Effects of midbrain lesions on lordosis and ultrasound production

Abstract

Previous studies suggest the control of lordosis by competing neural systems. A lordosis-inhibiting system is thought to originate in the lateral septum (LS) or preoptic area (POA) and project to midbrain sites, including the ventral tegmental area (VTA) and ventral half of the periaqueductal gray (vPAG). A lordosis-facilitating system is thought to originate in the ventromedial hypothalamus and project to the dorsal half of the PAG (dPAG). To test the generality of this model, we subjected female hamsters to control operations or lesions of the dPAG, vPAG or VTA. Subjects in hormone-induced estrus were observed for lordosis responses to males and manual stimulation and for rates of production of the “ultrasounds” used by hamsters for courtship. PAG lesions of both types depressed ultrasound rate, lordosis initiation and lordosis maintenance. VTA lesions failed to affect ultrasound rate, lordosis maintenance or lordosis responses to males. However, damage to the dorsomedial tegmentum was correlated with deficits in lordosis initiation. These results suggest the concentration in the PAG of mechanisms controlling vocalizations, including the ultrasounds used by hamsters for courtship. They confirm midbrain control of lordosis initiation and maintenance but fail to support any simple specialization of dorsal and ventral areas for these dimensions. They also fail to support a specialization of the dorsal and ventral halves of the midbrain for lordosis facilitation and inhibition, but do suggest several midbrain areas likely to be involved in the first of these functions.