Currents evoked by GABA and glycine in acutely dissociated neurons from the rat medial preoptic nucleus.
ABSTRACT The responses of acutely dissociated medial preoptic neurons to application of GABA, and glycine were studied using the perforated-patch whole-cell recording technique under voltage-clamp conditions. GABA, at a concentration of 1 mM, evoked outward currents in all cells (n = 33) when studied at potentials positive to -80 mV. The I-V relation was roughly linear. The currents evoked by GABA were partially blocked by 25-75 microM picrotoxin and were also partially or completely blocked by 100-200 microM bicuculline. Glycine, at a concentration of 1 mM, did also evoke outward currents in all cells (n = 12) when studied at potentials positive to -75 mV. The I-V relation was roughly linear. The currents evoked by glycine were largely blocked by 1 microM strychnine. In conclusion, the present work demonstrates that neurons from the medial preoptic nucleus of rat directly respond to the inhibitory transmitters GABA and glycine with currents that can be attributed to GABAA receptors and glycine receptors respectively.
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ABSTRACT: A common feature of general anaesthetic agents is their ability to potentiate neuronal inhibition through GABA(A) (gamma-aminobutyric acid) receptors. At concentrations relevant to clinical anaesthesia, these agents cause a dramatic stimulation of the chloride currents that are evoked by the binding of the natural ligand, GABA. Although there is widespread evidence that the sensitivity of GABA(A) receptors to anaesthetic agents is heterogeneous, the structural basis of these differences is largely unknown. Variations in subunit composition can have profound effects on the sensitivity of GABA(A) receptors to modulatory agents such as benzodiazepines. However, strict subunit specificity has not been demonstrated for the potentiating effects of anaesthetic agents. Here we describe a new class of human GABA(A) receptor subunit (epsilon) that can assemble with alpha- and beta-subunits and confer an insensitivity to the potentiating effects of intravenous anaesthetic agents. The epsilon-subunit also abolishes the normal outward rectification of recombinant receptors in which it assembles. The expression pattern of this subunit in the brain suggests a new target for manipulation of neuronal pathways within the basal ganglia.Nature 03/1997; 385(6619):820-3. · 38.60 Impact Factor
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ABSTRACT: Experiments were carried out to determine the temperature changes induced by the transmitter amino acids gamma-aminobutyric acid (GABA), taurine and glycine (representatives of the inhibitor class of amino acids), and of L-glutamic acid and L-aspartic acid (representatives of the excitatory functional class of amino acids). The amino acids were introduced directly into the preoptic anterial part of the hypothalamus (PO/AH). The experiments were made on male Wistar rats into which cannules were implanted in advance in PO/AH using a stereotaxic apparatus and coordinates of administration after König and Klippel. At ambient temperature of 22 degrees C GABA and taurine are found to cause a dose-dependent hypothermal response, L-aspartic acid and L-glutamic acid lead to dose-dependent hyperthermia, while glycine does not change the body temperature.Acta physiologica et pharmacologica Bulgarica 02/1989; 15(3):50-4.
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ABSTRACT: Extracellular recordings were made from preoptic-anterior hypothalamic neurones with combined recording and iontophoresis electrodes. Short iontophoretic applications of beta-alanine, GABA, glycine and taurine inhibited the discharge of the majority of neurones tested. Bicuculline metho-chloride reversibly and selectively antagonised GABA responses. Strychnine reversibly antagonised beta-alanine, glycine and taurine but not GABA responses. These results suggest the existence of two populations of inhibitory amino acid receptors in the preoptic-anterior hypothalamus. The function of inhibitory amino acids in the rostral hypothalamus was briefly discussed.Experimental Brain Research 02/1981; 43(2):154-8. · 2.22 Impact Factor