projections, including the nucleus basalis of Meynert, ventral limb of the diagonal band and the hippocampus, somatic motor nuclei and autonomic preganglionic motor nuclei. AT4 receptors are also observed in sensory regions, with moderate levels in spinal trigeminal, gracile, cuneate and thalamic ventral posterior nuclei, and the somatosensory cortex. The abundance of the AT4 receptor in motor and cholinergic neurons, and to a lesser extent, in sensory neurons, suggests multiple roles for the AT4 receptor in the primate brain.

Acetylcholinesterase↗
PubMed1987

An analysis of potentially converging inputs to the rostral ventral thalamic nuclei of the cat.

Potentially convergent inputs to cerebellar-receiving and basal ganglia-receiving areas of the thalamus were identified using horseradish peroxidase (HRP) retrograde tracing techniques. HRP was deposited iontophoretically into the ventroanterior (VA), ventromedial (VM), and ventrolateral (VL) thalamic nuclei in the cat. The relative numbers of labeled neurons in the basal ganglia and the cerebellar nuclei were used to assess the extent to which the injection was in cerebellar-receiving or basal ganglia-receiving portions of thalamus. The rostral pole of VA showed reciprocal connections with prefrontal portions of the cerebral cortex. Only the basal ganglia and the hypothalamus provided non-thalamic input to modulate these cortico-thalamo-cortical loops. In VM, there were reciprocal connections with prefrontal, premotor, and insular areas of the cerebral cortex. The basal ganglia (especially the substantia nigra), and to a lesser extent, the posterior and ventral portions of the deep cerebellar nuclei, provided input to VM and may modulate these cortico-thalamo-cortical loops. The premotor cortical areas connected to VM include those associated with eye movements, and afferents from the superior colliculus, a region of documented importance in oculomotor control, also were labeled by injections into VM. The dorsolateral portion of the VA-VL complex primarily showed reciprocal connections with the medial premotor (area 6) cortex. Basal ganglia and cerebellar afferents both may modulate this cortico-thalamo-cortical loop, although they do not necessarily converge on the same thalamic neurons. The cerebellar input to dorsolateral VA-VL was from posterior and ventral portions of the cerebellar nuclei, and the major potential brainstem afferents to this region of thalamus were from the pretectum. Mid- and caudo-lateral portions of VL had reciprocal connections with primary motor cortex (area 4). The dorsal and anterior portions of the cerebellar nuclei had a dominant input to this cortico-thalamo-cortical loop. Potentially converging brainstem afferents to this portion of VL were from the pretectum, especially pretectal areas to which somatosensory afferents project.

Afferent Pathways↗
PubMed1988

Segregation of lemniscal inputs and motor cortex outputs in cat ventral thalamic nuclei: application of a novel technique.

A double labeling method that permits accurate delineation of the terminals of medial lemniscal fibers was used to determine whether thalamic neurons projecting to motor cortex in the cat are in a position to be contacted by such terminals. Thalamic neurons in the VL nucleus were retrogradely labeled by injections of fluorogold placed in the cytoarchitectonically defined area 4, while lemniscal axons and their terminal boutons were anterogradely labeled, in a Golgi-like manner, from injections of Fast Blue placed under physiological control in different parts of the contralateral dorsal column nuclei. In additional experiments, spinothalamic fibers were similarly labeled by injections of Fast Blue in the spinal cord. The results reveal that there is no significant overlap in the distributions of lemniscal terminals and motor cortex-projecting neurons and that no somata or proximal dendrites of motor cortex-projecting neurons are in a position to receive lemniscal terminals. Spinothalamic terminals, on the other hand, end in clusters around motor cortex-projecting neurons in the VL nucleus as well as in other nuclei and are a more likely route for short latency somatosensory inputs to the motor cortex.

Amidines↗
PubMed1989

Dissociated mesencephalic responses to medial and ventral thalamic nuclei stimulation in rats. Relationship to analgesic mechanisms.

