Biomedical subjects

K E Moore

Publications and source records attributed to K E Moore.

At least 55 records · Page 3Linked to original sources

PubMed1994

Effects of the selective dopaminergic D2 agonist quinelorane on the activity of dopaminergic and noradrenergic neurons projecting to the diencephalon of the rat.

The purpose of the present study was to characterize dopaminergic D2 receptor-mediated regulation of catecholaminergic neurons in the diencephalon by examining the acute effects of the potent and selective D2 agonist quinelorane (LY163502; trans-(-)-5,5a,6,7,8,9,9a,10-octahydro-6-propylpyrimido [4,5-g] quinolin-2-amine dihydrochloride dihydrate) on concentrations of 3,4-dihydroxyphenylacetic acid, dopamine, 3-methoxy-4-hydroxyphenylethyleneglycol and norepinephrine in the dorsomedial nucleus of the hypothalamus and horizontal limb of the diagonal band of Broca of intact and norepinephrine-depleted male rats. For comparative purposes, various other diencephalic brain regions and the nucleus accumbens were also examined. The results of this study reveal that quinelorane decreases the activity of dopaminergic neurons in the nucleus accumbens, horizontal limb of the diagonal band of Broca and dorsomedial nucleus of the hypothalamus, whereas it increases the activity of noradrenergic neurons projecting to the dorsomedial nucleus of the hypothalamus, but not the horizontal limb of the diagonal band of Broca. These inhibitory and stimulatory actions of quinelorane are blocked by or reverse the effects of the D2-selective antagonist raclopride, indicating that quinelorane is acting at D2 receptors. Taken together, these results indicate that quinelorane inhibits DA neurons within the diencephalon, whereas it activates a subpopulation of noradrenergic neurons projecting to this brain region.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

gamma-Aminobutyric acid receptor-mediated regulation of periventricular-hypophysial dopaminergic neurons: possible role in mediating stress- and 5-hydroxytryptamine-induced decreases in neuronal activity.

The present study examined the effects of gamma-aminobutyric acid (GABA) agonists and antagonists on basal periventricular-hypophysial dopaminergic (PHDA) neuronal activity with a focus on the role of endogenous GABA in mediating 5-hydroxytryptamine- and stress-induced decreases in PHDA neuronal activity. PHDA neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in terminals of these neurons in the intermediate lobe of the pituitary. Plasma concentrations of alpha-melanocyte-stimulating hormone (alpha MSH) also were determined to provide a further index of PHDA neuronal activity. Administration of the GABAB agonist baclofen, but not the GABAA agonist isoguvacine, produced dose- and time-related decreases in intermediate lobe DOPAC concentrations and corresponding increases in plasma alpha MSH concentrations. Administration of either the GABAA antagonist SR-95,531 [2-(3-carboxypropyl)-3-amino-6-(4-methoxyphenyl)-pyridazinium bromide] or GABAB antagonists 2-hydroxysaclofen and CGP-35,348 [P-(3-aminopropyl)-P-diethoxymethyl-phosphinic acid; SR-95-531 did not alter basal intermediate lobe DOPAC concentrations or plasma alpha MSH concentrations per se, indicating that endogenous GABA does not tonically inhibit PHDA neuronal activity or alpha MSH secretion. 2-Hydroxysaclofen and CGP-35,348 did, however, reverse the baclofen-induced decrease in intermediate lobe DOPAC concentrations and increase in plasma alpha MSH concentrations. In a similar fashion, 2-hydroxysaclofen blocked the inhibitory effects of stress and the 5-hydroxytryptamine2/1c receptor agonist DOI [1-(2,5-dimethoxy-4-iodophenyl-2-aminopropane] on PHDA neuronal activity. These results indicate that GABAB and not GABAA receptor activation inhibits basal PHDA neuronal activity, and that GABAB receptor activation mediates the inhibitory effects of 5-hydroxytryptamine and stress on PHDA neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

5-Hydroxytryptamine2 receptor-mediated regulation of periventricular-hypophysial dopaminergic neuronal activity and the secretion of alpha-melanocyte-stimulating hormone.

