抄録
Striosome (or patch)/matrix compartments are one of the candidates of functional module in the striatum. We previously reported that activation of μ opioid receptor (MOR) suppressed GABAergic inhibitory postsynaptic currents (IPSCs) in medium-spiny projection neurons in compartment-specific manner. Interestingly, the inhibition of IPSCs was also observed in cholinergic interneurons. In this study, we investigated the MOR-mediated effects on the excitability of cholinergic interneurons. To identify the striosomes, we used a TH-GFP transgenic mouse strain expressing eGFP under the control of promoter of tyrosine hydroxylase, the rate-limiting enzyme for catecholamine synthesis. Because dopaminergic neurons densely innervate the striosomes in early postnatal stage, a striosome is identified as a bright area under a fluorescence microscope. Using corticostriatal slices obtained from TH-GFP mice, we made whole-cell recordings from cholinergic interneurons. GABAergic IPSCs were elicited in the presence of CNQX and AP5. Intrastriatal stimulation evoked multiphasic GABAergic IPSCs consisted of monosynaptic early and polysynaptic, nicotinic acetylcholine receptor (nAchR) mediated late components. DAMGO (1 microM), an agonist of MOR, suppressed only the early-IPSCs in the striosomes. Dihydro-β-erythroidine, an antagonist of non-α7 nAchR, suppressed only late-IPSCs, suggesting nAchR-mediated activation of GABAergic neurons. These studies would help to explain the MOR-mediated effects on the activity of local neural circuits in striosome/matrix compartments. [J Physiol Sci. 2008;58 Suppl:S57]