Ultrasonic vocalization induced by intracerebral carbachol in rats: localization and a dose-response study.

It has been recently demonstrated that application of a cholinergic agonist, carbachol, into the anterior hypothalamic-preoptic area in the rat can induce 22 kHz ultrasonic vocalization. Functional mapping of the response in the forebrain and diencephalic regions of the rat brain, as well as the relationship between the dose of carbachol and the multi-parameter recording of vocalization are analyzed in the present study. Direct pressure injection of carbachol into the brain of adapted rats induced a 22 kHz ultrasonic vocalization from a limited region of the anterior hypothalamic-preoptic area and the vicinity of the septum. The response was antagonized by a local pretreatment with atropine and could not be induced by injections of saline vehicle or by handling. Measurements of summed duration of individual calls and response duration showed a typical dose-response relationship for 32-fold range of carbachol doses with ED50 = 0.73 micrograms (4.0 nmol). The increasing dosage of carbachol did not influence the frequency of emitted ultrasounds. On the other hand, the sound intensity increased and the bandwidth decreased with the increasing dosage of carbachol. The mean duration of single calls was also significantly decreased with the carbachol dosage. However, higher doses of carbachol decreased the number of short calls (100-150 ms) but increased the number of longer calls (300-400 ms). The duration of individual calls appeared to be a sensitive index of the response intensity. The results suggest that the cholinergic input into the mediobasal forebrain may play a physiological role in initiating and emitting the 22 kHz ultrasonic vocalization in rats, and that changes in call duration, intensity and bandwidth may be involved in conveying information for conspecifics.