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  • Title: Contribution of the amygdala and nucleus accumbens to ventral pallidal responses to dopamine agonists.
    Author: Napier TC.
    Journal: Synapse; 1992 Feb; 10(2):110-9. PubMed ID: 1350111.
    Abstract:
    Neurons recorded from ventral pallidum/substantia innominata (VP) of the basal forebrain respond to dopaminergic agonists that activate either the D1 or D2 the receptor subtype. Major afferent systems to the VP originate within amygdaloid nuclei (AMN) and the nucleus accumbens (NA). Since both the AMN and the NA are dopaminoceptive, the present study sought to analyze the contribution of these afferent systems to VP responses to dopaminergic agonists. Single VP neurons were electrophysiologically recorded in vivo from chloral hydrate-anesthetized rats, and the following determinations were made. 1) Effects of pharmacologic inactivation of an afferent system were assessed by monitoring VP neurons during intracerebral microinjections of the local anesthetic procaine, administered directly into either the AMN or the NA. 2) With procaine-induced VP rate changes used to indicate an afferent influence on the recorded neuron, VP responses to apomorphine (an agonist that acts at D1 and D2 receptor subtypes), SKF38393 (a D1 agonist), or quinpirole (a D2 agonist) were determined and compared with responses in rats not receiving the procaine pretreatment. Following pharmacologic inactivation of either the AMN or the NA, approximately 80% of the VP neurons monitored demonstrated rate changes, illustrating that spontaneous neuronal firing in the Vp is dependent on tonically input systems. Following afferent cessation, responses to apomorphine and quinpirole remained intact, suggesting that the AMN or NA is not necessary for VP responding to the systemic administration of dopaminergic agonists that act at D2 receptors. In contrast, the number of neurons that responded to SKF38393 was diminished follow intra-AMN (but not intra-NA) procaine. This suggests that D1-induced VP responses are mediated, at least in part, via the AMN.
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