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K E Moore

Publications and source records attributed to K E Moore.

At least 91 records · Page 5Linked to original sources

Effects of photoperiod on lactotrophs and on dopaminergic and 5-hydroxytryptaminergic neurones in bull calves.

This study was conducted to determine whether photoperiod-induced changes in serum concentrations of prolactin in cattle were associated with changes in activity of dopamine or 5-hydroxytryptamine (5-HT) neurones in the infundibulum/pituitary stalk and the secretion rate and number of lactotrophs in the anterior pituitary gland. Sixteen prepubertal bull calves (approximately 8 weeks of age) were divided into two groups. One group of eight was maintained on a photoperiod of 8 h light: 16 h darkness (8L:16D) and the other group was exposed to 16L:8D for 4 weeks. At this time calves were injected with a decarboxylase inhibitor (m-hydroxybenzylhydrazine dihydrochloride, NSD 1015) which blocks the conversion of dihydroxyphenylalanine (DOPA) to dopamine and of 5-hydroxytryptophan (5-HTP) to 5-HT. Calves were killed with pentobarbital 15 min later. Accumulations of DOPA and 5-HTP in selected brain regions were used as indices of activity of dopamine and 5-HT neurones respectively. Secretory rate and number of prolactin-secreting lactotrophs were determined by reverse haemolytic plaque assay. Relative to calves exposed to 8L:16D, exposure to 16L:8D increased serum concentrations of prolactin by eightfold, anterior pituitary gland weight by 23%, release of prolactin from pituitary explants by 57% and the area of the plaque for prolactin-secreting lactotrophs by 70%. There was no difference in the rates of accumulation of DOPA and 5-HTP in the infundibulum/pituitary stalk of animals exposed to 4 weeks of 16L:8D or 8L:16D.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Temperature effects on serum prolactin concentrations and activity of dopaminergic neurons in the infundibulum/pituitary stalk of calves.

The effects of ambient temperature on serum concentrations of prolactin and neurochemical estimates of activity of dopaminergic neurons projecting to the infundibulum/pituitary stalk were investigated in Holstein bull calves. Accumulation of 3,4-dihydroxyphenylalanine (DOPA) in the infundibulum/pituitary stalk after intravenous injection of a decarboxylase inhibitor was used to estimate activity of these dopaminergic neurons. Increasing ambient temperature from 21 to 33 degrees C for 22 hr increased serum concentrations of prolactin and decreased activity of the dopaminergic neurons. Conversely, reducing ambient temperature from 22 degrees C to 11 degrees C decreased serum concentrations of prolactin and increased activity of these dopaminergic neurons. It is suggested that alterations in activity of dopaminergic neurons terminating in the infundibulum/pituitary stalk of bull calves may mediate acute temperature-induced changes in secretion of prolactin.

Acclimatization↗

Kappa opioid receptor-mediated regulation of dopaminergic neurons in the rat brain.

The effect of the kappa opioid receptor agonist U-50,488 [trans-3,4-dichloro-N-methyl-N-[2-pyrrolindinyl)-cyclohexyl]-benze ne- acetamide] was examined on the activity of dopamine (DA) neurons comprising the nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophysial systems in the male rat brain under basal and stimulated conditions. DA neuronal activity was estimated by measuring: 1) the accumulation of 3,4-dihydroxyphenylalanine after administration of a decarboxylase inhibitor and 2) the concentration of the DA metabolite 3,4-dihydroxyphenyla-cetic acid in brain (striatum, nucleus accumbens and median eminence) and pituitary regions (intermediate lobe and neural lobe) containing terminals of these neurons. Under basal (non-stimulated) conditions, U-50,488 produced a dose- and time-related decrease in the activity of tuberohypophysial DA neurons, but failed to alter the activity of nigrostriatal, mesolimbic or tuberoinfundibular DA neurons. The ability of U-50,488 to inhibit the basal activity of tuberohypophysial DA neurons was blocked by pretreatment with the kappa opioid antagonist nor-binaltorphimine. The activity of nigrostriatal, mesolimbic and intermediate lobe tuberohypophysial DA neurons was increased by haloperidol, whereas the activity of tuberoinfundibular DA neurons was increased by prolactin. U-50,488 decreased the activity of nigrostriatal, mesolimbic and tuberohypophysial DA neurons in haloperidol-treated rats, and decreased the activity of tuberoinfundibular DA neurons in prolactin-treated rats. These results indicate that activation of kappa opioid receptors inhibits all DA neuronal systems in the brain, but that this effect on nigrostriatal, mesolimbic and tuberoinfundibular DA neurons is evident only after these neurons have been activated.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Atrial natriuretic peptide-induced suppression of basal and dehydration-induced vasopressin secretion is not mediated by hypothalamic tuberohypophysial or tuberoinfundibular dopaminergic neurons.

