Muscarinic agonists modulate spontaneous and evoked unit discharge in auditory cortex of cat.
The present experiments studied the effects of cholinergic agonists and antagonists on the spontaneous and acoustic-evoked discharge of auditory cortical neurons and examined whether these effects were mediated by muscarinic cholinergic receptors. A primary focus of this report is the analysis of specific effects of these agents on the spontaneous and tone-evoked discharge and on different temporal components of the evoked discharge. Single neurons were recorded in the auditory cortex of chronically prepared, awake cats with multibarrel micropipette electrodes. The responses to acoustic stimuli were obtained before, during, and following continuous ejection of cholinergic agonist or antagonists by micropressure. The mean rate of discharge of the neurons was analyzed quantitatively for spontaneous discharge and for different peaks of the tone-evoked PSTH corresponding to tone "on," "through," and "off" responses. Acetylcholine (ACh) and acetyl-beta-methacholine (MCh) produced significant effects on spontaneous activity in 72% and 68% of neurons tested, respectively. Tone-evoked responses were effected in 92% and 82% of cells tested, respectively. The ability of these agonists to modify spontaneous or evoked activity was dose-dependent. Agonist effects on spontaneous and evoked activity were often different in the same cell; however, effects on spontaneous activity did predict effects on "through" responses. The most common effect of ACh or MCh on evoked activity was facilitation of the tone "on" response. For neurons with multicomponent discharge patterns in response to tones, the agonists had nonuniform effects on different response components. However, the effects of ACh on the "on" and "off" responses covaried. Hence cholinergic agonists produce heterogeneous, selective effects on different components of the responses of auditory cortical neurons rather than simple increases or decreases in discharge level. The effects of cholinergic agonists were modified in the presence of atropine. The effects of MCh were blocked by atropine in a higher proportion of cases than those of ACh.
McKenna
T M
TM
Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717.
Ashe
J H
JH
Hui
G K
GK
Weinberger
N M
NM
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001301:Audiometry, Pure-Tone; D001303:Auditory Cortex / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D002415:Cats; D005072:Evoked Potentials, Auditory / Q000187:drug effects; D008297:Male; D008688:Methacholine Compounds / Q000494:pharmacology; D010276:Parasympatholytics / Q000494:pharmacology; D010277:Parasympathomimetics / Q000494:pharmacology*; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000502:physiology*
D008688:Methacholine Compounds; D010276:Parasympatholytics; D010277:Parasympathomimetics; D011976:Receptors, Muscarinic; D001285:Atropine; D000109:Acetylcholine