Oxytocin and vasopressin/anti-diuretic hormone, the two peptide hormones of the posterior pituitary gland (the neurohypophysis), are secreted from the nerve endings of magnocellular neurosecretory neurons into the systemic circulation. The cell bodies of these oxytocin and vasopressin neurons are in the paraventricular nucleus and supraoptic nucleus respectively, and the electrical activity of these neurons is regulated by afferent synaptic inputs from other brain regions. By contrast, the hormones of the anterior pituitary gland (the adenohypophysis) are secreted from endocrine cells that, in mammals, are not directly innervated, yet the secretion of these hormones (adrenocorticotrophic hormone (ACTH), luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), prolactin and growth hormone) remains under the control of the brain. The brain controls the anterior pituitary gland by “releasing factors” and “release-inhibiting factors”; these are blood-borne substances released by hypothalamic neurons into blood vessels at the base of the brain, at the median eminence. These vessels, the hypothalamo-hypophysial portal vessels, carry the hypothalamic factors to the adenohypophysis where they bind to specific receptors on the surface of the hormone-producing cells.

For example, the secretion of growth hormone is controlled by two neuroendocrine systems: the growth hormone releasing hormone (GHRH) neurons and the somatostatin neurons, which stimulate and inhibit GH secretion respectively. The GHRH neurones are located in the arcuate nucleus of the hypothalamus, while the somatostatin cells involved in growth hormone regulation are in the periventricular nucleus. These two neuronal systems project axons to the median eminence where they release their peptides into portal blood vessels for transport to the anterior pituitary. Growth hormone is secreted in pulses, which arise from alternating episodes of GHRH release and somatostatin release, which may reflect neuronal interactions between the GHRH and somatostatin cells, and negative feedback from growth hormone.

So why are these systems of interest to physiologists and neuroscientists? Firstly, neuroendocrine systems regulate things that matter to most of us. They control reproduction in all its aspects, from bonding to sexual behavior, they control spermatogenesis and the ovarian cycle, parturition, lactation and maternal behaviour. They control the way we respond to stress and infection. They regulate our metabolism – they influence our eating and drinking behaviour, and influence how the energy intake is utilised – i.e. how fat we get. They influence our mood. They regulate body fluid and electrolyte homeostasis, and blood pressure. In other words, these are systems of central importance to many problems that are major health concerns, as well of sometimes of intimate personal interest.

Secondly, these neurons are large; they are mini “ factories” for producing secretory products; their nerve terminal are large and organised in coherent terminal fields; their output can often be measured easily in the blood; and what these neurons do and what stimuli they respond to are readily open to hypothesis and experiment. For these reasons and more, neuroendocrine neurons are good “model systems” for studying general questions, like “how does a neurone regulate the synthesis, packaging and secretion of its product?” and “how is information encoded in electrical activity?”