Nitric Oxide NO is emerging as an essential neurotransmitter within the CNS for erectile response. NO appears to act in several regions of the brain, including the MPOA and PVN.

Injection of NO-synthase (NOS) inhibitors into the PVN prevents penile erection induced by dopamine agonists and oxytocin.

NO production increased in the PVN of rats during noncontact erections, confirming the role of NO production during erection.

ACTH and a-MSH Adrenocorticotropic hormone (ACTH) and its related peptide a(alpha)-melanocyte stimulating hormone (a-MSH) have been shown to elicit erectile responses in addition to increased grooming, stretching, and yawning behaviors when given intracerebroventricularly to lab animals.

This proerectile effect appears to be due to the stimulation of melanocortin-3 (MC3) receptors which are prevalent in the hypothalamus and limbic system. The role of these peptides in erectile response is not entirely known, but they appear to induce erection by acting at sites distinct from those in the PVN stimulated by dopamine and oxytocin.  Additionally, Melanotan II, an a-MSH synthetic analog, has had proerectile effects in humans with psychogenic impotence.

Other Neurotransmitters Excitatory amino acids, such as l-glutamate, N-methyl-d-aspartate (NMDA), amino-3-hydroxy- 5-methyl-isoxazole-4-propionic acid (AMPA), and trans-1-amino-1,3-cyclo-pentadicarboxylic acid (ACPD) have been shown to have proerectile effects when injected into the MPOA or PVN of lab animals. Gamma-amino butyric acid (GABA) appears to function as an inhibitor in the reflex pathways for penile erection. Stimulation of opiod m receptors appears to centrally prevent penile erection and impair copulation likely through the prevention of the increased NO production in the PVN during sexual activity.