To investigate the mechanism of analgesia noted with electrical stimulation of the thalamic sensory relay nucleus and medial thalamus, modulations of neuronal activities in the periaqueductal gray matter (PAG) were studied in response to electrical stimulations of the ventroposterolateral nucleus (VPL) and parafascicular nucleus (Pf) and to peripheral noxious stimulations in rats. Extracellular single-unit activities were recorded from 102 neurons in the PAG and the adjacent area in animals under halothane anesthesia. A large population (83%) of the PAG neurons reacted to Pf stimulations with a predominantly excitatory response, whereas smaller numbers (43%) responded to VPL stimulations. There was a significant correlation between the response characteristics of Pf and noxious stimulations, whereas no correlation was found between VPL and noxious stimulations. The PAG neurons that were verified antidromically to project to the nucleus raphe magnus showed a similar pattern of response. The excitatory response to the Pf stimulation was partially attenuated by systemic administration of naloxone, whereas that to the VPL stimulation was not affected. These results suggest that part of the analgesic mechanism of medial thalamus stimulation involves activation of the descending pain suppression system by exciting the PAG neurons through the opioid system, while the analgesia produced by sensory relay nucleus stimulation does not involve the PAG neurons or the opioid system.

Afferent Pathways↗
PubMed1981

Projections of the cerebellar and dorsal column nuclei upon the thalamus of the rhesus monkey.

Projections from the cerebellar and dorsal column nuclei to the midbrain and thalamus of the rhesus monkey were traced with anterograde autoradiographic techniques, or, in a few cases, with the Fink-Heimer method. The cerebellar nuclei give rise to a massive projection to the contralateral midbrain and thalamus via the ascending limb of the superior cerebellar peduncle. Cerebellar efferent fibers terminate contralaterally in both divisions of the red nucleus, and bilaterally in the interstitial nucleus of Cajal, the nucleus of Darkschewitsch, the oculomotor nucleus, and the central gray. All the deep cerebellar nuclei project upon a broad area of the contralateral ventral thalamus as well as certain intralaminar nuclei. Corresponding ipsilateral thalamic terminations are sparse. The topographic organization of cerebellothalamic fibers does not correspond to individual cerebellar nuclei or to cytoarchitectonic divisions of the ventral thalamic nuclei. Rather there are longitudinally oriented strips of terminal labeling which extend through all divisions of the ventral lateral nucleus, i.e., the VLps, the VLc, the VLo, as well as nucleus X, the oral division of the ventral posterolateral nucleus (VPLo), the central lateral nucleus (CL), and the most caudal region of the ventral anterior nucleus (VA). The topography of the cerebellothalamic fibers is arranged in a mediolateral pattern with fibers originating from anterior zones of the dentate and interpositus ending most laterally and those from posterior dentate and interpositus terminating most medially. The fastigial contribution is relatively sparse. The longitudinal strips of terminal labeling in the ventral thalamic nuclei are made up of still smaller terminal units consisting of disk-like aggregates of silver grains separated from one another by grain-free spaces. The dorsal column nuclei terminate primarily in the contralateral caudal division of the VPL (VPLc) and never extend rostrally into VPLo. These results demonstrate a segregation of cerebellar and dorsal columnar inputs to motor and sensory regions of the thalamus, respectively. Since these regions are separate and discrete in their cortical associations as well (Kalil, '76), it seems unlikely that fast afferent pathways relaying to motor cortex (Lemon and Porter, '76) could arise from the dorsal column nuclei.

Afferent Pathways↗
PubMed2003

Localization of thalamic cells with tremor-frequency activity in Parkinson's disease and essential tremor.

It has been reported that parkinsonian and essential tremor can be controlled by deep brain stimulation or radiofrequency lesion within the cluster of cells with a tremor-frequency activity in the ventral thalamic nuclei. However, there have been very few reports about the exact localization of cells with tremor-frequency activity in the ventral thalamic nuclei. In the present study, we investigated the localization of cells with tremor-frequency activity in the ventral thalamic nuclei employing autopower spectrum and coherence analysis. Activity of a total of 130 cells, 63 in patients with parkinsonian tremor and 67 in patients with essential tremor, were recorded from the area anterior to the nucleus ventralis caudalis. Among these cells, 31 cells showed a coherence of greater than 0.4 to the electromyographic activity of both agonist and antagonist muscles. The proportion of cells exhibiting tremor-frequency activity were 26.8% in the nucleus ventralis intermedius (Vim) and 25.0% in the nuclei ventralis oralis posterior et anterior (Vop + Voa). There were no significant differences in proportion by nuclear location or disease. The present study demonstrated that cells with tremor-frequency activity are widely distributed over the area extending from the Vim to the Vop + Voa. This indicates that the best location for placing electrodes for deep brain stimulation or a radiofrequency lesion cannot be defined by identification of cells with tremor-frequency activity alone.

