ANALYSIS OF MASCULINE BEHAVIOR
Principal Investigator: Benjamin Sachs
Abstract: This project is an examination of the mechanical and neuroendocrine causes and effects of sexual potency in animals. This basic research on laboratory rats and other rodent species will promote our comparative understanding of the mechanisms underlying sexual reflexes in males, thereby also facilitating the use of appropriate animal models for the study of the organic origin of human erectile dysfunction and its treatment by pharmacological or surgical means. Sexual reflexes will be studied within and outside the context of copulation in three groups of studies. In one series of experiments, behavioral observations and electromyographic (EMG) recordings of long-term castrated male rats will be used (a) to examine the rate of androgen-induced restoration of activity in the two mechanical systems--i.e., the penile vasculature and the striated penile muscles-- that are normally coordinated in generating penile responses, and (b) to examine indirectly the relative roles of neural cytosol and membrane hormone receptors in the early stages of response restoration by androgen. A second group of studies uses behavioral observation, videorecording, and EMG recording to analyze the coordination of the vascular and striated penile muscle effector systems with each other and with the skeletal movements characteristic of mating in rats. In the third set of studies the mechanical and neuroendocrine effects of penile actions in copula will be compared in laboratory mice, hamsters, and meadow voles. These species were selected because they differ in important aspects of their mating behavior and female reproductive physiology from each other and from previously studied rats. Investigative techniques in this group of studies include surgical and endocrine manipulation of the penile response potential of the males, and scanning electron microscopy of the penile glands to record the changes resulting from castration and androgen replacement.
Funding Period: 1978-09-01 - 1995-06-30
more information: NIH RePORT