Ga. Marks et Hp. Roffwarg, CHOLINERGIC RESPONSIVENESS OF NEURONS IN THE VENTROPOSTERIOR THALAMUSOF THE ANESTHETIZED RAT, Neuroscience, 54(2), 1993, pp. 391-400
Acetylcholine has been implicated as an important neurotransmitter in
the mechanisms of thalamic activation. Cholinergic mechanisms are thou
ght to directly underlie the high level of excitability observed in th
alamic relay neurons during waking and rapid eye movement sleep. We so
ught to determine if the cholinergic responsiveness of neurons in the
ventroposterior nuclei of the thalamus in rat is consistent with this
view. Neurons in the chloral hydrate-anesthetized rat were studied wit
h extracellular recording and microiontophoretic application of cholin
ergic agents. In most cases (63% of 63 cells), the ejection of the ago
nist, carbachol, had no observable effect on spontaneous activity. Fac
ilitation (25%), inhibition (8%) and inhibition followed by facilitati
on (3%) were also observed. Carbachol ejections that by themselves wer
e ineffective in altering spontaneous activity proved capable, in 93%
of 28 cells, of antagonizing the uniformly facilitatory responses prod
uced by glutamate ejection. The putative M1-selective, cholinergic ago
nist, McN-A-343, was also ineffective alone in altering spontaneous ac
tivity in the majority of cases (74% of 27 cells) and produced only in
hibitory responses in the remaining seven neurons studied. Interacting
applications of McN-A-343 and glutamate resulted, in all cases, in an
tagonism of glutamate facilitation (N = 12). The various responses to
applied cholinergic agonists were all capable of being antagonized by
muscarinic receptor-blocking agents. Both the high proportion of inhib
itory responses and the antagonism of glutamate facilitatory responses
suggest that ventroposterior neurons in the rat differ from other tha
lamocortical relay neurons in the rat and cat with regard to cholinerg
ic responsiveness. Additionally, the lack of predominantly facilitator
y responding renders it unlikely that cholinergic mechanisms directly
underlie increases in excitability of ventroposterior neurons observed
during waking and rapid eye movement sleep.