The purpose of this study was to examine the effects of atrial natriuretic peptide (ANP) on the secretion of vasopressin and the activities of hypothalamic tuberohypophysial and tuberoinfundibular dopaminergic neurons in normal and dehydrated male rats. Neuronal activity was estimated by measuring the concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and dopamine (DA) in brain and posterior pituitary regions containing terminals of tuberohypophysial (neural lobe; intermediate lobe) and tuberoinfundibular (median eminence) DA neurons. Intracerebroventricular (icv) administration of 20 micrograms ANP decreased basal arginine vasopressin concentrations in the plasma, but had no effect on the concentrations of DOPAC or DA in any region examined. Water deprivation caused a time-dependent increase in plasma arginine vasopressin concentrations, with maximal levels measured 2 days after removal of water bottles. Water deprivation had no effect on DOPAC concentrations in the neural lobe, intermediate lobe or median eminence, but increased DA concentrations in the neural lobe. ANP (20 micrograms/rat; icv) decreased arginine vasopressin concentrations in the plasma of water-deprived rats without altering DOPAC or DA concentrations in the neural lobe, intermediate lobe or median eminence. These results indicate that ANP-induced suppression of basal and dehydration-induced vasopressin secretion is not mediated by tuberohypophysial or tuberoinfundibular DA neurons.

3,4-Dihydroxyphenylacetic Acid↗

3,4-Dihydroxyphenylacetic acid concentrations in the intermediate lobe and neural lobe of the posterior pituitary gland as an index of tuberohypophysial dopaminergic neuronal activity.

Tuberohypophysial dopamine (DA) neurons terminate in the intermediate and neural lobes of the posterior pituitary. The objective of this study was to determine if concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC), a major metabolite of DA in these regions, reflect the activity of tuberohypophysial DA neurons. The concentrations of DOPAC and DA in the intermediate lobe were approximately twice those in the neural lobe, so that the ratios of DOPAC/DA were similar between lobes. The administration of a monoamine oxidase inhibitor pargyline produced a rapid decline (by 5 min) of DOPAC concentrations in both the intermediate and neural lobes. The administration of nomifensine, an inhibitor of DA uptake at the nerve terminal, produced a modest 33% decline in DOPAC concentrations in the intermediate lobe, but was without effect in the neural lobe. Activation of tuberohypophysial DA neurons by electrical stimulation of the pituitary stalk increased both the rate of DA synthesis (accumulation of dihydroxyphenylalanine (DOPA) after administration of the decarboxylase inhibitor NSD 1015) and the concentrations of DOPAC in the intermediate and neural lobes. Administration of the DA antagonist haloperidol increased, and the DA agonist apomorphine decreased both the rate of DOPA accumulation and DOPAC concentrations in the intermediate lobe but not the neural lobe. The results of the present study demonstrate that: (1) elimination of DOPAC from the intermediate lobe and neural lobe is rapid and alterations in DOPAC concentrations reflect dynamic changes in metabolism of DA; (2) DA which is released and recaptured is a minor contributor to DOPAC concentrations; and (3) alterations in the activity of tuberohypophysial DA neurons are accompanied by corresponding changes in DOPAC concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

Activation of tuberoinfundibular but not tuberohypophysial dopaminergic neurons following intracerebroventricular administration of alpha-melanocyte-stimulating hormone.

