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Figure 5 | Molecular Pain

Figure 5

From: Differential modulation of nociceptive versus non-nociceptive synapses by endocannabinoids

Figure 5

Hypothetical model for opposing effects of 2AG on nociceptive (N) versus non-nociceptive (P) synapses. Both N- and P-cells have input onto the same postsynaptic targets (in this example, the L motor neuron) via glutamatergic synapses. Based on previous studies [10], 2AG directly depresses the nociceptive synapse via a TRPV-like receptor that reduces presynaptic neurotransmitter release. In the present study, 2AG was observed to potentiate the non-nociceptive synapse via an indirect mechanism in which the eCB reduces inhibitory input from an unknown GABAergic interneuron (int). This 2AG-mediated disinhibition appears to be mediated by the TRPV-like receptor as well. Nociceptive synapses are “protected” from this disinhibitory because they are depolarized by GABA. The same GABAergic interneuron is shown to act on both the N- and P-cells for diagrammatic purposes and it is not known whether these afferents receive GABAergic input from a common source or from distinct interneurons.

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