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Journal of Neuroscience, Vol 12, 4347-4357, Copyright © 1992 by Society for Neuroscience
Pharmacological characterization of calcium currents and synaptic transmission between thalamic neurons in vitro
FW Pfrieger, NS Veselovsky, K Gottmann and HD Lux
Department of Neurophysiology, Max-Planck-Institute for Psychiatry, Planegg-Martinsried, Germany.
We recorded from pairs of cultured, synaptically connected thalamic
neurons. Evoked excitatory postsynaptic currents (EPSCs) reversed at +17 mV
and were blocked reversibly by 1 mM kynurenic acid, a glutamate receptor
antagonist. NMDA and non-NMDA receptors mediated excitatory post-synaptic
responses, as shown by selective block of EPSC components with 50 microM
(+/-)-2-amino-5-phosphonopentanoic acid and 10 microM
6,7-dinitroquinoxaline-2,3-dione, respectively. Inhibitory postsynaptic
responses were evoked less frequently and were blocked by the GABAA
receptor antagonist (-)-bicuculline methochloride. The pharmacological
profiles of whole-cell calcium currents and evoked EPSCs were compared.
With 50 microM cadmium chloride (Cd), whole-cell low voltage-activated
(LVA) calcium currents were reduced in amplitude and high voltage-
activated (HVA) calcium currents and excitatory synaptic transmission were
completely blocked. This suggests that the residual calcium influx through
LVA channels into the presynaptic terminal does not suffice to trigger
transmitter release. A saturating concentration of omega- conotoxin GVIA
(omega-CgTx) (2.5 microM) blocked one-third of whole- cell HVA calcium
currents and evoked EPSCs. The dihydropyridine nifedipine (50 microM)
reversibly reduced whole-cell HVA calcium currents in a voltage-dependent
manner but not excitatory synaptic transmission. Cd and omega-CgTx did not
alter amplitude distributions of miniature EPSCs, demonstrating that the
inhibition of synaptic transmission was due to block of presynaptic calcium
channels. We conclude that excitatory glutamatergic transmission in
thalamic neurons in vitro was mediated mainly by HVA calcium currents,
which were insensitive to omega-CgTx and nifedipine.
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