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This Article Full Text Full Text (PDF) All Versions of this Article: 94/4/2549    most recent 00339.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Guo, J.-Z. Articles by Chiappinelli, V. A. Search for Related Content PubMed PubMed Citation Articles by Guo, J.-Z. Articles by Chiappinelli, V. A.

Synaptically Released and Exogenous ACh Activates Different Nicotinic Receptors to Enhance Evoked Glutamatergic Transmission in the Lateral Geniculate Nucleus

Department of Pharmacology and Physiology, The George Washington University, School of Medicine and Health Sciences, Washington, DC

Submitted 31 March 2005; accepted in final form 13 June 2005

The effects of activation of nicotinic acetylcholine receptors (nAChRs) on glutamatergic transmission in the ventral lateral geniculate nucleus (LGNv) were examined in chick brain slices. Whole cell recordings showed that monosynaptic postsynaptic currents (PSCs) evoked in LGNv neurons by optic tract stimulation were blocked by glutamate receptor antagonists. Exogenously applied nicotine (0.5 µM), choline (1 mM), or acetylcholine (ACh, 100 µM) markedly increased (>3-fold) these evoked PSCs. Potentiation by ACh was dose-dependent and did not desensitize during a 5-min application. In a second set of experiments, the effect of releasing endogenous ACh by stimulating the lateral portion of the LGNv through a separate conditioning electrode before optic tract stimulation was examined. Conditioning stimulation trains increased PSCs by an average of 5.2-fold, an effect dependent on both the intensity and number of conditioning pulses. This increase in PSC amplitude was most likely caused by released ACh activating 6- and/or 3-containing nAChRs because it was blocked by 100 nM -conotoxin MII, 100 nM dihydro--erythroidine (DHE), and 0.1–1.0 µM methyllycaconitine (MLA). In contrast, exogenously applied ACh increased PSC amplitude by activating a pharmacologically different population of nAChRs because this effect was inhibited by 100 nM -bungarotoxin, 50 nM MLA, and a high concentration (30 µM) of DHE, indicating that 7- and/or 8-containing receptors were involved. The results are consistent with a model whereby 6- and/or 3-containing nAChRs on retinal ganglion cell nerve terminals are located preferentially at cholinergic synapses, whereas 7- and/or 8-containing receptors are primarily extrasynaptic.