Tuberoinfundibular dopamine neurons

The dopamine neurons that project from the hypothalamus to the anterior pituitary are known as the tuberoinfundibular dopamine pathway (Fig. 10—13). Normally, these neurons are active and inhibit prolactin release. In the postpartum state, however, their activity is decreased, and therefore prolactin levels can rise during breastfeeding, so that lactation will occur. If the functioning of tuberoinfundibular dopamine neurons is disrupted by lesions or drugs, prolactin levels can also rise. Elevated prolactin levels are associated with galactorrhea (breast secretions), amenorrhea,... 

Berry SA, Gudelsky GA (1990) D receptors function to inhibit the activation of tuberoinfundibular dopamine neurons. J Pharmacol Exp Therap 254 677-682. 

Berry SA, Gudelsky GA (1991) Effect of D2 dopamine agonists on tuberoinfundibular dopamine neurons. Neuropharmacology 30 961-965. 

Demarest KT, Riegle GD, Moore KE (1985a) The interrelationship between the rapid tonic and delayed induced components of the prolactin-induced activation of tuberoinfundibular dopamine neurons. In Macleod RM, Thorner MO, Scapagnini U (Eds), Prolactin Basic and Clinical Correlates, pp. 533-542. Liviana Press, Padova. 

Durham RA, Eaton MJ, Moore KE, Lookingland KJ (1997) Effects of selective activation of dopamine D2 and D3 receptors on prolactin secretion and the acivity of tuberoinfundibular dopamine neurons. Eur J Pharmacol 335 37-42. 

Durham RA, Johnson JD, Eaton MJ, Moore KE and Lookingland KJ (1998) Opposing roles for dopamine D[ and D2 receptors in the regulation of hypothalamic tuberoinfundibular dopamine neurons. Eur J Pharmacol 355 141-147. 

Fuxe K, Hokfelt T, Nilsson O (1972) Effect of constant light and androgen-sterilization on the amine turnover of the tuberoinfundibular dopamine neurons blockade of cyclic activity and induction of a persistent high dopamine turnover in the median eminence. Acta Endocrinol <59 625-639. 

Gudelsky GA, Meltzer HY (1989) Activation of tuberoinfundibular dopamine neurons following the acute administration of atypical antipsychotics. Neuropsychopharmacology 2 45-51. 

Gudelsky GA, Berry SA, Meltzer HY (1989) Neurotensin activates tuberoinfundibular dopamine neurons and increases serum corticosterone concentration in the rat. Neuroendocrinology 49 604-609. 

He J-R, Molnar J, Barraclough CA (1994) Evidence that amplification of norepinephrine-induced LH release by morphine is indirectly due to suppression of tuberoinfundibular dopamine secretion. Brain Res 652 1-8. Hentschel K, Cheung S, Moore KE, Lookingland KJ (1998) Pharmacological evidence that neurotensin mediates prolactin-induced activation of tuberoinfundibular dopamine neurons. Neuroendocrinology 65 71-76. Hentschel K, Will YM, McMahon CD, Moore KE, Lookingland KJ (1999) Prolactin induces Fos-related antigen expression in neurotensin (NT)-IR neurons and increases numbers of NT-IR neurons in the arcuate nucleus. Soc Neurosci Abstr 25 1185. 

Krajnak K, Manzanares J, Lookingland KJ, Nunez AA (1994) The effect of short-photoperiod exposure on tuberoinfundibular dopamine neurons in male and female Syrian hamsters. J Biol Rhythms 9 125-135. 

McKay DW, Pasieka CA, Moore KE, Riegle GD, Demarest KT (1982) Semicircadian rhythm of tuberoinfundibular dopamine neuronal activity during early pregnancy and psuedopregnancy in the rat. 

Demarest KT, Moore KE, Riegle GD (1985b) Acute restraint stress decreases dopamine synthesis and turnover in the median eminence a model for the study of the inhibitory neuronal influences on tuberoinfundibular dopaminergic neurons. Neuroendocrinology 47 437 144. 

Manzanares J, Toney TW, Lookingland KJ, Moore KE (1991a) Activation of tuberoinfundibular and tuberohypophysial dopamine neurons following intracerebroventricular administration of bombesin. Brain Res 555 142-147. 

