MORPHINE MODULATION OF GABA-INDUCED AND GLUTAMATE-INDUCED CHANGES OF VENTRAL PALLIDAL NEURONAL-ACTIVITY

Microiontophoresis was used to investigate the influence of morphine o n the GABA- and glutamate-evoked responses of ventral pallidal neurons recorded extracellularly from chloral hydrate-anesthetized rats. Of t he GABA-sensitive neurons (50 of 69 tested) in the ventral pallidum, a ll displayed a decreased firing rate when GABA was applied, whereas al l of the glutamate-sensitive neurons (29 of 40 tested) increased neuro nal activity in the presence of glutamate. The majority of ventral pal lidal cells tested (65 of 83) were sensitive to iontophoretically appl ied morphine, and both increases and decreases in neuronal activity we re observed. The ability of morphine to alter the ratio between amino acid-evoked activity (''signal'') and spontaneous firing (''noise'') w as used as an indicator of morphine modulation. A morphine subthreshol d ejection current, i.e. one that did not change spontaneous firing ra te, and a morphine ejection current that produced approximately 50% of the maximum opioid-induced neuronal response were chosen for this eva luation. When morphine was co-iontophoresed with GABA or glutamate, at tenuation of the amino acid signal-to-noise ratio was generally seen, though some potentiations were observed. These changes were independen t of the direction of morphine-induced changes in spontaneous firing r ate. Both sub- and suprathreshold ejection currents were capable of af fecting GABA- and glutamate-evoked responses. These data suggest that morphine is a robust ventral pallidal neuromodulator. As ventral palli dal amino acid activity is important in the integration of sensorimoto r information, opioid modulation of amino acid transmission in the ven tral pallidum may have a profound effect on this integration. Copyrigh t (C) 1997 IBRO.