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Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons.

Publication ,  Journal Article
Naylor, JC; Li, Q; Kang-Park, M-H; Wilson, WA; Kuhn, C; Moore, SD
Published in: Eur J Neurosci
December 2010

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.

Duke Scholars

Published In

Eur J Neurosci

DOI

EISSN

1460-9568

Publication Date

December 2010

Volume

32

Issue

11

Start / End Page

1836 / 1842

Location

France

Related Subject Headings

  • gamma-Aminobutyric Acid
  • Synaptic Transmission
  • Salicylamides
  • Receptors, Dopamine D1
  • Rats, Sprague-Dawley
  • Rats
  • Presynaptic Terminals
  • Patch-Clamp Techniques
  • Neurons
  • Neurology & Neurosurgery
 

Citation

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MLA
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Naylor, J. C., Li, Q., Kang-Park, M.-H., Wilson, W. A., Kuhn, C., & Moore, S. D. (2010). Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons. Eur J Neurosci, 32(11), 1836–1842. https://doi.org/10.1111/j.1460-9568.2010.07457.x
Naylor, Jennifer C., Qiang Li, Maeng-hee Kang-Park, Wilkie A. Wilson, Cynthia Kuhn, and Scott D. Moore. “Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons.Eur J Neurosci 32, no. 11 (December 2010): 1836–42. https://doi.org/10.1111/j.1460-9568.2010.07457.x.
Naylor JC, Li Q, Kang-Park M-H, Wilson WA, Kuhn C, Moore SD. Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons. Eur J Neurosci. 2010 Dec;32(11):1836–42.
Naylor, Jennifer C., et al. “Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons.Eur J Neurosci, vol. 32, no. 11, Dec. 2010, pp. 1836–42. Pubmed, doi:10.1111/j.1460-9568.2010.07457.x.
Naylor JC, Li Q, Kang-Park M-H, Wilson WA, Kuhn C, Moore SD. Dopamine attenuates evoked inhibitory synaptic currents in central amygdala neurons. Eur J Neurosci. 2010 Dec;32(11):1836–1842.
Journal cover image

Published In

Eur J Neurosci

DOI

EISSN

1460-9568

Publication Date

December 2010

Volume

32

Issue

11

Start / End Page

1836 / 1842

Location

France

Related Subject Headings

  • gamma-Aminobutyric Acid
  • Synaptic Transmission
  • Salicylamides
  • Receptors, Dopamine D1
  • Rats, Sprague-Dawley
  • Rats
  • Presynaptic Terminals
  • Patch-Clamp Techniques
  • Neurons
  • Neurology & Neurosurgery