Navarro C E, Cabrera R J, Donoso A O
Laboratorio de Investigaciones Cerebrales, LINCE-CONICET, Facultad de Ciencias Médicas, Mendoza, Argentina.
Brain Res Bull. 1995;37(2):119-22. doi: 10.1016/0361-9230(94)00261-x.
Glutamate has been shown to stimulate noradrenaline (NA) release from hypothalamic nerve terminals. In the present study, we evaluated the possible interaction between the excitatory amino acid glutamate and gamma-aminobutyric acid (GABA), an inhibitory transmitter, on noradrenaline (NA) release from mediobasal hypothalamus (MBH) of adult male rats. Hypothalamic slices loaded in vitro with 3H-NA were superfused and exposed to glutamate, N-methyl-D-aspartic acid (NMDA), or kainate (KA). We found that 3H-NA release evoked by the excitatory amino acids glutamate and NMDA was dramatically decreased by GABA. The facilitatory effects of NMDA and KA were prevented concentration-dependently by the GABAB receptor antagonist 2-hydroxy saclofen which restored the NMDA effect. In addition, baclofen blocked K(+)-induced 3H-NA release. Activation of GABAA receptors by muscimol and THIP was ineffective. In conclusion, glutamate and GABA, through GABAB receptors, may interact to modulate NA release from the rat mediobasal hypothalamus.