The effect of alpha-melanocyte-stimulating hormone (alpha MSH) on the activity of different central dopaminergic neurons in the male rat was determined by measuring the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC) and the accumulation of 3,4-dihydroxyphenylalanine (DOPA) following the administration of a decarboxylase inhibitor in brain regions that contain terminals of nigrostriatal (striatum), mesolimbic (nucleus accumbens), tuberoinfundibular (median eminence) and tuberohypophysial (neural and intermediate lobe of the pituitary) dopaminergic neurons. Intracerebroventricular (i.c.v.) administration of alpha MSH caused a prompt (within 30 min) increase in the concentration of DOPAC and the accumulation of DOPA in the median eminence, but was without effect in the other brain regions. The alpha MSH-induced increase in tuberoinfundibular dopaminergic neuronal activity was temporally related to a decrease in circulating concentrations of prolactin. Twelve hours after the i.c.v. administration of prolactin DOPA accumulation increased in the median eminence but not in the neural or intermediate lobes of the pituitary. DOPA accumulation was not altered in any brain region 12 h after the i.c.v. administration of alpha MSH. These results suggest that alpha MSH acts acutely to selectively activate tuberoinfundibular dopaminergic neurons and thereby cause the secretion of prolactin from the anterior pituitary to decrease.

3,4-Dihydroxyphenylacetic Acid↗

Dopaminergic and beta-adrenergic receptor control of alpha-melanocyte-stimulating hormone secretion during stress.

The relative roles of dopaminergic and beta-adrenergic receptors in mediating the stress-induced increase in the secretion of alpha-melanocyte-stimulating hormone (alpha-MSH) from the intermediate lobe of the pituitary were determined in the male rat. Thirty minutes of physical immobilization (restraint stress) increased the circulating concentrations of alpha-MSH and decreased the 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA) ratio in the intermediate lobe of the pituitary, reflecting a decrease in the tuberohypophysial dopaminergic neuronal activity. Pretreatment with the beta-adrenergic antagonist propranolol reduced the stress-induced increase in the circulating levels of alpha-MSH, but had no effect on the basal plasma concentrations of this hormone or the stress-induced decrease in DOPAC/DA in the intermediate lobe. If the dopaminergic tone during stress was maintained by administration of the DA agonist apomorphine, the stress-induced increase in alpha-MSH secretion was prevented. In nonstressed animals the administration of the beta 2-adrenergic agonist metaproterenol increased the plasma levels of alpha-MSH, and the effect of this drug was augmented if the inhibitory dopaminergic tone on alpha-MSH secretion was blocked by the administration of the DA antagonist haloperidol. Severing neurons in the retrochiasmatic region of the hypothalamus blocked the stress-induced decrease in DOPAC/DA in the intermediate lobe and attenuated the stress-induced increase in plasma concentrations of alpha-MSH. Taken together, these results indicate that a decrease in tuberohypophysial dopaminergic neuronal inhibitory tone and an increase in beta-adrenergic stimulation are both necessary for the full expression of the stress-induced increase in secretion of alpha-MSH from melanotrophs in the intermediate lobe of the rat pituitary.

Afferent Pathways↗

Comparison of the effects of ether and restraint stress on the activity of tuberoinfundibular dopaminergic neurons in female and male rats.

The purpose of the present study was to characterize the acute inhibitory effects of restraint stress on the activity of tuberoinfundibular dopamine (DA) neurons as estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence. The time course of the effects of two types of physical restraint (immobilization in the supine position or confinement in an acrylic cylindrical tube) was determined in unanesthetized and diethylether (ether)-exposed female and male rats. The combination of brief (2 min) exposure to ether followed by 10 and 20 min of supine restraint increased concentrations of prolactin in plasma and decreased DOPAC concentrations in median eminence of both female and male rats. Thirty minutes of supine restraint decreased DOPAC concentrations in the median eminence of female rats that were not exposed to ether, and brief exposure to ether enhanced this effect. By contrast, 30 min of supine restraint failed to alter DOPAC concentrations in the median eminence in either unanesthetized or ether-exposed male rats. Tube restraint in the absence of ether failed to alter DOPAC concentrations in the median eminence of either female or male rats; but in female rats preexposed to ether, 30 min of tube restraint decreased DOPAC concentrations in the median eminence. On the other hand, in the absence of physical restraint, 2 min ether exposure caused a transient increase in prolactin secretion and a concurrent decrease of DOPAC concentrations in median eminence of both female and male rats.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

Kappa-opioid-receptor-mediated regulation of alpha-melanocyte-stimulating hormone secretion and tuberohypophyseal dopaminergic neuronal activity.

