Substantia Nigra Output to Prefrontal Cortex Via Thalamus in Monkeys. II. Activity of Thalamic Relay Neurons in Delayed Conditional Go/No-Go Discrimination Task

2009 ◽  
Vol 102 (5) ◽  
pp. 2946-2954 ◽  
Author(s):  
Ikuo Tanibuchi ◽  
Hiroyuki Kitano ◽  
Kohnosuke Jinnai

The present report investigated the involvement of primate nigro-thalamo-cortical projections in discrimination of visual signals with behavioral meaning. We tested the extracellular unit activity of mediodorsal (MD) and ventral anterior (VA) thalamic neurons monosynaptically receiving inhibitory input from the substantia nigra pars reticulata (SNr) and projecting to the frontal cortex in Japanese monkeys performing a delayed conditional go/no-go discrimination task. In the task two colored stimuli (S1, S2) intervened by delay period required the monkeys lifting a lever (go) or not (no-go); the same and different colored pairs of S1 and S2 meant go and no-go signals, respectively. Prominent task-relevant responses were sustained activity with color preference to S1 during delay period and S2-related activity with different firing rates between go and no-go trials. In particular, a high proportion of such go/no-go differential S2-related activity was found in thalamic relay neurons, receiving input from the caudolateral SNr and projecting to the prefrontal area (PSv) ventral to the principal sulcus, in the rostrolateral MD. The findings suggest that the caudolateral SNr–rostrolateral MD–PSv pathways may be possible conduits of signals coding the behavioral meaning of the visual stimuli and thus may be responsible for generating similar neuronal activity in the PSv.

2009 ◽  
Vol 102 (5) ◽  
pp. 2933-2945 ◽  
Author(s):  
Ikuo Tanibuchi ◽  
Hiroyuki Kitano ◽  
Kohnosuke Jinnai

A few studies have been performed in primate basal ganglia–thalamo–prefrontal pathways. Nevertheless, their electrophysiological properties and anatomical arrangements remain obscure. This study examined them in nigro-thalamo-cortical pathways from the substantia nigra pars reticulata (SNr) to the frontal cortex (FRC) via the mediodorsal (MD) and ventral anterior (VA) thalamus in monkeys. First, single thalamocortical neurons with SNr input were identified by antidromic responses to FRC stimulation and by inhibitory orthodromic responses with short latencies (<5 ms) to SNr stimulation. Second, single nigrothalamic neurons were found by antidromic responses to stimulation of the portions of the MD and VA where the thalamocortical neurons were recorded. The inhibitory orthodromic responses in the thalamocortical neurons were considered to be monosynaptically induced by nigral stimulation because the latency distribution of the orthodromic responses in the thalamocortical neurons was similar to that of the antidromic responses in the nigrothalamic neurons. Almost all relay neurons in the rostrolateral MD received inhibitory afferents from the caudolateral SNr and projected to the prefrontal area ventral to the principal sulcus, which constituted the densest nigro-thalamo-cortical projections. Meanwhile, neurons in the VA received inhibitory signals from the whole rostrocaudal extent of the SNr and projected to wide regions of the FRC; neurons in its pars magnocellularis mostly projected to different prefrontal areas, while those in its pars parvocellularis projected to motor areas. This report substantiated the topography of thalamocortical neurons monosynaptically receiving inhibitory SNr input and projecting to the FRC in the primate MD and VA at the single-neuron level.


