Title : Nicotine depresses facial stimulation-evoked molecular layer interneuron-Purkinje cell synaptic transmission via α7 nicotinic acetylcholine receptors in mouse cerebellar cortex.

Pub. Date : 2022 Apr 5

PMID : 35231469






3 Functional Relationships(s)
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1 Nicotine-induced depression in sensory stimulation-evoked MLI-PC synaptic transmission was abolished by either a non-selective nAChR blocker, hexamethonium, or the alpha7-nAChR antagonist methyllycaconitine (MLA), but not the selective alpha4beta2-nAChR antagonist dihydro-beta-erythroidine. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
2 Nicotine-induced depression in sensory stimulation-evoked MLI-PC synaptic transmission was abolished by either a non-selective nAChR blocker, hexamethonium, or the alpha7-nAChR antagonist methyllycaconitine (MLA), but not the selective alpha4beta2-nAChR antagonist dihydro-beta-erythroidine. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
3 Nicotine-induced depression in sensory stimulation-evoked MLI-PC synaptic transmission was abolished by either a non-selective nAChR blocker, hexamethonium, or the alpha7-nAChR antagonist methyllycaconitine (MLA), but not the selective alpha4beta2-nAChR antagonist dihydro-beta-erythroidine. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus