Calcium channels in the GABAergic presynaptic nerve terminals projecting to Meynert neurons of the rat

Citation
Js. Rhee et al., Calcium channels in the GABAergic presynaptic nerve terminals projecting to Meynert neurons of the rat, J NEUROCHEM, 72(2), 1999, pp. 800-807
Citations number
34
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROCHEMISTRY
ISSN journal
00223042 → ACNP
Volume
72
Issue
2
Year of publication
1999
Pages
800 - 807
Database
ISI
SICI code
0022-3042(199902)72:2<800:CCITGP>2.0.ZU;2-K
Abstract
Effects of selective Ca2+ channel blockers on GABAergic inhibitory postsyna ptic currents (IPSCs) were studied in the acutely dissociated rat nucleus b asalis of Meynert (nBM) neurons attached with nerve endings, namely, the "s ynaptic bouton" preparation, and in the thin slices of nBM, using nystatin perforated and conventional whole-cell patch recording modes, respectively. in the synaptic bouton preparation, nicardipine (3 x 10(-6) M) and omega-c onotoxin-MVIIC (3 x 10(-6) M) reduced the frequency of spontaneous postsyna ptic currents by 37 and 22%, respectively, whereas omega-conotoxin-GVIA had no effect. After blockade of L- and P/Q-type Ca2+ channels, successive rem oval of Ca2+ from external solution had no significant effect on the residu al spontaneous activities, indicating that N-, R-, and T-type Ca2+ channels are not involved in the spontaneous GABA release. Thapsigargin, but not ry anodine, increased the frequency of spontaneous IPSCs in both the synaptic bouton and slice preparations, suggesting the partial contribution of the i ntracellular Ca2+ storage site to the spontaneous GABA release. In contrast , omega-conotoxin-GVIA (3 x 10(-6) M) and omega-conotoxin-MVIIC (3 x 10-6 M ) suppressed the evoked IPSCs by 31 and 37%, respectively, but nicardipine produced no significant effect. the residual evoked currents were abolished in Ca2+-free external solution but not in the external solution containing 10(-5) M Ni2+ suggesting the involvement of N-, P/Q-, and R-type Ca2+ chan nels but not L- and T-type ones in the evoked IPSCs. Neither thapsigargin n or ryanodine had any significant effects on the evoked IPSCs. It was conclu ded that Ca2+ channel subtypes responsible for spontaneous transmitter rele ase are different from those mediating the transmitter release evoked by ne rve stimulation.