Plasma GH Responses to Hypothalamic, Hippocampal and Amygdaloid Electrical Stimulation: Effects of Variation in Stimulus Parameters and Treatment with α-Methyl-p-Tyrosine (α-MT)1
Plasma GH responses, as measured by radioimmunoassay, were determined in individual pentobarbital—anesthetized rats following electrical, stimulation of several neural sites. Significant increments in plasma GH levels occurred with stimulation of the ventromedial hypothalamic nucleus, the hippocampus and the basolateral amygdala. Electrical stimulation of the corticomedial amygdala inhibited GH release. Effective stimulation parameters varied from one site to another. Trains of stimuli (5 sec on, 10 sec off) delivered for 2 min via monopolar electrodes placed bilaterally in the ventromedial nucleus were effective in eliciting GH release. Total stimulation periods of 10 and 5 min were required to elicit responses from hippocampus and basolateral amygdala, respectively, using unilateral bipolar electrodes. Current intensities of 500–700 μA were effective in the ventromedial nucleus provided long pulse durations of 1–2 msec were employed. Long pulse durations (1–2 msec) were necessary for eliciting GH release after hippocampal stimulation. On the other hand, basolateral amygdaloid stimulation was effective with shorter pulse durations (0.2 to 0.5 msec). GH responses to ventromedial stimulation were not affected by pretreatment with α-MT (250 mg/kg, 24 and 10 hr before stimulation), whereas, hippocampal and basolateral amygdaloid—induced responses were blocked. These results suggest that several extrahypothalamic structures may have a role in excitation or inhibition of GH release and relay of these responses to the hypothalamus may involve catecholaminergic neurons. (Endocrinology92: 1354, 1973)