Cell‐specific spike‐timing‐dependent plasticity in GABAergic and cholinergic interneurons in corticostriatal rat brain slices

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Abstract
Striatum, the main input nucleus of basal ganglia, is involved in the learning of cognitive and motor sequences in response to environmental stimuli. Striatal output neurons (medium spiny neurons, MSNs) integrate cortical activity and the two main classes of interneurons (GABAergic and cholinergic interneurons) tightly regulate the corticostriatal information transfer. We have explored the transmission between cortex and striatal interneurons and their capability to develop activity‐dependent long‐term plasticity based on the quasi‐coincident cortical and striatal activities (spike‐timing‐dependent plasticity, STDP). We have observed glutamatergic monosynaptic connections between cortical cells and both striatal interneurons. Excitatory postsynaptic current latencies and rise times revealed that a cortical stimulation activates GABAergic interneurons before cholinergic, and both interneurons before MSNs. In addition, we have observed that striatal interneurons are able to develop bidirectional long‐term plasticity and that there is a cell‐specificity of STDP among striatal interneurons. Indeed, in GABAergic interneurons, long‐term depression (LTD) and long‐term potentiation (LTP) are induced by post‐pre and pre‐post STDP protocols, respectively. Cholinergic interneurons displayed a partially reversed STDP when compared to GABAergic interneurons: post‐pre protocols induced LTP as well as LTD (the induction of either LTP or LTD is correlated with rheobase) and pre‐post protocols induced LTD. The cell‐specificity of STDP also concerned the receptors activated for the induction of LTP and LTD in GABAergic and cholinergic interneurons: in GABAergic interneurons LTP and LTD required NMDA receptor‐activation whereas, in cholinergic interneurons, LTP was underlain by NMDA receptor‐activation and LTD by metabotropic glutamate receptors.