Diencephalic GABAergic Neurons in vitro Respond to Prolactin with a Rapid Increase in Intracellular Free Calcium

Kolbinger, Walter; Beyer, Cordian; Föhr, Karl J.; Reisert, Ingrid; Pilgrim, Christoph

doi:10.1159/000126222

Cited by 18 publications

(6 citation statements)

References 26 publications

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“…It is possible that this response also involves prolactin-induced activation of phosphoinositol-3 kinase and production of a range of inositol phosphate molecules (54). Similar prolactin-induced increases in intracellular Ca 2ϩ are also seen in glial cell lines (16,17) and neurons (29) that endogenously express the PRL-R. Hence, there is precedence for both rapid stimulatory and inhibitory actions of prolactin, and it is conceivable that either response could be induced, depending on the physiological state of the cell.…”

Section: Discussionmentioning

confidence: 88%

Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons

Kokay¹,

Bull²,

Davis³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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neurons of the supraoptic (SON) and paraventricular nuclei (PVN) show considerable plasticity during pregnancy and lactation. Prolactin receptors (PRL-R) have been identified in both these nuclei. The aim of this study was to investigate the cell type(s) expressing mRNA for the long form of prolactin receptor (PRL-R L) and to determine whether patterns of expression change during pregnancy and lactation. In addition, we examined effects of prolactin on excitability of oxytocin and vasopressin neurons. Sections from brains of nonpregnant, pregnant, and lactating rats were hybridized with an 35 S-labeled probe to label PRL-RL mRNA together with digoxigenin-labeled probes to detect either oxytocin or vasopressin mRNA. In the SON, PRL-R L mRNA was predominantly colocalized with oxytocin mRNA, with over 80% of oxytocin neurons positive for PRL-R L mRNA. Very few (Ͻ10%) vasopressin neurons expressed PRL-R L mRNA. In the PVN, PRL-RL mRNA was also predominantly found in oxytocin neurons, and the proportion of PRL-R L-positive oxytocin neurons increased significantly during pregnancy and lactation. As in the SON, relatively few vasopressin cells contained PRL-R L mRNA. For in vivo electrophysiology, nonpregnant rats were anesthetized, and then extracellular single neuron activity was recorded in identified oxytocin and vasopressin neurons. After a period of baseline recording, the effect of prolactin (1 g icv) on firing rate was examined. Prolactin treatment of nonpregnant rats induced a significant decrease in firing rates of oxytocin neurons. There was no effect of prolactin on the activity of vasopressin neurons. Together, these data provide strong evidence that prolactin directly and specifically regulates activity of oxytocin neurons. pregnancy; lactation; magnocellular neurons; in situ hybridization IN ADDITION TO ITS CRITICAL actions in mammary gland function during pregnancy and lactation, the anterior pituitary hormone prolactin exerts important actions within the brain. Prolactin is thought to gain access to the brain through a carrier-mediated transport system (74), likely involving prolactin receptors in the choroid plexus (51, 64). Prolactin receptor (PRL-R) mRNA (3,4,11,45) and protein (13, 46) have been identified in many hypothalamic nuclei. Interestingly, PRL-R expression in the choroid plexus is markedly increased during pregnancy and lactation (2), suggesting increased access of prolactin to brain structures during these conditions. Similarly, levels of PRL-R protein in the hypothalamus appear to increase during lactation compared with nonpregnant rats (47-49). These observations suggest that prolactin may be a major regulator of hypothalamic function, particularly during pregnancy and lactation, when prolactin levels are elevated (22,23).Within the hypothalamus, the neurons that undergo one of the most dramatic changes during pregnancy and lactation are the magnocellular neurons of the supraoptic (SON) and paraventricular (PVN) nuclei (26). PRL-R mRNA has been identified in both of these nuclei (3, 4...

