Single unit responses of substantia nigra pars reticulata neurons to apomorphine: effects of striatal lesions and anesthesia.

Abstract:

:Many of the behavioral consequences of dopamine system activation are thought to be mediated by substantia nigra pars reticulata output pathways. Extracellular, single unit recording studies were conducted to determine how i.v. administration of the dopamine agonist, apomorphine, affects the activity of these pars reticulata neurons. Results revealed that a 320 micrograms/kg dose of the drug, considered sufficient to stimulate striatal postsynaptic dopamine receptors, caused highly variable changes in reticulata cell firing. Cells exhibited increases, decreases, or no changes in firing. Many cells also displayed marked minute to minute changes in firing. This non-uniform pattern of responses was not related to state of consciousness since similar responses were observed in both chloral hydrate-anesthetized as well as conscious, paralyzed rats. Both the increases and decreases could be reversed by subsequent administration of haloperidol. The variable responses to apomorphine were reduced but not totally prevented by striatal kainic acid lesions, suggesting that changes in striatonigral transmission may account for some but not all of the firing changes which were observed. A lower dose of apomorphine (20 micrograms/kg), thought to act primarily at dopamine cell autoreceptors, had little effect on reticulata cell firing and did not modify the variable responses normally observed after the higher dose. These results contrast strikingly with the consistent excitatory responses to apomorphine which have previously been observed in the globus pallidus and suggest that complex or multiple indirect effects of the drug may contribute to the varied reticulata responses.

journal_name

Brain Res

journal_title

Brain research

authors

Waszczak BL,Lee EK,Ferraro T,Hare TA,Walters JR

doi

10.1016/0006-8993(84)90380-9

subject

Has Abstract

pub_date

1984-07-23 00:00:00

pages

307-18

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(84)90380-9

journal_volume

306

pub_type

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