Action Potentials↗
PubMed2003

Group II and III metabotropic glutamate receptors and the control of the nucleus reticularis thalami input to rat thalamocortical neurones in vitro.

Intracellular recordings were made from neurones in the thalamic reticular nucleus (TRN) and ventro-basal (VB) thalamus in slices of rat midbrain in vitro. Electrical stimulation of the medial lemniscus or TRN resulted in the generation of complex synaptic potentials containing disynaptic inhibitory post-synaptic potentials (IPSPs) in VB thalamocortical neurones. Analysis of the excitatory synaptic responses in TRN neurones indicates they can produce burst output response irrespective of the level of sub-threshold membrane potential. This suggests that network-evoked IPSPs in VB thalamocortical neurones occur following a burst of TRN action potentials. Using ionotropic glutamate receptor antagonists, the activation of these disynaptic events was blocked, and the monosynaptic IPSPs that resulted from the direct activation of the TRN could be isolated. The selective Group II agonists LY354740 (1-10 microM) and N-acetyl-aspartyl-glutamate (NAAG; 100-500 microM) both caused a reversible depression of these monosynaptic TRN IPSPs without any effect on membrane potential or input resistance. Likewise, the specific Group III agonist L-2-amino-4-phosphonobutanoate (10-500 microM), but not (RS)-4-phosphonophenylglycine (1 and 30 microM) also caused a reversible depression of these IPSPs, again without any effect on membrane potential or input resistance.Thus, the IPSPs recorded in VB thalamocortical neurones, evoked by TRN activation, can be depressed by the activation of either Group II or III metabotropic glutamate receptors. This is consistent with the location of these receptor types on the presynaptic terminals of TRN axons in the VB thalamus. This raises the possibility that, during periods of intense excitatory activity, glutamate release could influence the release of GABA from TRN axon terminals in the thalamus. In addition, as NAAG is located in the axons and terminals arising from the TRN, there is the possibility that this dipeptide is also released by these terminals to control the release of GABA during periods of high activity in the TRN.

Animals↗
PubMed2001

Axonal conduction properties of antidromically identified neurons in rat barrel cortex.

Physiological studies of the rodent somatosensory cortex have consistently described considerable heterogeneity in receptive field properties of neurons outside of layer IV, particularly those in layers V and VI. One such approach for distinguishing among different local circuits in these layers may be to identify the projection target of neurons whose axon collaterals contribute to the local network. In vivo, this can be accomplished using antidromic stimulation methods. Using this approach, the axonal conduction properties of cortical efferent neurons are described. Four projection sites were activated using electrical stimulation: (1) vibrissal motor cortex, (2) ventrobasal thalamus (VB), (3) posteromedial thalamic nucleus (POm), and (4) cerebral peduncle. Extracellular recordings were obtained from a total of 169 units in 21 animals. Results demonstrate a close correspondence between the laminar location of the antidromically identified neurons and their anatomically known layer of origin. Axonal properties were most distinct for corticofugal axons projecting through the crus cerebri. Corticothalamic axons projecting to either VB or POm were more similar to each other in terms of laminar location and conduction properties, but could be distinguished using focal electrical stimulation. It is concluded that, once stimulation parameters are adjusted for the small volume of the rat brain, the use of antidromic techniques may be an effective strategy to differentiate among projection neurons comprising different local circuits in supra- and infragranular circuits.

Animals↗
PubMed2000

Regionally selective blockade of GABAergic inhibition by zinc in the thalamocortical system: functional significance.

