Long‐term plasticity of corticostriatal synapses is modulated by pathway‐specific co‐release of opioids through κ‐opioid receptors

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12404-list-0001">Both endogenous opioids and opiate drugs of abuse modulate learning of habitual and goal‐directed actions, and can also modify long‐term plasticity of corticostriatal synapses.Striatal projection neurons of the direct pathway co‐release the opioid neuropeptide dynorphin which can inhibit dopamine release via κ‐opioid receptors.Theta‐burst stimulation of corticostriatal fibres produces long‐term potentiation (LTP) in striatal projection neurons when measured using whole‐cell patch recording.Optogenetic activation of direct pathway striatal projection neurons inhibits LTP while reducing dopamine release.Because the endogenous release of opioids is activity dependent, this modulation of synaptic plasticity represents a negative feedback mechanism that may limit runaway enhancement of striatal neuron activity in response to drugs of abuse.