The effects of the kappa-opioid receptor agonist trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzene- acetamide methanesulfonate hydrate (U-50488) were examined on alpha-melanocyte-stimulating hormone (alpha-MSH) secretion and the activity of tuberohypophysial dopamine (DA) neurons in the male rat. Tuberohypophysial DA neuronal activity was estimated by measuring: (1) the rate of DA synthesis [accumulation of 3,4-dihydroxyphenylalanine (DOPA) following inhibition of aromatic L-amino acid decarboxylase], and (2) DA metabolism [concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC)] in the intermediate lobe of the pituitary. U-50488 produced a dose- and time-dependent increase in plasma concentrations of alpha-MSH which was accompanied by a decrease in the accumulation of DOPA and in the intermediate lobe. The effects of U-50488 were blocked by pretreatment with the DA agonist apomorphine but not by the beta-adrenergic antagonist propranolol. The effects of U-50488 on plasma alpha-MSH concentrations and intermediate-lobe DOPA accumulation were blocked by pretreatment with the selective kappa-opioid receptor antagonist nor-binaltorphimine. These results indicate that U-50488, by acting on kappa-opioid receptors, inhibits the activity of intermediate-lobe tuberohypophysial DA neurons, and through this action increases the secretion of alpha-MSH from melanotrophs.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Prolactin regulation of dopaminergic neurons in the infundibulum pituitary stalk of bull calves.

The effects of elevated circulating concentrations of prolactin were examined on neurochemical estimates of activity of dopaminergic neurons in the infundibulum/pituitary stalk of Holstein bull calves (8-10 weeks of age). Activity of these neurons was estimated by measuring the accumulation of dihydroxyphenylalanine, the immediate precursor of dopamine, 15 min after an intravenous injection of the aromatic L-amino acid decarboxylase inhibitor, 3-hydroxybenzylhydrazine. Subcutaneous injections of the dopamine antagonist haloperidol every 6 hr for 1 day increased serum concentrations of prolactin and accumulation of dihydroxyphenylalanine in the infundibulum/stalk. Intravenous infusions of prolactin for 1 or 9 days increased accumulation of dihydroxyphenylalanine in the infundibulum/stalk, indicating that these neurons remain responsive to elevated prolactin for at least 9 days. It is concluded that elevated concentrations of prolactin in blood stimulate dopaminergic neurons in the infundibulum/pituitary stalk of bull calves. We speculate that these neurons may be analogous to the tuberoinfundibular dopaminergic neurons that regulate prolactin in rats.

Animals↗

A sex difference in the stimulatory afferent regulation of tuberoinfundibular dopaminergic neuronal activity.

The involvement of afferent neuronal systems in the maintenance of basal and prolactin-stimulated tuberoinfundibular dopaminergic (TIDA) neuronal activity was examined in female and male rats. The synthesis and turnover of dopamine (DA) was measured in the median eminence, the terminal region of the TIDA neurons, to estimate the activity of these neurons. Complete and retrochiasmatic deafferentations of the mediobasal hypothalamus were made 7 days prior to experimentation to either completely isolate the TIDA neurons from the rest of the brain or to interrupt neuronal connections from rostral brain regions to the TIDA neurons, respectively. Both complete and retrochiasmatic deafferentations decreased the basal rate of DA synthesis and turnover in the median eminence of female, but not of male rats. These results suggest that neuronal afferents originating rostral to the mediobasal hypothalamus stimulate TIDA neurons in the female but not in the male rat. Intracerebroventricular administration of rat prolactin increased DA synthesis in the median eminence of both sham and retrochiasmatic deafferentiated female and male rats showing that the stimulatory action of prolactin is not blocked by retrochiasmatic deafferentation. Ovariectomy reduced the rate of DA synthesis in the median eminence but retrochiasmatic deafferentation did not cause a further decrease in ovariectomized rats. These results suggest that retrochiasmatic deafferentation and ovariectomy may remove a stimulatory input to the TIDA neurons which is mediated through a common afferent neuronal pathway. These afferent influences do not appear to be operational in the adult male rat since retrochiasmatic deafferentation did not reverse the castration-induced increase in the rate of DA synthesis in the median eminence of male rats.

Animals↗

Autoradiographic identification of prolactin binding sites in rat median eminence.

