Title : Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats.

Pub. Date : 2006 Mar

PMID : 16553775






3 Functional Relationships(s)
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1 (2) The nicotine-facilitated LTP was blocked by dihydro-beta-erythroidine (DHbetaE), a non-alpha7 nAChR antagonist, whereas long-term depression (LTD) was produced by the combination of nicotine and methyllycaconitine, a alpha7-nAChR antagonist. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
2 (2) The nicotine-facilitated LTP was blocked by dihydro-beta-erythroidine (DHbetaE), a non-alpha7 nAChR antagonist, whereas long-term depression (LTD) was produced by the combination of nicotine and methyllycaconitine, a alpha7-nAChR antagonist. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
3 This suggested that several nAChR subtypes were involved in the nicotine-facilitated synaptic plasticity. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus