Lack of evidence for functional TRPV1 vanilloid receptors in rat hippocampal nerve terminals - PubMed (original) (raw)

. 2006 Jul 31;403(1-2):151-6.

doi: 10.1016/j.neulet.2006.04.030. Epub 2006 May 2.

Affiliations

Lack of evidence for functional TRPV1 vanilloid receptors in rat hippocampal nerve terminals

Attila Köfalvi et al. Neurosci Lett. 2006.

Abstract

Although TRPV(1) vanilloid receptors (TRPV(1)Rs) have been assumed to be present in the brain, their role is not well-defined. Here, we tested the widely used TRPV(1)R agonists (E)-capsaicin (0.1-100 microM) and resiniferatoxin (RTX, 0.1 microM) on resting and K(+)-evoked Ca(2+) entry and radiolabelled GABA release in rat hippocampal nerve terminals. (E)-capsaicin and RTX failed to evoke Ca(2+) transients or to trigger [(3)H]GABA outflow. Both (E)-capsaicin (EC(50), 40.4 microM) and its enantiomer (Z)-capsaicin (EC(50), 22.9 microM), which is inactive at the TRPV(1)R, inhibited the K(+)-evoked Ca(2+) entry, and to similar extent, the Ca(2+)-dependent K(+)-evoked [(3)H]GABA release. The TRPV(1)R enhancer/partial agonist 2-aminoethoxydiphenyl borate (1-300 microM) induced rapid Ca(2+) entry. None of the above-mentioned findings proved to be sensitive to the TRPV(1)R antagonists iodoresiniferatoxin (I-RTX; 3 microM) and SB366791 (3 microM). The CB(1) cannabinoid receptor antagonist AM251 (EC(50), 1.1 microM) and I-RTX (EC(50), 4.6 microM) also diminished the K(+)-evoked Ca(2+) entry per se. We observed competitive antagonism between I-RTX and AM251, indicating that the two molecules may act at the same site. In conclusion, there is a need to examine the discrepancy between ex vivo and in vitro data to understand the neurochemical and physiological functions of brain TRPV(1)Rs.

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