Binding sites for prolactin were localized and quantified in the female rat brain by in vitro autoradiographic analysis with iodine-125-labeled ovine prolactin. Following incubation, labeled prolactin bound preferentially to the median eminence and choroid plexus of the lateral and third ventricles. The addition of excess unlabeled ovine prolactin blocked binding of the labeled hormone in the choroid plexus, and attenuated prolactin binding in the median eminence. These results provide evidence for median eminence. These results provide evidence for prolactin-specific recognition sites in the median eminence, a region intimately involved in the hypothalamic regulation of prolactin secretion.

Animals↗

Alterations in concentrations of dihydroxyphenylacetic acid in the median eminence of rats euthanatized with pentobarbital.

Concentrations of dopamine (DA) and one of its major metabolites, dihydroxyphenylacetic acid (DOPAC), were determined in selected brain regions of rats that were euthanatized either by decapitation or by intravenous injections of pentobarbital or Fatal Plus, a commercial preparation that contains pentobarbital. When compared with values in decapitated brains, pentobarbital increased the concentration of DOPAC in the median eminence, which contains terminals of tuberoinfundibular dopaminergic (TIDA) neurons. Fifteen minutes of restraint reduced the concentration of DOPAC in the median eminence of rats killed by decapitation or by injections of pentobarbital, indicating that pentobarbital does not mask restraint-induced decrease in TIDA neuronal activity. In contrast, none of the manipulations altered DA or DOPAC concentrations in the striatum, which contains terminals of nigrostriatal dopaminergic neurons. Thus, changes in the concentrations of DOPAC in the median eminence (an index of TIDA neuronal activity) induced by stress can be detected in rats euthanatized by either decapitation or an injection of pentobarbital.

3,4-Dihydroxyphenylacetic Acid↗

In vitro insertion of leader peptidase into Escherichia coli membrane vesicles.

Leader peptidase is an integral protein of the Escherichia coli cytoplasmic membrane whose topology is known. We have taken advantage of this knowledge and available mutants of this enzyme to develop a genetic test for a cell-free protein translocation reaction. We report that leader peptidase inserted into inverted plasma membrane vesicles in its correct transmembrane orientation. We have examined the in vitro membrane assembly characteristics of a variety of leader peptidase mutants and found that domains required for insertion in vivo are also necessary for insertion in vitro. These data demonstrate the physiological validity of the in vitro insertion reaction and strengthen the use of this in vitro protein translocation reaction for the dissection of this complex sorting pathway.

Cell Membrane↗

Neuroleptics and neuroendocrine function.

Neuroleptics have been developed primarily to treat psychoses, but they have become invaluable research tools. Because of their selective action on DA receptors, neuroleptics are commonly employed to study the function and regulation of DA neurotransmission. The relationship between the antipsychotic efficacy and the DA receptor affinity of the various neuroleptic drugs has lead to the development of new DA antagonists in hopes of discovering novel antipsychotic agents. This approach has produced interesting new compounds selective for the DA receptor subtypes. The use of DA receptor antagonism as a measure of the potential antipsychotic efficacy of a compound will undoubtedly change as the mechanisms behind the antipsychotic actions of neuroleptics become better understood. Although endocrine side effects of neuroleptic administration are undesired in the clinic, they have provided insight into the neuroendocrine regulation of pituitary hormones. Through the use of neuroleptics, DA neurons in the hypothalamus have been shown to play a role in the regulation of prolactin, GH, and TSH secretion. The ability of DA to act at the pituitary and thereby inhibit the secretion of these three hormones suggests that other regulatory factors must provide the specificity needed for the differential secretion of the individual hormones during varying physiological states. Future research will certainly explore the interactions of DA and these regulatory factors at the pituitary. The role of DA in neuroendocrine regulation is not limited to the pituitary. The presence of DA neurons within the hypothalamus offers the possibility of DA regulation of hypothalamic neurosecretory activity.

Animals↗

Effect of electrical stimulation of the ventromedial nucleus and the dorsomedial nucleus on the activity of tuberoinfundibular dopaminergic neurons.

