(129) A Neurological Excitation/Inhibition “Faucet Model” for Orgasm and Pain

Abstract

Abstract Introduction A prevalent concept of neuronal inhibition in sexual response is that it opposes the effects of neuronal excitation, e.g., the classical arm balance in which excitation and inhibition are on opposite arms of the balance; when one is up, the other is down (Perelman: Curr Sex Health Rep 2018;10:38). However, there is extensive evidence that neuronal inhibition can increase jointly and concurrently with neuronal excitation. Objective To review extensive evidence of neuronal inhibition increasing concurrently with neuronal excitation in various contexts including sexual response and orgasm. Methods Review neurological evidence and propose a novel model of neuronal excitation and inhibition acting jointly to enable intense sexual response and orgasm. Results The intensity of neuronal inhibition can increase concurrently with an increase in excitation, thereby actually enabling the excitation intensity to increase, as in the most basic functions of the nervous system, i.e., the spinal reflexes, and in graceful, non-spastic movement of precision, and intense movement. Sensorially, pain activates the endogenous pain-inhibiting system. In sexual response, as the intensity of response to vaginal self-stimulation increased from pressure to pleasure to orgasm, the intensity of pain inhibition also increased. The spinothalamic tract, which transmits pain, also transmits the genital stimulation leading to orgasm. In the brain, major components that are activated by pain are also activated by orgasm, evidence of sites of inhibitory interactions between genital afferent activity and pain perception. When the intensity of excitation surpasses that of concurrent inhibition, the excitation is perceived as aversive or painful (Komisaruk & delCerro: Sex Med Rev 2022;10:481). We propose a model of this view of concurrent excitation and inhibition, both increasing in intensity jointly to orgasm, as hot (excitatory) and cold (inhibitory) water flowing from a faucet. This model differs from that of a classical balance in that it incorporates variations in intensity of excitation and inhibition independently of each other as well as concurrently and jointly, rather than just reciprocally. Thus, a low versus high flow rate of hot water would represent mild or intense pain, whereas a high flow rate of both hot and cold water would represent intense, but non-painful, comfortable excitation, as in orgasm, with perhaps the hot water intensity just exceeding the cold at orgasm. Weak, “anhedonic” orgasm, or premature ejaculation are represented by the “faucet model” as hot and cold water at a very low flow rate; anorgasmia and/or “HSDD” as cold consistently surpassing hot at any flow rate, from low to high, depending on the dynamic qualities of the anorgasmia, i.e., not “getting going”, or “getting close, but not there”, with regard to orgasm. In the latter case e.g., a titrated combination of excitatory (hot) and inhibitory (cold) pharmaceuticals might enable a more delayed and intense orgasm. Conclusions Our proposed “faucet model” of neuronal excitation and inhibition mediating sexual response and orgasm, which is based on extensive neurological evidence, we believe can account for a variety of healthy and pathological sexual responses, and provide a rational basis for therapeutic application. Disclosure Any of the authors act as a consultant, employee or shareholder of an industry for: Adamo Bioscience (first author); many others (last author).