Caudate stimulation and substantia nigra activity in the rat.

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Abstract
The responses of spontaneously active single neurons in the substantia nigra and overlying mesencephalic reticular formation were analyzed during the electrical stimulation of the ipsilateral caudate nucleus. Experiments were performed in rats anesthetized with urethane or pentobarbitone. All recordings were made extracellularly with multibarrelled glass micropipettes which were also used to test neuronal responsiveness to electrophoretically administered substances. The micropipette tip position was marked and the distribution of neurons studied was analyzed. Single shock stimulation of the caudate nucleus inhibited neuronal activity in the substantia nigra (270/320 cells: mean latency 5.4 ms) and in the mesencephalic reticular formation (62/72 cells: mean latency 16.6 ms). These effects were often accompanied by periods of excitation. In pentobarbitone anesthetized animals the latency and duration of these substantia nigra inhibitions was increased. Compared with the zona reticulata, fewer neurons in the zona compacta of the substantia nigra responded to caudate stimulation in both urethane or pentobarbitone anesthetized animals. The activity of most cells was depressed by electrophoretically administered GABA or glycine and increased by acetylcholine or glutamate. Neurons of the mesencephalic reticular formation were less sensitive to GABA and glycine than substantia nigra neurons. Within the substantia nigra, both zona compacta and zona reticulata neurons were more sensitive to GABA than to glycine. Over-all, glutamate was a more potent excitant than acetylcholine (ACh). Electrophoretic bicuculline methochloride (BMC) consistently reduced GABA but not glycine depression of substantia nigra neurons. Approximately twice as much BMC was required to reduce the endogenous inhibition of the same substantia nigra neurons 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. Electrophoretic strychnine consistently reduced glycine but not GABA depression of substantia nigra neurons, and did not modify caudate evoked inhibition of these neurons or the accompanying field potential. There may be a slowly conducting caudatonigral pathway which has both facilitatory and inhibitory components. The inhibitory pathway may use 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.