The present study examined the effects of the 5-hydroxytryptaminergic (5HT)2/1c agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on periventricular-hypophysial dopaminergic (DA) neuronal activity and the secretion of alpha-melanocyte-stimulating hormone (alpha MSH). For comparison, the effects of DOI on tuberoinfundibular DA neuronal activity and the secretion of prolactin were also examined. Periventricular hypophysial and tuberoinfundibular DA neuronal activities were estimated by measuring the concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the terminal regions of these neurons; i.e., in the intermediate lobe of the pituitary and median eminence, respectively. Acute administration of DOI produced dose- and time-related decreases in intermediate lobe DOPAC concentrations and corresponding increases in plasma alpha MSH concentrations. Pretreatment of animals with either the 5HT2/1c antagonist ritanserin or the selective 5HT2 antagonist alpha-phenyl-1-(2-phenylethyl)-4-piperidine methanol (MDL-11,939) blocked the DOI-induced decrease in intermediate lobe DOPAC concentrations and increase in plasma alpha MSH concentrations. Acute administration of DOI produced dose- and time-related increases in plasma prolactin concentrations but did not alter DOPAC concentrations in the median eminence. Furthermore, the DOI-induced increase in plasma prolactin concentrations was blocked by ritanserin, but not MDL-11,939 pretreatment. Taken together, these data suggest that DOI inhibits periventricular hypophysial DA neuronal activity and increases the secretion of alpha MSH by activating 5HT2 receptors, whereas the DOI-induced prolactin secretion is independent of a decrease in tuberoinfundibular DA neuronal activity and is most likely mediated by 5HT2/1c receptor activation.

Amphetamines↗

PubMed1994

Differential effects of histamine on the activity of hypothalamic dopaminergic neurons in the rat.

The effect of intracerebroventricular administration of histamine on hypothalamic dopaminergic neuronal activity was estimated in male rats by measuring concentrations of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in brain regions containing terminals or perikarya of these neurons. Three distinct, regionally specific neurochemical responses were apparent. In the median eminence and intermediate lobe of the pituitary, histamine affected neither DOPAC nor dopamine concentrations, suggesting no effect on tuberoinfundibular or periventricular-hypophysial dopaminergic neuronal activity. In the medial zona incerta and in the dorsomedial, rostral periventricular and medial preoptic hypothalamic nuclei, histamine effected a dose- and time-related increase in both DOPAC and dopamine concentrations; these effects were blocked by destruction of noradrenergic neurons projecting to these regions, suggesting that these changes are attributable to noradrenergic neuronal activation, and that histamine does not affect the activity of incertohypothalamic or periventricular-preoptic dopaminergic neurons located in these brain regions. In the suprachiasmatic, caudal periventricular and paraventricular hypothalamic nuclei, histamine effected a dose- and time-related increase in DOPAC, but not dopamine, concentrations; these effects were blocked by the H1 antagonist mepyramine, but not the H2 antagonist zolantidine. Destruction of noradrenergic neurons projecting to these regions did not prevent the histamine-induced increases in DOPAC concentrations. These data indicate that histamine increases the activity of dopaminergic neurons projecting to the suprachiasmatic, caudal periventricular and paraventricular nuclei via an action at H1 receptors. Overall, these results reveal that i.c.v. administration of histamine differentially affects the activity of the various dopaminergic neuronal systems of the rat hypothalamus.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Comparison of the effects of the dopamine D2 agonist quinelorane on tuberoinfundibular dopaminergic neuronal activity in male and female rats.

