Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons.

Published

Journal Article

The central nucleus of the amygdala (CeA) plays a critical role in regulating the behavioral, autonomic and endocrine response to stress. Dopamine (DA) participates in mediating the stress response and DA release is enhanced in the CeA during stressful events. However, the electrophysiological effects of DA on CeA neurons have not yet been characterized. Therefore, the purpose of this study was to identify and characterize the effect of DA application on electrophysiological responses of CeA neurons in coronal brain sections of male Sprague-Dawley rats. We used whole-cell patch-clamp electrophysiological techniques to record evoked synaptic responses and to determine basic membrane properties of CeA neurons both before and after DA superfusion. DA (20-250 μM) did not significantly alter membrane conductance over the voltage range tested. However, DA significantly reduced the peak amplitude of evoked inhibitory synaptic currents in CeA neurons. Pretreatment with the D(2) receptor antagonist eticlopride failed to significantly block the inhibitory effects of DA. In contrast, pretreatment with the D(1) receptor antagonist SCH-23390 significantly reduced the effects of DA on evoked inhibitory neurotransmission in these neurons. Moreover, bath superfusion of the specific D(1) receptor agonist SKF-39393, but not the D(2) receptor agonist quinpirole, significantly reduced peak amplitude of evoked inhibitory synaptic events. DA reduced the frequency of miniature IPSCs without altering the amplitude, while having no effect on the amplitude of IPSCs elicited by pressure application of GABA. These results suggest that DA may modulate inhibitory synaptic transmission in CeA through D(1) receptor activation primarily by a presynaptic mechanism.

Full Text

Duke Authors

Cited Authors

  • Naylor, JC; Li, Q; Kang-Park, M-H; Wilson, WA; Kuhn, C; Moore, SD

Published Date

  • December 2010

Published In

Volume / Issue

  • 32 / 11

Start / End Page

  • 1836 - 1842

PubMed ID

  • 20955472

Pubmed Central ID

  • 20955472

Electronic International Standard Serial Number (EISSN)

  • 1460-9568

Digital Object Identifier (DOI)

  • 10.1111/j.1460-9568.2010.07457.x

Language

  • eng

Conference Location

  • France