Journal of Neuroscience, Vol 6, 1702-1711, Copyright © 1986 by Society for Neuroscience
The rat ventromedial thalamic nucleus and motor control: role of N- methyl-D-aspartate-mediated excitation, GABAergic inhibition, and muscarinic transmission
T Klockgether, M Schwarz, L Turski and KH Sontag
The rat ventromedial thalamic nucleus (VM) is a point of convergence of
several pathways that are supposed to be involved in motor control.
Cortical fibers terminating within this nucleus use an excitatory amino
acid, possibly L-glutamate, as their transmitter. Excitatory amino acids
are known to interact with N-methyl-D-aspartate (NMDA), kainate, and
quisqualate receptors, the presence of which has been demonstrated within
the thalamus, gamma-Amino-butyrate (GABA) has been identified as the
transmitter of the basal ganglia afferents to the VM, whereas cerebellar
afferents to the VM are supposed to release ACh acting on muscarinic
receptors. The present study investigates the behavioral and motor
consequences of local injections of drugs into the VM, which specifically
interact with NMDA, GABA, and muscarine receptors. Both the NMDA antagonist
(-)2-amino-7-phosphonoheptanoate [(-)AP7], and the GABA agonist muscimol,
but not the muscarinic antagonist scopolamine, induced catalepsy and limb
rigidity. Both the (-)AP7- and muscimol- induced catalepsy were antagonized
by coadministration of NMDA and the GABA antagonist bicuculline. The
(-)AP7-induced catalepsy was characterized as an akinetic-rigid syndrome,
in which the ability to induce a phasic activation of a set of muscles is
lost and replaced by exaggerated tonic muscular responses. NMDA,
bicuculline, and the muscarinic agonist bethanechol induced an increase in
locomotor activity. The present study provides evidence that an imbalance
between NMDA-mediated excitation and GABAergic inhibition within the rat VM
leads to disturbances of motility, whereas muscarinic transmission within
this nucleus appears to be of minor importance.