Perikarya and terminals of tuberoinfundibular dopaminergic (TIDA) neurons are located in the arcuate nucleus (ARN) and in the median eminence (ME), respectively. Dopamine (DA) released from TIDA terminals in the ME inhibits prolactin secretion from the anterior pituitary. Anatomical studies have described the sources of afferents to ARN and ME, but not to TIDA neurons per se. The ventromedial nucleus (VMN) and the dorsomedial nucleus (DMN) of the hypothalamus project to ARN and ME and have a role in prolactin regulation. In the present study, VMN and DMN were investigated as possible sources of TIDA afferents. Alterations in the activity of TIDA neurons were estimated by measuring plasma concentrations of prolactin and the rates of DA synthesis (3,4-dihydroxyphenylalanine - DOPA - accumulation after administration of the decarboxylase inhibitor NSD 1015) and metabolism (concentrations of the DA metabolite 3,4-dihydroxyphenylacetic acid - DOPAC) in the ME following electrical stimulation of ARN, VMN, and DMN in ovariectomized female rats. Thirty minutes of bilateral stimulation of ARN or DMN increased DOPA accumulation in the ME; stimulation of the VMN had no effect. 5-Hydroxytryptamine synthesis in the ME was unaffected by stimulation of any region. Plasma prolactin levels declined during DMN stimulation, varying with the frequency and duration of the electrical stimulus. DA metabolism within TIDA neurons increased with DMN stimulation, as evidenced by increased DOPAC concentrations in the ME. In females whose basal TIDA activity has been increased by haloperidol treatment or decreased by bromocriptine treatment, DMN stimulation was still able to increase DOPA accumulation in the ME. The present data suggest the presence of stimulatory TIDA afferents originating from or passing through the DMN.

3,4-Dihydroxyphenylacetic Acid↗

The anterior hypothalamus provides stimulatory input to tuberoinfundibular dopamine neurons which is not mediated by prolactin.

Complete or retrochiasmatic deafferentations of the mediobasal hypothalamus were made in female rats 7 days prior to experimentation in order to determine the role played by putative afferent neuronal connections (1) in maintaining the basal neuronal activity of tuberoinfundibular dopaminergic (TIDA) neurons, and (2) in the stimulatory actions of prolactin on these neurons. The neuronal activity of TIDA neurons was estimated by measuring the rates of synthesis, turnover or metabolism of dopamine (DA) in the terminals of these neurons in the median eminence. Complete deafferentation of the mediobasal hypothalamus reduced the basal rate of DA synthesis, and retrochiasmatic deafferentation decreased the rates of synthesis, turnover and metabolism of DA in the median eminence. A knife cut 1 mm rostral to the retrochiasmatic cut failed to alter basal TIDA neuronal activity. These results suggest that afferent neuronal inputs originating in or coursing through the caudal portion of the anterior hypothalamus mediate a tonic stimulatory influence on TIDA neurons in the female rat. Intracerebroventricular administration of rat prolactin or systemic administration of haloperidol (which increases circulating levels of prolactin) increased DA synthesis in the median eminence of both sham-operated rats and retrochiasmatic-deafferentated rats. Thus, the stimulatory action of prolactin was not blocked by retrochiasmatic deafferentation. In addition, elimination of the basal stimulatory action of endogenous prolactin by pretreating animals with bromocriptine reduced the rate of DA synthesis in the median eminence of both sham- and retrochiasmatic-deafferentated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of alterations in the activity of tuberohypophysial dopaminergic neurons on the secretion of alpha-melanocyte stimulating hormone.

Administration of gamma-butyrolactone (GBL), an anesthetic which reduces dopaminergic neuronal activity, decreased the concentration of the dopamine (DA) metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the intermediate lobe of the pituitary gland, and increased alpha-melanocyte stimulating hormone (alpha MSH) concentrations in the serum of male rats. Bilateral electrical stimulation of the rostral arcuate nucleus, which contains perikarya of tuberohypophysial DA neurons, increased DOPAC concentrations in the intermediate lobe and decreased alpha MSH concentrations in the serum of GBL-anesthetized rats. Administration of the DA antagonist haloperidol prevented the decline in serum alpha MSH levels following arcuate nucleus stimulation, but had no effect on serum alpha MSH concentrations in sham-stimulated GBL-treated rats. These results indicate that GBL-induced decreases or stimulation-induced increases in the activity of tuberohypophysial DA neurons are accompanied by corresponding changes in the metabolism of DA in the intermediate lobe of the rat pituitary gland, and by reciprocal changes in the secretion of alpha MSH.

3,4-Dihydroxyphenylacetic Acid↗