Corticotropin-releasing factor (CRF) plays an important role in the activation of centrally mediated responses to stress. The amygdala, a limbic structure involved in the stress response, has a significant number of CRF cell bodies and CRF receptors. Activation of glutamatergic projections to the amygdala has been implicated in the stress response. Few studies have evaluated neurotransmitter-stimulated CRF release in the amygdala. We measured the effects of glutamate (0.1–1000 μ M ) and N -methyl- d -aspartate (NMDA, 0.1–1000 μM) on CRF release from the amygdala using primary neuronal cultures from embryonic rat brains (E18–19). Experiments were performed after the cultures grew for 17–20 days. CRF was measured using radioimmunoassay. The excitatory amino acid neurotransmitters, glutamate and NMDA, stimulated CRF release in a concentration-dependent manner. The apparent EC 50 values for glutamate and NMDA were 17.5 μM and 12 μM, respectively. Consistent with a NMDA receptor-driven event, glutamate-stimulated CRF release was blocked by the NMDA antagonist, 2-amino-5-phosphonovaleric acid (AP-5, 1–100 μM) and antagonized by the addition of 1.2 mM MgCl 2 to the incubation medium. These results implicate an inhibition of CRF release in the amygdala as a possible mechanism for the reported anxiolytic effects of NMDA antagonists.
Peptides – Elsevier
Published: Jan 1, 1999
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