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Section: Discussionmentioning

confidence: 88%

Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons

Kokay¹,

Bull²,

Davis³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…There is considerable evidence that hyperprolactinemia can inhibit GnRH secretion in both male and female rats [31, 32, 33, 34]. While it is possible that the inhibitory action of prolactin could be mediated by a stimulation of hypothalamic GABAergic neurons [14, 15, 16], we have been unable to demonstrate increased GABA turnover associated with the PRL-induced suppression of postcastration LH secretion in males [21]. There is also evidence that endogenous opioids [35, 36, 37]and corticotropin-releasing hormone (CRH) [38]may also be involved in inhibition of GnRH neurons during lactation.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperprolactinemia has also been reported to increase activity of hypothalamic GABAergic neurons in some studies [14, 15, 16]. Hence, it seemed possible that suckling-induced increases in GABAergic neuronal activity in the hypothalamus might be involved in the inhibition of GnRH neurons during lactation.…”

Section: Introductionmentioning

confidence: 99%

Lactation Alters γ-Aminobutyric Acid Neuronal Activity in the Hypothalamus and Cerebral Cortex in the Rat

Kornblatt¹,

Grattan²

2001

Neuroendocrinology

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γ-Aminobutyric acid (GABA) neurons terminating in the hypothalamus have been implicated in the neuroendocrine regulation of reproductive hormones, particularly luteinizing hormone (LH) and prolactin. The aim of this study was to examine whether GABAergic neuronal activity in the hypothalamus was modified during lactation, and whether any observed changes correlated with changes in secretion of these hormones. Animals were divided into three experimental groups: diestrous controls, lactating with pups present (with pups), and lactating with pups removed for 4 h (without pups). Animals were decapitated either without treatment, or 60 min after inhibition of GABA degradation by aminooxyacetic acid (AOAA) (100 mg/kg, i.p.). The rate of GABA accumulation in the tissue after AOAA is a measure of GABA turnover. GABA turnover was estimated in 13 microdissected brain regions, and serum prolactin and LH measured by radioimmunoassay. Suckling was associated with significantly increased prolactin and significantly decreased LH compared with diestrous rats. In lactating rats with pups, GABA turnover was significantly increased in the cingulate cortex compared with diestrous rats. GABA turnover was significantly increased in the ventrolateral preoptic nucleus of lactating rats with pups compared with diestrous rats or lactating rats without pups. There was significantly lower GABA turnover in the anterior hypothalamic area, ventromedial and dorsomedial hypothalamic nuclei in lactating rats without pups compared with diestrous rats. There were no significant changes in other brain regions examined. The results demonstrate that activity of GABAergic neurons in specific parts of the hypothalamus and cerebral cortex is altered during lactation.

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“…Whether PRL secreted from the anterior pituitary or produced in neurons in the brain (33-35) is responsible for the effect on GnRH remains to be elucidated. Effects on GnRH neurons do not eliminate the possibility that PRL could act at additional sites in the brain to inhibit the release of GnRH, possibly through an action on GABAergic (GABA, y-aminobutyric acid) neurons (36).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of gonadotropin hormone-releasing hormonerelease by prolactin from GT1 neuronal cell lines through prolactinreceptors.

Milenković¹,

D’Angelo²,

Kelly³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

107

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High levels of prolactin (PRL) are associated with inhibition of luteinizing hormone secretion in several mammalian species. We asked whether this phenomenon could be explained by a direct inhibitory action of PRL on hypothalamic gonadotropin hormone-releasing hormone (GnRH) neurons. The ability of PRL to suppress GnRH release and expression was tested in the highly differentiated GT1 GnRH cell lines. In static culture, nanomolar concentrations of either rat or mouse PRL inhibited the release of GnRH in a dose-dependent fashion. PRL treatment for 24 hr also decreased GnRH mRNA levels determined by Northern analysis. The cells were shown to express the PRL receptor gene, and the mRNAs for both the short and long forms were present by Northern and PCR analysis, although the short form was more abundant. In Western blots with monoclonal antibody against the rat liver PRL receptor, the short 42-kDa form of the receptor was observed. These results demonstrate that PRL inhibits GnRH release and possibly gene expression in GnRH neurons. This action appears to be mediated through prolactin receptors expressed by the cells.

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Diencephalic GABAergic Neurons in vitro Respond to Prolactin with a Rapid Increase in Intracellular Free Calcium

Cited by 18 publications

References 26 publications

Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons

Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons

Lactation Alters γ-Aminobutyric Acid Neuronal Activity in the Hypothalamus and Cerebral Cortex in the Rat

Inhibition of gonadotropin hormone-releasing hormonerelease by prolactin from GT1 neuronal cell lines through prolactinreceptors.

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