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OtherNEUROPHARMACOLOGY

Corticotropin-Releasing Factor Increases Dihydropyridine- and Neurotoxin-Resistant Calcium Currents in Neurons of the Central Amygdala

Baojian Yu and Patricia Shinnick-Gallagher
Journal of Pharmacology and Experimental Therapeutics January 1998, 284 (1) 170-179;
Baojian Yu
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Patricia Shinnick-Gallagher
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Abstract

Corticotropin-releasing factor (CRF) is an important mediator of stress responses in the brain, and CRF receptors and CRF-containing neurons and terminals are located within the central nucleus of the amygdala (CeA). CeA neurons possess multiple types of Ca++ channels, including L, N and Q types and a current resistant to saturating concentrations of dihydropyridine and neurotoxin antagonists. In this study, we used whole-cell patch-clamp techniques to study the effects of CRF on whole-cell Ca++ current (ICa) in acutely dissociated CeA neurons and determine components of the current affected. CRF (1–400 nM) increased the peak of the ICa in ≈50% of the CeA neurons recorded. In the remaining neurons, CRF had little effect. The CRF-induced increase in the ICa was concentration dependent and the estimated EC50 value was 14.9 nM. CRF (50 nM) increased the peak ICa by 25 ± 5% (n = 9). CRF produced an increase in both the transient and the steady state current but did not shift the peak of the current-voltage relationship. CRF did not affect the voltage dependence of activation and inactivation, and the CRF effect on ICas was not significantly different when the neuron was held at −80 or −40 mV. The competitive CRF receptor antagonist (α-helical CRF9–41, 3 μM) blocked the CRF-induced increase in ICa, suggesting that the effect of CRF is receptor mediated. CRF (50 nM) enhanced the ICa(20 ± 3%) in the presence of saturating concentrations of the L-type blocker nimodipine and neurotoxin N- and Q-type blockers ω-conotoxin GVIA and ω-conotoxin MVIIC. We conclude that CRF increased, through a receptor mechanism, dihydropyridine- and neurotoxin-resistant current(s) in CeA neurons.

Footnotes

  • Send reprint requests to: Dr. Patricia Shinnick-Gallagher, Department of Pharmacology, University of Texas Medical Branch, Galveston, TX 77555-1031. E-mail: patricia.shinnick-gallagher{at}utmb.edu

  • 1 This work was supported by National Institute of Neurological Diseases and Stroke Grants NS29265 and NS24643 (P.S.G.).

  • Abbreviations:
    CRF
    corticotropin-releasing factor
    CeA
    central nucleus of the amygdala
    NIM
    nimodipine
    DHP
    dihydropyridine
    CRF-ir
    corticotropin-releasing factor immunoreactive
    GABA
    γ-aminobutyric acid
    ACTH
    adrenocorticotropin
    HPA
    hypothalamic-pituitary-adrenal
    TEA
    tetraethylammonium chloride
    HEPES
    4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid
    BAPTA
    1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid TTX, tetrodotoxin
    4-AP
    4-aminopyridine
    Aga IVA
    ω-agatoxin IVA
    HVA
    high voltage activated calcium current
    • Received January 10, 1997.
    • Accepted September 12, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 284, Issue 1
1 Jan 1998
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OtherNEUROPHARMACOLOGY

Corticotropin-Releasing Factor Increases Dihydropyridine- and Neurotoxin-Resistant Calcium Currents in Neurons of the Central Amygdala

Baojian Yu and Patricia Shinnick-Gallagher
Journal of Pharmacology and Experimental Therapeutics January 1, 1998, 284 (1) 170-179;

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OtherNEUROPHARMACOLOGY

Corticotropin-Releasing Factor Increases Dihydropyridine- and Neurotoxin-Resistant Calcium Currents in Neurons of the Central Amygdala

Baojian Yu and Patricia Shinnick-Gallagher
Journal of Pharmacology and Experimental Therapeutics January 1, 1998, 284 (1) 170-179;
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