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Chloral hydrate anesthesia alters the responsiveness of identified midbrain dopamine neurons to dopamine agonist administration
Author(s) -
Kelland Mark D.,
Freeman Arthur S.,
Chiodo Louis A.
Publication year - 1989
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890030105
Subject(s) - quinpirole , apomorphine , agonist , chloral hydrate , dopamine , dopamine agonist , amphetamine , dopamine receptor , chemistry , dopamine receptor d2 , endocrinology , medicine , pharmacology , anesthesia , dopaminergic , receptor
Single‐unit electrophysiological recording techniques were used to sample the basal activity of antidromically identified nigrostriatal and mesoaccumbens dopamine (NSDA and MADA, respectively) neurons and to examine the responsiveness of these cells to dopamine agonist‐induced inhibition of cell firing rate in either chloral hydrate‐anesthetized or paralyzed rats. Paralyzed rats exhibited a greater percentage of burst‐firing cells (69%) than did anesthetized animals (37%). Furthermore, paralyzed rats were less sensitive to the mixed D1/D2 DA receptor agonist apomorphine and the selective D2 DA receptor agonist quinpirole. However, significantly higher doses of d‐amphetamine were required in paralyzed animals only with respect to inhibiting MADA neurons. The abilities of apomorphine and quinpirole to inhibit NSDA cell firing were rate‐dependent in both anesthetized and paralyzed rats, whereas d‐amphetamine‐induced inhibition was rate dependent only in anesthetized animals. In contrast, apomorphine‐ and quinpirole‐induced inhibition of MADA neurons were rate‐dependent only in anesthetized rats, whereas d‐amphetamine‐induced inhibition was rate‐dependent only in paralyzed animals. These results suggest that general anesthesia exerts subtle effects on the basal activity and pharmacological responsiveness of midbrain dopamine neurons.