In the present article we report that in vivo LHRH output as measured at the anterior pituitary following castration significantly increased, due to larger and more frequent LHRH signals arriving to this gland. This contrasts with the decreased amplitude and overall mean LHRH release of castrate males bearing a push-pull cannula within the hypothalamus. These divergent results have generated a new thesis regarding the role of gonadal steroids upon the LHRH pulse generator. This thesis submits that following castration there is an increased frequency and decreased amplitude of the LHRH signal from discrete loci within the medial basal hypothalamus, but an increased synchrony of LHRH release throughout the entire hypothalamus, resulting in an increased frequency and amplitude of LHRH arriving at the anterior pituitary.