Caudate stimulation and substantia nigra activity in the rat.

Abstract

SUMMARY1. The responses of spontaneously active single neurones in the substantia nigra and overlying mesencephalic reticular formation have been analysed during the electrical stimulation of the ipsilateral caudate nucleus. Experiments were performed in rats anaesthetized with urethane or pentobarbitone. All recordings were made extracellularly with multibarrelled glass micropipsttes which were also used to test neuronal responsiveness to electrophoretically administered substances. The micropipette tip position was marked and the distribution of neurones studied has been analysed.2. Single shock stimulation of the caudate nucleus inhibited neuronal activity in the substantia nigra (270/320 cells: mean latency 5-4 msec) and in the mesencephalic reticular formation (62/72 cells: mean latency 16-6 msec). However, these effects were often accompanied by periods of excitation. In pentobarbitone anaesthetized animals the latency and duration of these substantia nigra inhibitions was increased.3. Compared with the zona reticulate, fewer neurones in the zona compacta of the substantia nigra responded to caudate stimulation in both urethane or pentobarbitone anaesthetized animals.4. The activity of most cells was depressed by electrophoretically administered GABA or glycine and increased by acetylcholine or glutamate. Neurones of the mesencephalic reticular formation were less sensitive to GABA and glycine than substantia nigra neurones. Within the substantia nigra, both zona compacta and zona reticulate neurones were more sensitive to GABA than to glycine. Over-all, glutamate was a more potent excitant than acetylcholine (ACh).5. Electrophoreticbicuculline methochloride (BMC) consistently reduced "ABA but not glycine depression of substantia nigra neurones. Approximately twice as much BMC was required to reduce the endogenous A. DRAY, T. J. GONYE AND N. R. OAKLEY inhibition of the same substantia nigra neurones and the amplitude of the concomitantly evoked positive field potential as was required to abolish exogenous GABA responses. Some evoked substantia nigra inhibitions were resistant to BMC.6. Electrophoretic strychnine consistently reduced glycine but not GABA depression of substantia nigra neurones, and did not modify caudate evoked inhibition of these neurones or the accompanying field potential.7. The results support the concept of a slowly conducting caudatonigral pathway which has both facilitatory and inhibitory components. The inhibitory pathway uses GABA as the neurotransmitter. The identity of the possible excitatory transmitter is unknown. The monosynaptic nature of this pathway is uncertain and the possible contribution of other bicuculline insensitive nigral inhibitory processes is discussed.

Do silent dopaminergic neurons exist in rat substantia nigra in vivo?

“…24 However, when a higher stimulus intensity (>500 µA) was used, dopaminergic neurons were inhibited, 24 consistent with the majority of reports on the effects of striatal stimulation on identified dopaminergic neurons. 15,16,29,37,38,42,50,52 Since the stimulus parameters used in the present study were 1.0 mA with a duration of 500 µs, the stimulus would be expected to inhibit, not excite, dopaminergic neurons, and is thus unlikely to account for the failure to detect any silent dopaminergic neurons.…”

In vivo release of dopamine from rat striatum, substantia nigra and prefrontal cortex: differential modulation by baclofen

“…The present results are in agreement with the inhibition by GABAB receptors of the nigral dopaminergic activity, since baclofen infusion into the SN decreased the release of '** dopamine in the SN. It has been reported that intranigral injection of GABA decreases dopamine release in the ipsilateral ST (Reid et al, 1988), while nigral perfusion of baclofen (10 JM) decreases dopamine release in the same SN 150 180 210 and in the ipsilateral ST (Westerink et al, 1992 (Aghajanian & Bunney, 1975;Dray et al, 1976).…”

Tetanus toxin and synaptic inhibition in the substantia nigra and striatum of the rat.

“…To this end an examination was made of the effects of tetanus toxin on the inhibitory effect of striatal stimulation on neurones in the substantia nigra. Electrophysiological and neurochemical data indicates that this pathway is relatively long and that the inhibitory effect of striatal stimulation is mediated by GABA or a GABA-like substance (Frigyesi & Purpura, 1967;Feltz, 1971;Precht & Yoshida, 1971;Crossman, Walker & Woodruff, 1973;Fonnum, Grofova, Rinvik, Storm-Mathisen & Walberg, 1974;Dray, Gonye & Oakley, 1976). …”