The purpose of the present study was to examine the effects of quinelorane (LY163502), a potent and selective D2 dopaminergic (DA) receptor agonist, on the activity of tuberoinfundibular DA neurons in male and female rats as estimated by determining the concentration of the primary metabolite of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), in terminals of these neurons in the median eminence (ME). In males, quinelorane produced dose- and time-related increases in the concentration of DOPAC in the Me which was blocked by the D2 receptor antagonist raclopride. The activity of tuberoinfundibular neurons in female rats is higher than it is in males because circulating levels of prolactin tonically stimulate these neurons in the female. In female rats, quinelorane markedly lowered plasma concentrations of prolactin but failed to alter DOPAC concentrations in the ME. Pretreatment of female rats with prolactin antiserum induced hypoprolactinemia and reduced DOPAC concentrations in the ME; in these animals quinelorane increased ME DOPAC concentrations. These results indicate that by acting on D2 receptors quinelorane is able to stimulate tuberoinfundibular DA neurons in both male and female rats, but in female rats the ability of quinelorane to reduce circulating levels of prolactin indirectly reduces the activity of tuberoinfundibular DA neurons and thereby masks the stimulatory action of this drug on these neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

delta-Opioid receptor-mediated regulation of central dopaminergic neurons in the rat.

Effects of intraventricular injections of the delta-opioid receptor agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) and antagonist 17-cyclopropylmethyl-6,7-dehydro-4,5-epoxy-3,14-dihydroxy-6,7,2',3'-indo l morphinan (naltrindole) hydrochloride were determined on the activities of mesolimbic, nigrostriatal, tuberoinfundibular and periventricular-hypophysial dopaminergic neurons in brains of male rats. Dopaminergic neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of the decarboxylase inhibitor 3-hydroxybenzylhydrazine in regions of the brain (nucleus accumbens, striatum, median eminence) and the intermediate lobe of the pituitary which contain terminals of these neurons. DPDPE produced a dose- and time-related increase in concentrations of DOPAC and accumulation of DOPA in nucleus accumbens and median eminence, but had no effect in striatum or intermediate lobe of the pituitary. Naltrindole hydrochloride had no effect per se, but blocked the ability of DPDPE to increase DOPAC concentrations in nucleus accumbens and median eminence. These results reveal that activation of delta-opioid receptors selectively increases the activities of mesolimbic and tuberoinfundibular but not of nigrostriatal or periventricular-hypophysial dopaminergic neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Sexual differences in N-methyl-D-aspartate receptor-mediated regulation of tuberoinfundibular dopaminergic neurons in the rat.

The purpose of the present study was to examine the effects of N-methyl-D-aspartate (NMDA) receptor blockade on the activity of tuberoinfundibular dopaminergic (TIDA) neurons in male and female rats. TIDA neuronal activity was estimated by measuring either the accumulation of 3,4-dihydroxyphenylalanine (DOPA) 30 min after the administration of the decarboxylase inhibitor NSD-1015 or the concentration of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence. The non-competitive NMDA receptor antagonist MK-801 markedly reduced prolactin secretion in both male and female rats. MK-801 also produced a dose- and time-dependent decrease in the activity of TIDA neurons in female rats, but had no effect on the activity of TIDA neurons in either intact, orchidectomized or orchidectomized, testosterone-treated male rats. Removal of the tonic stimulatory effects of prolactin on TIDA neurons in female rats by immunoneutralization of endogenous prolactin failed to alter the responsiveness of TIDA neurons to the inhibitory effects of MK-801. On the other hand, MK-801 was unable to inhibit TIDA neurons in ovariectomized female rats, but the responsiveness of TIDA neurons to MK-801 in ovariectomized female rats was restored following estrogen replacement, even in the absence of prolactin. Like MK-801, the competitive NMDA receptor antagonist CGS-19755 produced a dose-dependent decrease in TIDA neuronal activity in female rats, which was prevented in a dose-dependent manner by the NMDA receptor agonist D,L-(tetrazol-5-yl) glycine. Taken together, these results reveal a sexual difference in the responsiveness of TIDA neurons to NMDA receptor antagonists, and suggest that estrogen positively modulates NMDA receptor-mediated, tonic stimulation of TIDA neurons in female rats by a prolactin-independent mechanism.

Animals↗

PubMed1993

Neurochemical evidence that 5-hydroxytryptaminergic neurons tonically inhibit noradrenergic neurons terminating in the hypothalamus.

