There is a functional interaction between the neurotrophin brain-derived neurotrophic factor and our endogenous cannabinoid (endocannabinoid) signaling.  Activation of the cannabinoid (CB1) receptors cross talk and regulates GABA release.

The effects of BDNF at inhibitory cortical synapses are mediated by the release of endocannabinoids. These endocannabinoids act retrogradely at presynaptic CB1 receptors.

Acute application of BDNF rapidly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) via postsynaptic trkB receptor activation.

Furthermore, BDNF seem to induce the release of a retrograde messenger from the postsynaptic cell that regulates presynaptic neurotransmitter release. Ihibiting endocannabinoid synthesis or transport disrups the BDNF effect, implicating postsynaptic endocannabinoid release triggered by BDNF.^[1]

These findings are highly important, and a might threw a new light on the putative analgesic effects of anandamine-likes such as palmitoylethanolamide (PEA). 

Prof. dr Jan M. Keppel Hesselink, october 2010 

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