The thalamocortical (TC) system is a tightly coupled synaptic circuit in which GABAergic inhibition originating from the nucleus reticularis thalami (NRT) serves to synchronize oscillatory TC rhythmic behavior. Zinc is colocalized within nerve terminals throughout the TC system with dense staining for zinc observed in NRT, neocortex, and thalamus. Whole cell voltage-clamp recordings of GABA-evoked responses were conducted in neurons isolated from ventrobasal thalamus, NRT, and somatosensory cortex to investigate modulation of the GABA-mediated chloride conductance by zinc. Zinc blocked GABA responses in a regionally specific, noncompetitive manner within the TC system. The regional levels of GABA blockade efficacy by zinc were: thalamus > NRT > cortex. The relationship between clonazepam and zinc sensitivity of GABA(A)-mediated responses was examined to investigate possible presence or absence of specific GABA(A) receptor (GABAR) subunits. These properties of GABARs have been hypothesized previously to be dependent on presence or absence of the gamma2 subunit and seem to display an inverse relationship. In cross-correlation plots, thalamic and NRT neurons did not show a statistically significant relationship between clonazepam and zinc sensitivity; however, a statistically significant correlation was observed in cortical neurons. Spontaneous epileptic TC oscillations can be induced in vitro by perfusion of TC slices with an extracellular medium containing no added Mg(2+). Multiple varieties of oscillations are generated, including simple TC burst complexes (sTBCs), which resemble spike-wave discharge activity. A second variant was termed a complex TC burst complex (cTBC), which resembled generalized tonic clonic seizure activity. sTBCs were exacerbated by zinc, whereas cTBCs were blocked completely by zinc. This supported the concept that zinc release may modulate TC rhythms in vivo. Zinc interacts with a variety of ionic conductances, including GABAR currents, N-methyl-D-aspartate (NMDA) receptor currents, and transient potassium (A) currents. D-2-amino-5-phosphonovaleric acid and 4-aminopyridine blocked both s- and cTBCs in TC slices. Therefore NMDA and A current-blocking effects of zinc are insufficient to explain differential zinc sensitivity of these rhythms. This supports a significant role of zinc-induced GABAR modulation in differential TC rhythm effects. Zinc is localized in high levels within the TC system and appears to be released during TC activity. Furthermore application of exogenous zinc modulates TC rhythms and differentially blocks GABARs within the TC system. These data are consistent with the hypothesis that endogenously released zinc may have important neuromodulatory actions impacting generation of TC rhythms, mediated at least in part by effects on GABARs.

2-Amino-5-phosphonovalerate↗
PubMed2001

Kinetic and pharmacological properties of GABA(A) receptors in single thalamic neurons and GABA(A) subunit expression.

Synaptic inhibition in the thalamus plays critical roles in sensory processing and thalamocortical rhythm generation. To determine kinetic, pharmacological, and structural properties of thalamic gamma-aminobutyric acid type A (GABA(A)) receptors, we used patch-clamp techniques and single-cell reverse transcriptase polymerase chain reaction (RT-PCR) in neurons from two principal rat thalamic nuclei-the reticular nucleus (nRt) and the ventrobasal (VB) complex. Single-channel recordings identified GABA(A) channels with densities threefold higher in VB than nRt neurons, and with mean open time fourfold longer for nRt than VB [14.6 +/- 2.5 vs. 3.8 +/- 0.7 (SE) ms, respectively]. GABA(A) receptors in nRt and VB cells were pharmacologically distinct. Zn(2+) (100 microM) reduced GABA(A) channel activity in VB and nRt by 84 and 24%, respectively. Clonazepam (100 nM) increased inhibitory postsynaptic current (IPSC) decay time constants in nRt (from 44.3 to 77.9 ms, P < 0.01) but not in VB. Single-cell RT-PCR revealed subunit heterogeneity between nRt and VB cells. VB neurons expressed alpha1-alpha3, alpha5, beta1-3, gamma2-3, and delta, while nRt cells expressed alpha3, alpha5, gamma2-3, and delta. Both cell types expressed more subunits than needed for a single receptor type, suggesting the possibility of GABA(A) receptor heterogeneity within individual thalamic neurons. beta subunits were not detected in nRt cells, which is consistent with very low levels reported in previous in situ hybridization studies but inconsistent with the expected dependence of functional GABA(A) receptors on beta subunits. Different single-channel open times likely underlie distinct IPSC decay time constants in VB and nRt cells. While we can make no conclusion regarding beta subunits, our findings do support alpha subunits, possibly alpha1 versus alpha3, as structural determinants of channel deactivation kinetics and clonazepam sensitivity. As the gamma2 and delta subunits previously implicated in Zn(2+) sensitivity are both expressed in each cell type, the observed differential Zn(2+) actions at VB versus nRt GABA(A) receptors may involve other subunit differences.

