RESUMO
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.
Assuntos
Glicina/metabolismo , Bulbo/metabolismo , Animais , Masculino , Bulbo/efeitos dos fármacos , Potássio/farmacologia , Radioisótopos , Ratos , Ratos Wistar , Veratridina/farmacologiaRESUMO
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.
Assuntos
Masculino , Animais , Ratos , Glicina/biossíntese , Bulbo/metabolismo , Análise de Variância , Potássio/farmacocinética , Ratos Wistar , Veratrina/farmacologiaRESUMO
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
Assuntos
Masculino , Animais , Ratos , Ácido gama-Aminobutírico , Córtex Cerebelar , Técnicas In VitroRESUMO
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