Relative Contributions of Thalamic Reticular Nucleus Neurons and Intrinsic Interneurons to Inhibition of Thalamic Neurons Projecting to the Motor Cortex. Ando, N., Y. Izawa, and Y. Shinoda. Department of Physiology, School of Medicine, Tokyo Medical and Dental University, 1 - 5 - 45, Yushima, Bunkyo-ku, Tokyo, Japan.
APStracts 2:0001N, 1995.
SUMMARY AND CONCLUSIONS
1. Intracellular responses to stimulation of the cerebral cortex (Cx) and cerebellum were analyzed in thalamocortical neurons (TCNs) in the ventroanterior-ventrolateral (VA-VL) complex of the thalamus and neurons in the thalamic reticular nucleus (RN) of anesthetized cats, and the contribution of reticular nucleus neurons (RNNs) and thalamic interneurons (TINs) to cerebral and cerebellar inhibition of TCNs was determined. 2. Single TCNs projecting to area 4 or 6 received convergent monosynaptic excitatory and disynaptic inhibitory inputs from both the dentate nucleus (DN) and the interpositus nucleus (IN). These TCNs also received monosynaptic EPSPs and disynaptic IPSPs from the pericruciate cortex (areas 4 and 6). Each TCN received the strongest excitatory and inhibitory inputs from the cortical area to which that TCN projected, and weaker inhibitory inputs from adjacent cortical areas. 3. RNNs were identified morphologically by intracellular injection of horseradish peroxidase (HRP). Stimulation of the brachium conjunctivum (BC) evoked disynaptic EPSPs with a long decay phase in RNNs in the anterior ventrolateral part of the RN. Single RNNs received convergent disynaptic excitatory inputs from both the DN and the IN. Stimulation of the Cx produced monosynaptic long-lasting EPSPs with two different latencies in these RNNs : early EPSPs with latencies of 0.9 - 2.1 msec and late EPSPs with latencies of 1.8 - 3.5 msec. Collision experiments with BC- and Cx-evoked EPSPs in RNNs indicated that BC-evoked disynaptic EPSPs and Cx-evoked early EPSPs were produced by axon collaterals of TCNs to RNNs. The latencies of the Cx-evoked late EPSPs in RNNs were almost identical to those of Cx-evoked monosynaptic EPSPs in TCNs, indicating that corticothalamic neurons (CTNs) exert monosynaptic excitatory effects on RNNs and TCNs. 4. Stimulation of the Cx produced IPSPs in TCNs with short latencies of 1.8 - 2.7 msec and longer latencies of 2.8 msec or more. The Cx-evoked early IPSPs with latencies of 1.8 - 2.7 msec were mediated by RNNs. The origin of Cx-evoked late IPSPs with latencies of 2.8 msec or longer in TCNs was two-fold. Cx-induced early IPSPs in TCNs were facilitated by conditioning cortical stimulation that induced late IPSPs in the TCNs. The same conditioning cortical stimulation also facilitated BC-evoked disynaptic IPSPs. The time course of this facilitation indicated that CTNs produce long-lasting excitation in TINs. These results indicated that Cx-evoked IPSPs with latencies of more than 2.7 msec were mediated at least in part by RNNs and inhibitory TINs in the VA-VL complex. 5. The shortest latencies of BC-evoked IPSPs in TCNs were at least 0.8 msec longer than those of BC-evoked monosynaptic EPSPs in TCNs, and were almost equal to the latencies of BC-evoked EPSPs in RNNs. Therefore, these BC-evoked disynaptic IPSPs could not be mediated via RNNs. However, the interaction between Cx-induced early IPSPs and BC-evoked late IPSPs in TCNs indicated that BC-evoked IPSPs contained a trisynaptic component via RNNs. 6. These electrophysiological results were confirmed by the anatomical findings that the main axons of HRP-stained RNNs receiving disynaptic excitatory input from the BC and monosynaptic excitatory input from the Cx ran dorsomedially or caudomedially and spread into the VA-VL complex, where TCNs receiving cerebellar input were located. 

Received 12 December 1994; accepted in final form 8 February 1995.
APS Manuscript Number J772-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  3 April 1995.