An Aplysia-like synaptic switch for rapid protection against ethanol-induced synaptic inhibition in a mammalian habit circuit.
Decades of work in Aplysia californica established the general rule that principles of synaptic plasticity and their molecular mechanisms are evolutionarily conserved from mollusks to mammals. However, an exquisitely sensitive, activity-dependent homosynaptic mechanism that protects against the depression of neurotransmitter release in Aplysia sensory neuron terminals has, to date, not been uncovered in other animals, including mammals. Here, we discover that depression at a mammalian synapse that is implicated in habit formation and habit learning acceleration by ethanol, the fast-spiking interneuron (FSI) to medium spiny principal projection neuron (MSN) synapse of the dorsolateral striatum, is subject to this type of synaptic protection. We show that this protection against synaptic depression is calcium- and PDZ domain interaction-dependent. These findings support activity dependent protection against synaptic depression as an Aplysia-like synaptic switch in mammals that may represent a leveraging point for treating alcohol use disorders.
['Patton|Mary H|MH|', 'Padgett|Katherine E|KE|', 'McKeon|Paige N|PN|', 'Lu|Shao-Gang|SG|', 'Abrams|Thomas W|TW|', 'Mathur|Brian N|BN|']
D000818:Animals D001048:Aplysia D002118:Calcium D002492:Central Nervous System Depressants D003342:Corpus Striatum D000431:Ethanol D005260:Female D006184:Habits D008297:Male D008822:Mice, Transgenic D009433:Neural Inhibition D009473:Neuronal Plasticity D009474:Neurons D054731:PDZ Domains D011493:Protein Kinase C D013569:Synapses D046509:Tissue Culture Techniques
FSI MSN Striatum Alcohol Delta opioid receptor LTD PKA PKC Parvalbumin