1993 ◽  
Vol 70 (1) ◽  
pp. 20-27 ◽  
Author(s):  
J. M. Chung ◽  
J. R. Huguenard ◽  
D. A. Prince

1. The alterations of voltage-sensitive calcium currents produced in thalamic cells by injury were investigated under voltage clamp using patch-clamp recordings in the whole-cell configuration. 2. One day after unilateral cortical ablation in immature rats (postnatal day 7), low-threshold transient calcium (T) currents in acutely isolated thalamic relay neurons (RNs) were increased by 68% compared with contralateral controls (P < 0.001). Three days after the operation, T currents in injured neurons were at 44% of control levels (P < 0.001). On the other hand, high-threshold (L) calcium currents in RNs did not change over the same interval. 3. To investigate the mechanism for the increase of T current, both kinetics and voltage dependency of activation and inactivation were examined. At a test voltage of -40 mV, the activation time constant decreased from 4.1 to 3.2 ms (P < 0.05); however, this small change was insufficient to explain the large increase in T current. Time constants for both fast and slow inactivation did not change significantly, nor did voltage dependence of activation or inactivation of thalamic T currents. 4. Methyl-phenyl-succinimide (MPS, 1 mM), a compound known to block T currents, was used to examine possible alterations in the pharmacological properties of T channels after injury. MPS was more effective in reducing T currents in normal versus injured RNs (24 and 20% reductions, respectively; P < 0.05), suggesting that pharmacological properties of T channels in the injured RNs may be different from those of the normal RNs.(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 71 (6) ◽  
pp. 2576-2581 ◽  
Author(s):  
J. R. Huguenard ◽  
D. A. Prince

1. Experiments were carried out using patch-clamp techniques in rat thalamic slices, maintained in vitro, to examine the effects of the benzodiazepine compound, clonazepam (CZP), on intrathalamic inhibition. Bath-applied CZP reduced the gamma-aminobutyric acid-B (GABAB) component of inhibitory postsynaptic potentials and currents (IPSPs and IPSCs, respectively) evoked in rat thalamic somatosensory relay neurons by stimulation of nucleus reticularis thalami (nRt), without consistently affecting the GABAA IPSP. Secondary IPSPs, which occur as a result of intrathalamic oscillations, were dramatically reduced. 2. Voltage-clamp experiments combined with local or bath perfusion of the GABAA antagonist bicuculline methiodide (BMI), demonstrated that nRt is a site of GABAA-mediated postsynaptic inhibition that affects inhibitory output onto relay neurons. BMI enhanced both GABAA and GABAB postsynaptic inhibition in relay neurons when applied to nRt. Focal applications in the ventrobasal relay nucleus near the recording electrode blocked the GABAA-mediated IPSP but had no effects on GABAB inhibitory potentials. 3. Results suggest that CZP acts to facilitate recurrent inhibition in nRt and decrease its inhibitory output onto relay neurons. Intra-nRt GABAA-mediated inhibition thus has an important role in controlling thalamic excitability and in the anti-absence actions of CZP.


2016 ◽  
Vol 116 (5) ◽  
pp. 2368-2382
Author(s):  
Lu Li ◽  
Ford F. Ebner

Cortex actively modulates the responses of thalamic relay neurons through corticothalamic (CT) projections. Here we investigated the temporal precision of CT modulation on sensory responses of relay neurons in rat ventral posterior medial thalamus (VPM) to direction-specific whisker stimuli. CT feedback levels were either augmented by cortical electrical microstimulation or depressed by cortical application of muscimol, a potent agonist of γ-aminobutyric acid A-type (GABAA) receptors. To evaluate the temporal specificity of CT influence, we compared the early (3–10 ms after stimulus onset) and late (10–100 ms) response components of VPM single units to whisker deflections in preferred or nonpreferred directions before and after altering CT feedback levels under urethane anesthesia. The data showed that cortical feedback most strongly affected the late responses of single VPM units to whisker stimulation. That is, cortical stimulation consistently increased the late responses of VPM units in the corresponding (homologous) barreloids to the stimulus direction preferred by neurons in the cortical locus stimulated. However, cortical stimulation could either increase or decrease the early response, depending on whether or not cortical and thalamic loci were tuned to the same direction. Such bidirectional regulation of the early and late VPM responses is consistent with a mechanism of circuit-level disinhibition in vivo. The results support the theory that CT feedback on thalamic sensory responses is mediated by a time-dependent shift of the excitation-inhibition balance in the thalamo-cortico-thalamic loop, such as would occur during sensory feature integration, plasticity, and learning in the awake state.


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