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|Title:||Evidence for neuronal release of isotopically labelled glycine from the rat ventral medullary surface in vivo|
Assumpção, Jurandyr D'Avila [UNIFESP]
Confessor, Yara Queiroga [UNIFESP]
Guertzenstein, Pedro Gaspar [UNIFESP]
Cravo, Sergio Luiz [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
|Publisher:||Assoc Bras Divulg Cientifica|
|Citation:||Brazilian Journal Of Medical And Biological Research. Sao Paulo: Assoc Bras Divulg Cientifica, v. 29, n. 4, p. 527-532, 1996.|
|Abstract:||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 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%, 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 [H-3]-leucine or [H-3]-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.|
|Appears in Collections:||Artigo|
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