Pb2+ via protein kinase C inhibits nicotinic cholinergic modulation of synaptic transmission in the hippocampus

The Journal of Pharmacology and Experimental Therapeutics
M F BragaEdson X Albuquerque

Abstract

The present study was designed to investigate the effects of Pb(2+) on modulation of synaptic transmission by nicotinic receptors (nAChRs) in the rat hippocampus. To this end, inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs, respectively) were recorded by means of the whole-cell mode of the patch-clamp technique from rat hippocampal neurons in culture. Acetylcholine (ACh, 1 mM; 1-s pulses) triggered GABA release via activation of alpha4beta2* and alpha7* nAChRs. It also triggered glutamate release via activation of alpha7* nAChRs. Pb(2+) (0.1 and 1 microM) blocked ACh-triggered transmitter release. Blockade by Pb(2+) of ACh-triggered IPSCs was partially reversible upon washing of the neurons. In contrast, even after 30- to 60-min washing, there was no reversibility of Pb(2+)-induced blockade of ACh-triggered EPSCs. The effects of Pb(2+) on GABA release triggered by activation of alpha7* and alpha4beta2* nACRs were mimicked by the protein kinase C (PKC) activator phorbol-12-myristate-13-acetate (1 microM) and blocked by the indolocarbazole Go 7874 (50 nM) and the bisindolylmaleimide Ro-31-8425 (150 nM), which are selective PKC inhibitors. After washing of fully functional neuronal networks that had been exposed ...Continue Reading

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Citations

Aug 12, 2008·Neurobiology of Disease·Paul GierkeKarl-Heinz Braunewell
Jul 14, 2009·Brain Research·Sudarshana PurkayasthaProbal Banerjee
Nov 7, 2013·Toxicology and Industrial Health·Izabela GutowskaEwa Stachowska
Jun 20, 2020·Biological Trace Element Research·Emilia MetrykaIrena Baranowska-Bosiacka
Feb 3, 2021·Toxics·Daniela Ramírez OrtegaVerónica Pérez de la Cruz

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