The role of the GABAergic system in the production of ultrasonic vocalization in rats /

Abstract

Ultrasonic vocalization plays an important role in intraspecies communication for rats. It has been well demonstrated that rats will emit 22kHz vocalization in stressfiil or threatening situations. Although the neural mechanism underlying vocahzation is not well understood, it is known that chohnergic input to the basal forebrain induces such alarm calls. A number of experiments have found that intracerebral injection of carbachol, a predominantly muscarinic agonist, into die anterior hypothalamic/preoptic area (AH/POA) rehably induces vocalization similar to naturally emitted ultrasonic calls. It has also been shown that carbachol has extensive inhibitory effects on neuronal firing in the same area. This result impUes that the inhibitory effects of carbachol in the AH/POA could trigger vocahzation, and that the GABAergic system could be involved. The purpose of this study is to investigate the effects ofGABA agonists and antagonists on flie production of carbachol induced 22kHz vocalization. The following hypotheses were examined: 1) apphcation ofGABA (a naturally occurring inhibitory neurotransmitter) will have a synergistic effect with carbachol, increasing vocalization; and 2) tiie apphcation ofGABA antagonists (picrotoxin or bicuculline) will reduce caibachol-induced vocalization. A total of sixty rats were implanted with stainless steel guide cannulae in the AH/POA area. After recovery, animals were locally pretreated with 1) GABA (l-40ng), 2) picrotoxin (1 .5^g) or bicuculhne (0.03ng), or 3) sahne; before injection with carbachol (1 .5^g). The resulting vocalization was measured and quantitated. The results indicate that pretreatment with GABA or GABA antagonists had no significant effect on vocalization. Local pretreatment with GABA did not potentiate the vocal response as measured by its duration, latraicy, and total number of calls. Similarly, pretreatment with picrotoxin or bicuculline had no effects on the same measures of vocalization. The results suggest tfiat chohnoceptive neurons involved in the production of alarm calls are not under direct GABAergic control.