Animals↗
PubMed1976

[Reactions of neurons of the reticular and ventral anterior thalamic nuclei of the cat to electric stimulation of the relay nuclei of the optic thalamus].

Responses of 92 reticular (R) and 105 ventral anterior (VA) thalamic neurons to electrical stimulation of relay nuclei, ventrobasal complex (VB), lateral (GL) and medial (GM) geniculate bodies, were studied in cats immobilized with d-tubocurarine. 72.2% of R and 76.2% of VA investigated neurons responded to VB stimulation, while GM stimulation caused responses only in 15.0% of R and 27.1% of VA neurons and GL stimulation in 10.2% of R and 19.6% of VA neurons. The responses of R-VA neurons to relay nuclei stimulation were expressed, as a rule in excitation. Two types of excited neurons were distinguished: the first group responded to stimulation of afferent inputs by the discharge of 5-15 spikes at a frequency of 250-300 p/s, the second group responded by single action potential. According to peculiarities of their responses, the neurons of the first group are resembling inhibitory interneurons. 2.2% of R and 7.8% of VA neurons responded to relay nuclei stimulation by antidromic spikes. Among R and VA neurons there are cells which respond to stimulation of one, two and even three different relay nuclei. If stimulation of one relay nucleus is followed by a response of R or VA neuron, the preceding stimulation of another relay nucleus, with the time interval between the conditioning and testing stimuli being less than 30-50 ms, induced the inhibition of the response to the testing stimulus.

Animals↗
PubMed1978

[Reactions of neurons in the reticular and ventral anterior thalamic nuclei to stimulation of the ventrolateral nucleus of the thalamus and motor cortex].

Responses of 137 neurons located in oral parts of reticular (R) and ventral anterior (VA) thalamic nuclei to electrical stimulation of the ventrolateral nucleus (VL) and motor cortex (MI) were studied in 17 cats immobilized with d-tubocurarine. 10.5% of the investigated neurons responded to VL stimulation by antidromic spike (latency 0.7--3.0 ms). 11.0% of the neurons responded antidromically to MI stimulation (latency 0.4--4.0 ms). Neurons with axon sending one branch to VL and the other to MI were found. 78.9% of the neurons responded to VL stimulation with orthodromic excitation (after stimulation of MI this type of response was found only in 52.5% of neurons). 55.6% of R and VA neurons responded to VL stimulation by discharges composed of 3--20 spikes with frequency of 130--530/per second. After MI stimulation discharges of the same type were observed only in 30.5% of the investigated neurons. Inhibition was found in 6.8% of the studied neurons. 55.7% of R and VA neurons demonstrated the convergence of the effects from VL and MI. Corticofugal influences from MI on responses of R and VA neurons to the VL testing stimuli could be inhibitory as well as excitatory.

Action Potentials↗
PubMed1980

[Reactions of neurons of the reticular and ventral anterior thalamic nuclei to electrical stimulation of the centrum medianum of the thalamus].

Responses of 145 reticular (R) and 158 ventral anterior (VA) thalamic neurons to electrical stimulation of centrum medianum (CM) were studied in cats anaesthetized with thiopental sodium (30-40 mg/kg intraperitoneally) and immobilized with d-tubocurarine (1 mg/kg). 4.1% of R and 4.4% of VA neurons under study responded to CM stimulation by antidromic spike (latency 0.3-2.0 ms). The conduction velocity of antidromic excitation in axons of those neurons was found to be 1.7-7.6 m/s. There were neurons which responded by antidromic spike to the other thalamic nuclei stimulation as well as to CM. This fact is the electrophysiological proof of the axonal branching in these neurons. 53.8% of R and 46.9% of VA neurons responded to CM stimulation with orthodromic excitation. Two groups of cells were separated among neurons excited orthodromically. The first group neurons responded to CM stimulation by discharges composed of 6-12 spikes with frequency of 130-640 per second. The neurons of the second group generated a single spike. Inhibitory reactions were noticed only in 0.7% of R and in 4.4% of VA neurons. It is shown that afferent impulses from relay nuclei, lateral posterior nucleus and motor cortex converged to some R and VA neurons responding to CM.

Action Potentials↗