The medial zona incerta (MZI) and dorsomedial nucleus of the hypothalamus (DMN), which contain cell bodies and terminals of incertohypothalamic dopaminergic (DA) neurons, are densely innervated by both noradrenergic (NE) and 5-hydroxytryptaminergic (5-HT) neurons. In view of emerging anatomical and pharmacological evidence suggesting possible interactions between 5-HT and catecholaminergic neurons, the effects of experimental procedures that inhibit or disrupt 5-HT neurons on the activities of catecholaminergic neurons terminating in these regions were examined in the present study. Catecholaminergic neuronal activity was estimated by measuring catecholamine synthesis (accumulation of 3,4-dihydroxyphenylalanine [DOPA] after administration of a decarboxylase inhibitor) and metabolism (concentrations of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) and the norepinephrine metabolite 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG)) in the MZI and DMN of both male and female rats. Inhibition of 5-HT neurons following administration of the 5-HT1A autoreceptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) increased the accumulation of DOPA in the DMN and the concentrations of DOPAC in the MZI and DMN, indicating an activation of catecholaminergic neurons in these regions. Concentrations of MHPG were increased in the MZI and DMN by 8-OH-DPAT or 5,7-dihydroxytryptamine-induced lesions of 5-HT neurons, revealing that NE neurons terminating in these regions were activated following procedures that decrease 5-HT neuronal function. Following destruction of NE neurons projecting to the MZI and DMN, 8-OH-DPAT no longer increased DOPAC concentrations in these brain regions.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Comparison of the effects of losulazine and reserpine on central aminergic neurons.

The purpose of this study was to examine the effects of both acute and chronic administration of the peripheral sympatholytic antihypertensive agent losulazine on central dopaminergic, noradrenergic, and 5-hydroxytryptaminergic neurons in the rat. For comparison, the acute effects of reserpine were also examined. Acute systemic administration of losulazine produced marked dose- and time-dependent decreases in dopamine and norepinephrine concentrations in regions outside the blood-brain barrier (i.e., the median eminence, intermediate lobe, and neural lobe), that were accompanied by an increase in plasma concentrations of prolactin and alpha-melanocyte-stimulating hormone. By comparison, losulazine caused a relatively modest, transient depletion of dopamine and norepinephrine (but not 5-hydroxytryptamine) in regions of the brain protected by the blood-brain barrier (i.e., the striatum, nucleus accumbens, and dorsomedial nucleus of the hypothalamus). In contrast to losulazine, acute systemic administration of reserpine caused a prolonged depletion of dopamine, norepinephrine, and 5-hydroxytryptamine in all brain and pituitary regions examined. These results suggest that regional differences in the response of aminergic neurons to acute administration of losulazine and reserpine reflect differences in the ability of these drugs to penetrate the blood-brain barrier. Chronic systemic administration of losulazine produced a similar decrease in dopamine and norepinephrine in the median eminence, intermediate lobe, and neural lobe, suggesting that tolerance does not develop to the ability of losulazine to deplete catecholamines in these regions. Chronic losulazine administration also decreased dopamine concentrations in the striatum, and norepinephrine concentrations in the dorsomedial nucleus, suggesting that losulazine may have cumulative effects on central catecholamine neurons terminating in these brain regions.

Animals↗

PubMed1993

Activation of mesolimbic dopaminergic neurons following central administration of histamine is mediated by H1 receptors.

The effect of intracerebroventricular administration of histamine on the activity of mesolimbic and nigrostriatal dopaminergic (DA) neurons was determined in male rats. The activity of these neurons was estimated by measuring: (1) the accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of a decarboxylase inhibitor, and (2) the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC) in the nucleus accumbens and striatum, which contain the terminals of these neurons. Central administration of histamine increased both DOPA accumulation and DOPAC concentrations in the nucleus accumbens, but was without effect in the striatum. The increase in DOPAC concentrations in the nucleus accumbens occurred within 10 min and was sustained for at least 120 min. The H1 antagonist mepyramine blocked whereas the H2 antagonist zolantidine did not affect histamine-induced increases in DOPAC concentrations in the nucleus accumbens. Neither mepyramine nor zolantidine affected basal DOPAC concentrations in the nucleus accumbens. These results indicate that central administration of histamine stimulates mesolimbic DA neurons through an action at the H1 receptor, but has no effect upon the activity of nigrostriatal DA neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Kappa opioid receptor-mediated regulation of prolactin and alpha-melanocyte-stimulating hormone secretion in male and female rats.