Nishikawa Y, Ikegami H, Jikihara H, Koike K, Masumoto N, Kasahara K, Tasaka K, Hirota K, Miyake A, Tanizawa O (1993) Effects of thyrotropin-releasing hormone and phorbol ester on dopamine release from dispersed rat tuberoinfundibular dopaminergic neurons. Peptides 74 839-844. 

Selemon LD, Sladek JR (1981) Aging of tuberoinfundibular (A-12) dopamine neurons in the C57B1/6N mouse. Brain Res Bull 7 585-594. 

The intermediate length systems include the tuberoinfundibular system, which projects from the arcuate and periventricular nuclei into the intermediate lobe of the pituitary and the median eminence. This system is responsible for the regulation of such hormones as prolactin. The inter hypothalamic neurons send projections to the dorsal and posterior hypothalamus, the lateral septal nuclei and the medullary periventricular group, which are linked to the dorsal motor nucleus of the vagus such projections may play a role in the effects of dopamine on the autonomic nervous system. 

Dopamine agonists decrease pituitary prolactin secretion through a dopamine-mimetic action on the pituitary at two central nervous system loci (1) they decrease dopamine turnover in the tuberoinfundibular neurons of the arcuate nucleus, generating increased hypothalamic dopamine and (2) they act directly on pituitary dopamine receptors to inhibit prolactin release. 

Maternal prolactin via the milk is required for normal development of the tuberoinfundibular neuronal system of the hypothalamus during the neonatal period in rats (Shyr et al., 1986). Blocking the suckling-induced rise in maternal prolactin levels causes abnormal tuberoinfundibular function, with decreased inhibition by dopamine of prolactin secretion in the offspring later in life. The resulting chronically elevated prolactin levels cause prostatitis in the male offspring (Tangbanluekal Robinette, 1993). 

Demarest KT, Moore KE (1979b) Comparison of dopamine synthesis regulation in terminals of nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophyseal neurons. J Neural Transm 45 263-277. 

Lookingland KJ, Jarry HD, Moore KE (1987a) The metabolism of dopamine in the median eminence reflects the activity of tuberoinfundibular neurons. Brain Res 479 303-310. 

Lookingland KJ, Gunnet JW, Moore KE (1987b) Electrical stimulation of the arcuate nucleus increases the metabolism of dopamine in terminals of tuberoinfundibular neurons in the median eminence. Brain Res 436 161-164. 

An inhibitory role for morphine on the release of dopamine into hypophysial portal blood and on the synthesis of dopamine in tuberoinfundibular neurons... 

Like other anterior pituitary hormones, prolactin is secreted in a pulsatile manner. Prolactin is unique among the anterior pituitary hormones in that hypothalamic regulation of its secretion is predominantly inhibitory. The major regulator of prolactin secretion is dopamine, which is released by tuberoinfundibular neurons and interacts with the Dj receptor on lactotropes to inhibit prolactin secretion. A number of putative prolactin-releasing factors have been described, but their physiological roles are unclear. Under certain pathophysiological conditions, such as severe primary hypothyroidism, persistently elevated levels of TRH can induce hyperprolactinemia and consequent galactorrhea. 

In addition to the common neural mechanism, primer pheromones have a common endocrine effect expressed principally by changing prolactin secretion from the anterior pituitary. Our own studies have shown that lowering prolactin by injections of bromocriptine (a dopamine agonist) is able to reproduce the actions of all the described primer pheromones in female mice with identical timing (Keverne, 1982). Direct measurement of prolactin has also demonstrated that exposure of female mice to males results in rapid decreases of serum prolactin (Ryan and Schwartz, 1980). Such decreases in prolactin are probably brought about by increases in the release of hypothalamic dopamine from the tuberoinfundibular dopaminergic (TIDA) neurons into the hypophyseal portal circulation. Indeed, our recent studies show there to be an increase in the synthesis of dopamine in this... 

The secretion of prolactin (PRL) is controlled by both stimulatory and inhibitory factors of hypothalamic origin. The inhibitory control is exerted primarily by dopamine, which is released from the tuberoinfundibular dopaminergic (TIDA) neurons into the pituitary portal circulation. Evidence based on peripheral administration of serotonin precursors, agonists or antagonists, intraventricular injection of serotonin, and electrical stimulation of the raphe nucleus indicates that central serotonergic projections to the hypothalamus are involved in the stimulation of PRL. Administration of pyridoxine to deficient rats resulted in a significant increase in plasma PRL (14). 

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