Electrophysiological analysis of reciprocal caudato-nigral relations

Frigyesi, Tamas L.; Purpura, Dominick P.

doi:10.1016/0006-8993(67)90057-1

Cited by 191 publications

(27 citation statements)

References 25 publications

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“…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). …”

Section: Introductionmentioning

confidence: 99%

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

Davies¹,

Tongroach²

1979

The Journal of Physiology

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SUMMARY1. The effects of tetanus toxin were determined on GABA-mediated synaptic inhibition of substantia nigra neurones evoked by striatal stimulation and on the presumed dopamine-and 5-hydroxytryptamine-mediated synaptic inhibition of striatal neurones evoked by nigral and dorsal raphe nucleus stimulation, respectively, in the urethane-anaesthetized rat.2. Following an intranigral injection of tetanus toxin, striatal-evoked inhibition of substantia nigra neurones, which is sensitive to bicuculline, was rapidly abolished. This effect was not accompanied by any significant change in the responses of nigral neurones to ionophoretically administered GABA or other putative neurotransmitters and thus indicates a presynaptic site of action of the toxin. 3. The rate of onset of action of the toxin in the substantia nigra was extremely rapid (1-4 min) and appeared to be related to the rate of activation of the inhibitory pathway.4. Injections into the substantia nigra of tetanus toxin neutralized with antitoxin had no significant effect on striatal-evoked inhibition in the substantia nigra.5. Injections of tetanus toxin into the striatum failed to influence the inhibition of striatal neurones evoked by stimulation of the ipsilateral substantia nigra or the dorsal raphe nucleus, suggesting that tetanus toxin does not impair monoaminemediated inhibition in the central nervous system. 6. Synaptic excitation which preceded substantia-nigra-evoked inhibition in striatal neurones and which occasionally preceded striatal-evoked inhibition in nigral neurones was also unaffected by tetanus toxin.7. It is suggested that tetanus toxin selectively abolishes GABA-mediated synaptic inhibition in the central nervous system and may be a useful tool in the identification of such synaptic inhibitory mechanisms.

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Section: Introductionmentioning

confidence: 99%

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

Davies¹,

Tongroach²

1979

The Journal of Physiology

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“…Both the uptake of GABA into nerve terminals in the substantia nigra (Hattori, McGeer, Fibiger & McGeer, 1973) and its release from slices of substantia nigra (Hokfelt, Jonsson & Ljungdahl, 1970;Okada & Hassler, 1973) have been demonstrated. Furthermore, electrophysiological studies have shown that the activity of neurones in the substantia nigra may be reduced by electrical stimulation of the ipsilateral caudate nucleus (Grossman, 1966;Frigyesi & Purpura, 1967;Feltz, 1971;Goswell & Sedgwick, 1971;Crossman, Walker & Woodruff, 1973;Feger & Ohye, 1975) and also by GABA applied by micro-electrophoresis (Feltz, 1971;Crossman et al 1973). In addition, both the caudate evoked depression of substantia nigra neurones and that produced by GABA may be reduced by picrotoxin Crossman et al 826 1973) and on this evidence it has been suggested that the striato-nigral pathway is inhibitory and utilizes GABA as the neurotransmitter.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, the possibility of an additional excitatory input to the substantia nigra has been raised by Frigyesi & Purpura (1967) who showed that stimulation of the caudate nucleus induced an e.p.s.p.-i.p.s.p. sequence in substantia nigra neurones and both Feltz (1971) and Feger & Ohye (1975) have demonstrated an excitation of substantia nigra neurones which preceded inhibition.…”

Section: Introductionmentioning

confidence: 99%

Caudate stimulation and substantia nigra activity in the rat.

Dray¹,

Gonye²,

Oakley³

1976

The Journal of Physiology

174

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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.

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“…Since 1967, many in vivo electrophysiological studies have investigated the effects of electrical stimulation of the dopaminergic nigrostriatal pathway on striatal neurons (Frigyesi and Purpura, 1967;Siggins, 1978;Wilson et al, 1982). None of the observed effects, however, have been unequivocally attributed to the evoked DA release (Siggins, 1978;Wilson et al, 1982).…”

Section: Kinetics Of the Dopaminergic Transmission Mediated By D1 Recmentioning

confidence: 99%

Prolonged and Extrasynaptic Excitatory Action of Dopamine Mediated by D1 Receptors in the Rat StriatumIn Vivo

1997

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The spatiotemporal characteristics of the dopaminergic transmission mediated by D1 receptors were investigated in vivo. For this purpose dopamine (DA) release was evoked in the striatum of anesthetized rats by train electrical stimulations of the medial forebrain bundle (one to four pulses at 15 Hz), which mimicked the spontaneous activity of dopaminergic neurons. The resulting dopamine overflow was electrochemically monitored in real time in the extracellular space. This evoked DA release induced a delayed increase in discharge activity in a subpopulation of single striatal neurons. This excitation was attributable to stimulation of D1 receptors by released DA because it was abolished by acute 6-hydroxydopamine lesion and strongly reduced by the D1 antagonist SCH 23390. Striatal neurons exhibiting this delayed response were also strongly excited by intravenous administration of the D1 agonist SKF 82958. Whereas the DA overflow was closely time-correlated with stimulation, the excitatory response mediated by DA started 200 msec after release and lasted for up to 1 sec. Moreover, functional evidence presented here combined with previous morphological data show that D1 receptors are stimulated by DA diffusing up to 12 m away from release sites in the extrasynaptic extracellular space. In conclusion, DA released by bursts of action potentials exerts, via D1 receptors, a delayed and prolonged excitatory influence on target neurons. This phasic transmission occurs outside synaptic clefts but still exhibits a high degree of spatial specificity.

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Electrophysiological analysis of reciprocal caudato-nigral relations

Cited by 191 publications

References 25 publications

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

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

Caudate stimulation and substantia nigra activity in the rat.

Prolonged and Extrasynaptic Excitatory Action of Dopamine Mediated by D1 Receptors in the Rat StriatumIn Vivo

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