Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the role of the GABA(A) receptor mediating systems in the control of gonadotropin-releasing hormone (GnRH) release from the ventromedial-infundibular region (VEN/IN) of anestrous ewes, the extracellular concentrations of GnRH, beta-endorphin, noradrenaline (NE), dopamine (DA), 4-hydroxy-3-methoxy-phenylglycol (MHPG) and 3,4-dihydroxy-phenylacetic acid (DOPAC) were quantified during local stimulation or blockade of GABA(A) receptors with muscimol or bicuculline respectively. In most animals stimulation of GABA(A) receptors significantly attenuates GnRH release with concomitant increase of beta-endorphin and DA release, and MHPG and DOPAC levels. Blockade of the GABA(A) receptors generally did not affect GnRH and NE release but inhibited in most animals beta-endorphin release and decreased dopaminergic activity. These results suggest, that GABA may suppress GnRH release directly by GABA(A) receptor mechanism on the axon terminal of GnRH neurons or indirectly by GABA(A) receptor processes activating beta-endorphin-ergic and dopaminergic neurons in the VEN/NI. On the basis of these results in could not be distinguish between these two events. The decrease in extracellular beta-endorphin and dopamine concentration without evident changes in the GnRH level during GABA(A) receptor blockade may suggest that other neuronal systems are involved in this effect.
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PMID:The involvement of GABA(A) receptors in the control of GnRH and beta-endorphin release, and catecholaminergic activity in the ventromedial-infundibular region of hypothalamus in anestrous ewes. 1159 66

To examine the role of gamma-aminobutyric acid (GABA)(A) receptor mediating systems in the control of gonadotropin-releasing hormone (GnRH) release from the medial preoptic area (MPOA) of ewes during the follicular phase of the estrous cycle, the extracellular concentrations of GnRH, beta-endorphin, noradrenaline (NE), dopamine (DA), 4-hydroxy-3-methoxy-phenyl-glycol (MHPG) and 3,4-dihydroxy-phenylacetic acid (DOPAC) were quantified during the local infusion of muscimol and bicuculline (agonist and antagonist of GABA(A) receptors, respectively) to this structure. Stimulation of GABA(A) receptors markedly attenuated GnRH release, increased beta-endorphin release and noradrenergic system activity in the MPOA. The decrease of the luteinizing hormone (LH) concentration in blood plasma and LH pulse amplitude suggests that a GABA(A) receptor agonist in the MPOA also suppresses GnRH release from the GnRH axon terminals in the ventromedial hypothalamus/nucleus infundibularis region (VEN/NI). Blockade of GABA(A) receptors had no evident effect on GnRH/LH secretion but decreased beta-endorphin release and increased the extracellular DOPAC concentration. The suppressive influence of muscimol in the MPOA on GnRH release might be considered a net result of its direct inhibitory effect on GnRH release, indirect inhibitory influence on GnRH release through activation of the beta-endorphinergic system, and facilitation of GnRH neurons by increasing noradrenaline release. The results obtained during bicuculline perfusion on these systems' activity are not sufficiently consistent to provide a clear understanding of the lack of changes in the GnRH/LH release under blockade of GABA(A) receptors. We conclude that the MPOA in ewes during the follicular phase is an important regulatory site where stimulation of GABA(A) receptors both decreases GnRH secretion and increases beta-endorphin release.
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PMID:The role of GABA(A) receptors in the neural systems of the medial preoptic area in the control of GnRH release in ewes during follicular phase. 1265 29

To examine the role of gamma-aminobutyric acid (GABA)B receptor mediating systems in the ventromedial hypothalamus-infundibular nucleus region (VMH/NI) of anoestrous ewes in controlling gonadotropin-releasing hormone (GnRH) release, the extracellular concentrations of GnRH, beta-endorphin, norepinephrine, dopamine, 4-hydroxy-3-methoxy-glycol and 3,4-dihydroxy-phenylacetic acid were quantified during infusion of baclofen or phaclofen (agonist and antagonist of GABAB receptors, respectively) in this structure. The stimulation of GABAB receptors activates GnRH/luteinising hormone (LH) release, attenuates noradrenergic and beta-endorphinergic tone but has no evident effect on the dopaminergic system. Blockade of GABAB receptors in this structure increases the extracellular beta-endorphin concentration but has no significant influence on GnRH release or catecholaminergic activity. It is suggested that activation of GnRH/LH release in the VMH/NI of anoestrous ewes may result from a decrease of norepinephrine output and hence its inhibitory effect on GnRH secretion. Activation of GABAB receptors, as well as their blockade, did not change dopaminergic system activity, indicating that GABAB does not affect GnRH release indirectly by a GABAB receptor mechanism acting on dopaminergic neurones in the VMH/NI. Increased activity of the beta-endorphinergic system during blockade of GABAB receptors does not change GnRH release, suggesting that beta-endorphin does not play a significant role in the control of GnRH secretion in anoestrous ewes.
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PMID:Effects of GABAB receptor modulation on gonadotropin-releasing hormone and beta-endorphin release, and on catecholaminergic activity in the ventromedial hypothalamus-infundibular nucleus region of anoestrous ewes. 1572 Apr 75