Abstract
In the first experiment the role of γ-aminobutyric acid (GABA) in the display of lordosis behavior was examined in septal-lesioned and sham-operated ovariectomized rats. Following estradiol benzoate (EB) priming, septal-lesioned rats were tested for lordosis behavior before and after bilateral infusion of picrotoxin or saline directly into the substantia nigra (SN). Sham animals were given the same behavioral tests but received intranigral infusion of either hydrazinopropionic acid (HPA) or saline. Picrotoxin, which blocks GABA receptors, was effective in suppressing the hhgh levels of lordosis behavior seen in the EB-primed septal-lesioned female rat 30 min after infusion, but not at 120 min. Conversely, HPA, which elevates endogenous GABA levels, was effective in facilitating lordosis behavior in sham-operated rats treated with EB only. The lordosis quotient was moderately increased 30 min after HPA infusion, reached high levels at 120 min, and returned to low levels by 360 min post-infusion, demonstrating the reversibility of the drug effect. Saline infusions in lesioned and sham-operated controls were without effect. In the second experiment septal-lesioned and sham-operated rats were primed with EB and infused with the drugs as in the first experiment, but were sacrificed at the time the maximal behavioral effect has been observed in the first experiment. Tyrosine hydroxylase (TH) activity and dopamine (DA) and homovanillic acid (HVA) levels were measured. No effect on TH activity was found. However, sham-operated rats receiving HPA infusions had lower DA and receiving picrotoxin infusions had higher DA and HVA levels than those of lesioned saline-injected controls. Septal-lesioned saline-infused rats also showed decreased DA and HVA levels relative to sham-operated saline-infused animals. These results support the concept of a GABA inhibitory neuronal feedback system which modulates DA turnover and perhaps plays a critical role in the neural control of lordosis behavior.
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