The purpose of this study was to examine the effects of the kappa opioid receptor agonist U-50,488 and antagonist nor-binaltorphimine (NOR-BNI) on the secretion of prolactin and alpha-melanocyte-stimulating hormone (alpha MSH) in male and female rats. Activation of kappa opioid receptors with U-50,488 increased plasma prolactin concentrations in both male and female rats, whereas blockade of kappa opioid receptors with NOR-BNI decreased plasma prolactin concentrations in male, but not in female rats. U-50,488 also increased and NOR-BNI decreased plasma concentrations of alpha MSH; similar effects were observed in both male and female rats. These results reveal a sexual difference in kappa opioid receptor-mediated regulation of prolactin, but not alpha MSH secretion.

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

PubMed1993

Differential effects of the D2 receptor agonist quinelorane on the secretion of prolactin and alpha-melanocyte-stimulating hormone.

The purpose of the present study was to determine the effects of quinelorane, a selective D2 receptor agonist, on concentrations of prolactin and alpha-melanocyte-stimulating hormone (alpha-MSH) in plasma of male rats. Quinelorane decreased plasma concentrations of prolactin but not of alpha-MSH, whereas, the D2 receptor antagonist raclopride increased plasma concentrations of both hormones. Quinelorane reversed the effects of raclopride on circulating levels of prolactin, but not alpha-MSH. The results of this study suggest that secretion of hormones from melanotrophs and lactotrophs is regulated by different subtypes of D2 receptors.

Analysis of Variance↗

PubMed1993

Neurochemical evidence that the inhibitory effect of galanin on tuberoinfundibular dopamine neurons is activity dependent.

The purpose of the present study was to examine the effects of galanin on the basal and stimulated activity of tuberoinfundibular dopaminergic (TIDA) neurons in male and female rats. TIDA neuronal activity was estimated by measuring dopamine (DA) synthesis [accumulation of 3,4-dihydroxyphenylalanine(DOPA) after administration of a decarboxylase inhibitor] and metabolism [ratio of 3,4-dihydroxyphenylacetic acid (DOPAC) to DA concentrations] in terminals of these neurons in the median eminence. Central administration of galanin (2 micrograms/rat, i.c.v.) produced a rapid (by 15 min) increase in plasma prolactin concentrations, but had no effect on the ratio of DOPAC to DA in the median eminence of either male or female rats. In contrast, galanin decreased the ratio of DOPAC to DA in the median eminence of both male and female rats whose TIDA neuronal activity was stimulated following administration of the DA antagonist haloperidol (1 mg/kg, s.c., 12 h). The galanin receptor antagonist galanin-(1-13)-bradykinin-(2-9)-amide had no effect on the accumulation of DOPA in the median eminence of male rats per se, but blocked the inhibitory effects of either exogenous or endogenous galanin on median eminence DOPA accumulation in haloperidol-treated rats. These results indicate that in both male and female rats, galanin-induced activation of prolactin secretion is not mediated by changes in tonic inhibition of hormone release by TIDA neurons, and that TIDA neurons are responsive to the inhibitory effects of galanin only under activated conditions.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

5HT2 receptors mediate the effects of stress on the activity of periventricular hypophysial dopaminergic neurons and the secretion of alpha-melanocyte-stimulating hormone.

