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Spontaneous and stimulus-induced release of isotopically labelled glycine was studied in the superfused rat dorsal or ventral medullary surface in vivo. Superfusion of the ventral medullary surface of anesthetized (urethane, 1.2 g/kg, ip) male adult Wistar rats (250-350 g) with high K+ (40 mM) surrogate cerebrospinal fluid (CSF) produced an average increase of 45% over the spontaneous efflux of exogeneously applied glycine (N = 5, P < 0.01). In experiments in which the calcium of the CSF was replaced by an equimolar amount of magnesium, the increase in glycine efflux in response to high K+ was reduced to 15%, a value not statistically different from that observed in control experiments (N = 6). Veratridine stimulation evoked a large (80%) increase in glycine efflux (N = 5, P < 0.001), which was inhibited by tetrodotoxin. High potassium or veratridine failed to modify spontaneous release of glycine on the dorsal medullary surface. Results obtained in control experiments showed that neither high K+ nor veratridine is effective in modifying spontaneous efflux of [3H]-leucine or [3H]-inulin on the ventral or dorsal medullary surface. These data support the hypothesis that glycine is a neurotransmitter on the ventral medullary surface and that it may be part of neural pathways involved in cardiorespiratory regulation present in this region.

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Spontaneous and stimulus-induced release of isotopically labelled glycine was studied in the superfused rat dorsal or ventral medullary surface in vivo. Superfusion of the ventral medullary surface of anesthetized (urethane, 1.2 g/kg, ip) male adult Wistar rats (250-350 g) with high K+ (40 mM) surrogate cerebrospinal fluid (CSF) produced an average increase of 45 per cent over the spontaneous efflux of exogenously applied glycine (N = 5, P<0.01). In experiments in which the calcium of the CSF was replaced by an equimolar amount of magnesium, the increase in glycine efflux in response to high K+ was reduced to 15 per cent, a value not statistically different from that observed in control experiments (N = 6). Veratridine stimulation evoked a large (80 per cent) increase in glycine efflux (N = 5, P<0.001), which was inhibited by tetrodotoxin. High potassium or veratridine failed to modify spontaneous release of glycine on the dorsal medullary surface. Results obtained in control experiments showed that neither high K+ nor veratridine is effective in modifying spontaneous efflux of [(3)H]-leucine or [(3)H]-inulin on the ventral or dorsal medullary surface. These data support the hypothesis that glycine is a neurotransmitter on the ventral medullary surface and that it may be part of neural pathways involved in cardiorespiratory regulation present in this region.

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Stimulus-induced release of labelled taurine has been studied in the superfused rat cerebellar cortex and dorsal medulla in vivo. In the cerebellum both elevated potassium and electrically induced depolarization consistently produced marked increases in the efflux of exogenously applied taurine in a calcium-dependent fashion. Veratridine-stimulation evoked a large Ca2+-independent taurine efflux which was, however, prevented by tetrodotoxin. In the dorsal medulla, both high K+ and veratridine induced a clear Ca2+-independent increase in taurine efflux. Electrical stimulation was always ineffective in changing taurine efflux from the dorsal medulla. These data strongly support a possible neurohumoral role for taurine in the cerebellum but not in the dorsal medulla.

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Estudou-se a liberacao in vivo de GABA, taurina e glicina radiativos, induzida por diferentes agentes despolarizadores aplicados diretamente ao cortex cerebelar exposto de ratos antestesiados. Os resultados obtidos indicam que a glicina provavelmente nao e neurotransmissora no cortex cerebelar, enquanto que o GABA e a taurina devem estar envolvidos na transmissao sinaptica naquela estrutura, como neurotransmissores e talvez, tambem, como moduladores da excitabilidade neuronal

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GABA, taurina e glicina isotopicamente marcdos, em preparacoes in vivo, induzida marcados, em preparacoes in vitro induzida por diferentes agentes despolarizadores aplicados diretamente sobre a superficie pial da regiao dorsal da medula (MD). Os resultados obtidos permitem concluir que o GABA e, provavelmente, o principal neurotransmissor inibidor nessa regiao, a taurina provavelmente esta envolvida como moduladora da excitabilidade neuronal, enquanto que a glicina nao deve ter acao neurotransmissora da MD

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1 The recently discovered benzodiazepine receptor exists in high concentration in the cerebral cortex. We have, therefore, examined the effects of diazepam and chlordiazepoxide on cortical neurone responses to excitatory and inhibitory amino acids and acetylcholine, in the cortex of rats anaesthetized with urethane.2 Chlordiazepoxide applied by microiontophoresis reduced the responses to glutamate and aspartate but acetylcholine responses were unaffected on most cells even by much higher doses of benzodiazepine. gamma-Aminobutyric acid (GABA) and taurine responses were unaffected on most cells, but were reduced on 4 of 25 units. After intravenous diazepam, responses to GABA and taurine were reduced on 3 cells and unchanged on 11.3 On Purkinje cells in the cerebellum a number of cells (5 of 16) exhibited a substantial increase in responses to GABA and taurine following intravenous or iontophoretic application of benzodiazepines.4 It is suggested that the highly selective reduction of excitatory amino acid responses in the cerebral cortex may be of particular relevance to the behavioural effects of benzodiazepines.

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Release patterns for exogenously applied [14C] labelled alpha-amino-n-butyric-acid (GABA) have been investigated in rat cerebellar cortex in vivo. An increase in [14C] GABA release could be evoked by stimulating with high (40 mM) K+ or veratridine (10(-4)M) but not with direct electrical stimulation. Biphasic patterns for high K+ and possibly veratridine stimulated release of GABA suggest the existence of two separate anatomical sources of isotope which are sensitive to these depolarising stimuli. Both K+ and veratridine-evoked GABA release are calcium dependent. Studies involving partial replacement of Na+ with HEPES, (N-2-hydroxyethyl-piperazine-N-2-ethane-sulphonic acid), sucrose or choline chloride also reveal a sodium dependency of [14C] GABA release. These studies collectively indicate a neuronal source for evoked GABA release, a criterion for transmitter identification not previously satisfied in the cerebellar cortex.

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High potassium and electrical stimulation consistently increase efflux of labelled GABA from the in vivo superfused rat dorsal medulla in a calcium-dependent fashion. The depolarizing alkaloid, veratridine, also evokes a large increase in efflux of labelled GABA. These data strongly suggest release from a neurotransmitter pool in this region.

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High (40 mM) potassium stimulation has been shown to increase the efflux in vivo of [1-3H] taurine from the superfused rat cerebellar cortex by 46%, P less than 0.001. During superfusion with calcium-free media this increase in efflux is abolished. The cellular location of [1-3H] taurine in the cerebellar cortex is not yet known, but this region of the brain contains exceptionally high levels of endogenous taurine. The calcium dependency of the release of labelled taurine raises the possibility that taurine has some neuro-humoral role in the cerebellar cortex.

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Replacement of extracellular chloride with isethionate or methylsulphate causes an increased efflux of 1-[14C]-GABA from the in vivo superfused rat cuneate nucleus. This raises the question of the suitability of these anions as inert substitutes for chloride in studies on the ionic dependency of membrane phenomena in the central nervous system.

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