The effects of adrenergic stimulation on the pulsatile release of LH were investigated in ovariectomized rats with acute depletion of brain norepinephrine (NE) levels. Rats bearing atrial cannula were pretreated with NE synthesis inhibitors, diethyldithiocarbamate (DDC) or bis (4-methyl-1-homopiperanzinyl thiocarbanyl) disulfide (FLA-63) and blood was withdrawn at 15-min intervals beginning 1 h later. DDC and FLA-63 markedly dampened pulsatile LH secretion. Administration of the α-adrenergic agonist clonidine (CLON) resulted in immediate LH release and apparent resumption of pulsatile LH secretion. The facilitatory effect of CLON on LH secretion was more pronounced in FLA-63 than in DDC-pretreated rats. Additional characterization of the pattern of LH secretion in FLA-63-pretreated rats showed that the interval between LH pulses was significantly lengthened after acute NE depletion; however, CLON treatment increased LH pulse frequency to that found in ovariectomized rats. To further investigate the ability of CLON to augment pulsatile LH release, the LH secretory pattern was determined between 2 and 4 h after CLON administration in FLA-63-pretreated rats. 8 of 10 rats receiving CLON (0.3 mg/kg) responded with episodic LH release 2–4 h following treatment while saline-treated rats continued to show dampened LH secretory patterns. These studies demonstrate that following acute depletion of NE in ovariectomized rats, a single injection of CLON can enhance both the amplitude and frequency of LH pulses. Further, the data suggest that central noradrenergic neurons exert only a permissive effect on pulsatile LH release and that the pulsatile mechanism may predominately be resident in LHRH neurons.

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