2014 Apr 9. pii: S0149-7634(14)00083-9. doi: 10.1016/j.neubiorev.2014.03.026. [Epub ahead of print]
Modulation of defensive behavior by Transient Receptor Potential Vanilloid Type-1 (TRPV1) Channels.
Abstract
Aguiar DC, Moreira FA, Terzian AL, Fogaça MV, Lisboa SF, Wotjak CT, Guimaraes FS. NEUROSCI BIOBEHAV REV. Modulation of defensive behavior by Transient Receptor Potential Vanilloid Type-1 (TRPV1) Channels.
The Transient Receptor Potential Vanilloid Type-1 (TRPV1) was first characterized in primary afferent fibers as a receptor for capsaicin (the pungent ingredient of chili peppers). Later on, this cation-permeable ion channel was also described in the central nervous system, where its main putativeendogenous ligand is N-arachidonoyl ethanolamide (an endocannabinoid, also known as anandamide). Recent results employing genetic, pharmacological and histochemical techniques indicate that TRPV1 tonically modulate anxiety, fear and panic responses in brain regions related to defensive responses, such as the dorsal periaqueductal gray, the hippocampus and the medial prefrontal cortex. Genetic deletion or antagonism of this ion channel induces anxiolytic-like effects in several animal models. The main mechanism responsible for TRPV1-mediated effects on anxiety seems to involve facilitation of glutamatergic neurotransmission. In addition, there is evidence for interactions with other neurotransmitter systems, such as nitric oxide and endocannabinoids.
Copyright © 2014. Published by Elsevier Ltd.
The Transient Receptor Potential Vanilloid Type-1 (TRPV1) was first characterized in primary afferent fibers as a receptor for capsaicin (the pungent ingredient of chili peppers). Later on, this cation-permeable ion channel was also described in the central nervous system, where its main putativeendogenous ligand is N-arachidonoyl ethanolamide (an endocannabinoid, also known as anandamide). Recent results employing genetic, pharmacological and histochemical techniques indicate that TRPV1 tonically modulate anxiety, fear and panic responses in brain regions related to defensive responses, such as the dorsal periaqueductal gray, the hippocampus and the medial prefrontal cortex. Genetic deletion or antagonism of this ion channel induces anxiolytic-like effects in several animal models. The main mechanism responsible for TRPV1-mediated effects on anxiety seems to involve facilitation of glutamatergic neurotransmission. In addition, there is evidence for interactions with other neurotransmitter systems, such as nitric oxide and endocannabinoids.
Copyright © 2014. Published by Elsevier Ltd.
KEYWORDS:
Anandamide, Anxiety, Endocannabinoids, Endovanilloids, Fear
- PMID:
24726577
[PubMed – as supplied by publisher]
