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Nigral GABAergic inhibition upon mesencephalic dopaminergic cell groups in rats
Author(s) -
Saitoh Kazuya,
Isa Tadashi,
Takakusaki Kaoru
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.0953-816x.2004.03337.x
Subject(s) - gabaergic , dopaminergic , neuroscience , midbrain , dopaminergic pathways , chemistry , pharmacology , dopamine , medicine , psychology , central nervous system , inhibitory postsynaptic potential
Synaptic inhibition from the substantia nigra pars reticulata (SNr) to the mesencephalic dopaminergic neurons, which was mediated by gamma (γ)‐amino‐butyric acid (GABA), was investigated in a midbrain slice preparation of Wistar rats. Whole‐cell patch‐clamp recordings were used to record synaptic potentials/currents from the dopaminergic neurons ( n = 93) located in the retrorubral field ( n = 22), the substantia nigra pars compacta ( n = 47) and the ventral tegmental area ( n = 24). In the presence of ionotropic glutamate receptor antagonists electrical stimulation of the SNr induced inhibitory postsynaptic potentials (IPSPs) and/or currents (IPSCs) in 83 neurons. The IPSPs/IPSCs were comprised early and late components. The early IPSPs/IPSCs were mediated by chloride currents through GABA A receptors. The late IPSPs/IPSCs were mediated by potassium currents through GABA B receptors. Both GABA A ‐ and GABA B ‐IPSPs were amplified by repetitive stimuli with frequencies between 25 and 200 Hz. This frequency range covers the firing frequencies of SNr neurons in vivo . It was observed that an application of a GABA B receptor antagonist increased the amplitude of the GABA A ‐IPSPs. The amplification was followed by a rebound depolarization that induced transient firing of dopaminergic neurons. These properties of the IPSPs were common in all of the three dopaminergic nuclei. These results suggest that postsynaptic GABA A ‐ and GABA B ‐inhibition contribute to transient and persistent alternations of the excitability of dopaminergic neurons, respectively. These postsynaptic mechanisms may be, in turn, regulated by presynaptic GABA B ‐inhibition. Nigral GABAergic input may provide the temporospatial regulation of the background excitability of mesencephalic dopaminergic systems.