The roles of 5-hydroxytryptaminergic (5HT) neurons and receptor subtypes in mediating the effects of stress on the activity of periventricular hypophysial dopaminergic (PHDA) neurons and the secretion of alpha-melanocyte-stimulating hormone (alpha MSH) were examined in female rats. Periventricular hypophysial dopaminergic neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid in the intermediate lobe of the pituitary. Brief exposure to diethylether followed by 30 min of supine restraint decreased intermediate lobe 3,4-dihydroxyphenylacetic acid concentrations and increased plasma concentrations of alpha MSH. These stress-induced effects were not observed in animals in which 5HT neurons had been previously destroyed by 5,7-dihydroxytryptamine or inhibited by the administration of the 5HT1A receptor agonist 8-hydroxy-2-(di-n-propyl-amino)-tetralin. Pretreatment of rats with the 5HT2 receptor antagonist MDL-11,939 blocked the inhibitory effects of stress on intermediate lobe 3,4-dihydroxyphenylacetic acid concentrations and the corresponding increase in plasma alpha MSH concentrations, whereas the 5HT3 receptor antagonist ondansetron was without effect. These results reveal that 5HT neurons, acting via 5HT2 receptors, mediate the inhibitory effects of stress on periventricular hypophysial dopaminergic neurons and the consequent increase in secretion of alpha MSH.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Sexual differences in the stimulatory effects of bombesin on tuberoinfundibular dopaminergic neurons.

The purpose of this study was to (1) examine the effects of central administration of bombesin on the activity of tuberoinfundibular dopaminergic (DA) neurons in male and female rats, and (2) determine if sexual differences in the responsiveness of these neurons to bombesin were due to the presence of prolactin or gonadal steroids. The activity of tuberoinfundibular DA neurons was estimated by measuring the concentrations of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in terminals of these neurons in the median eminence. The effects of bombesin on the secretion of prolactin and alpha-melanocyte stimulating hormone (alpha MSH), and the activities of nigrostriatal, mesolimbic, and periventricular-hypophysial DA neurons were also determined in gonadally intact male and female rats. Central administration of bombesin (10 ng/rat; i.c.v.) decreased prolactin secretion in gonadally intact male and female rats, but only in males was this associated with an increase in the activity of tuberoinfundibular DA neurons. In contrast, bombesin increased the activity of periventricular-hypophysial DA neurons terminating in the intermediate lobe of both male and female rats, and this was associated with a decrease in alpha MSH secretion in both sexes. Bombesin had no effect on the activities of nigrostriatal, mesolimbic, or periventricular-hypophysial DA neurons terminating in the neural lobe in either sex. The loss of endogenous gonadal hormones following ovariectomy rendered tuberoinfundibular DA neurons responsive to the stimulatory effects of bombesin, whereas immunoneutralization of endogenous prolactin following administration of prolactin antiserum had no effect on the inability of bombesin to alter the activity of these neurons in female rats.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Characterization of opioid receptor-mediated regulation of incertohypothalamic dopamine neurons: lack of evidence for a role of 5-hydroxytryptaminergic neurons in mediating the stimulatory effects of morphine.

The purpose of the present study was to characterize opioid receptor-mediated regulation of incertohypothalamic dopaminergic (DA) neurons in the rat brain by examining the acute effects of selective mu or kappa opioid receptor agonists and antagonists on concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the medial zona incerta (MZI) and the dorsomedial hypothalamic nucleus (DMN) which contain cell bodies and terminals, respectively, of these neurons. Morphine caused a dose- and time-related increase in concentrations of DOPAC in MZI and DMN; this stimulatory effect was blocked by the mu opioid receptor antagonist naltrexone. In contrast, activation or blockade of kappa opioid receptors following administration of U-50,488 or nor-binaltorphimine, respectively, had no effect on DOPAC concentrations in either the MZI or DMN. The basal activity of incertohypothalamic DA neurons and their response to morphine was similar in male and female rats. Morphine also increased the concentrations of 5-hydroxyindoleacetic acid in MZI and DMN, indicating that morphine increases the activity of 5-hydroxytryptamine (5HT) neurons projecting to these regions. This might suggest that morphine-induced activation of incertohypothalamic DA neurons is mediated by 5HT neurons; but 5,7-dihydroxytryptamine-induced lesions of 5HT neurons did not alter the ability of morphine to increase DOPAC concentrations in MZI and DMN. These results indicate that the stimulatory effects of mu opioid receptor activation on incertohypothalamic DA neurons is not dependent upon the presence of 5HT neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Effects of immunoneutralization of dynorphin1-17 and dynorphin1-8 on the activity of central dopaminergic neurons in the male rat.

The effects of administration of antibodies against dynorphin1-17 (DYN1-17-AB) and dynorphin1-8 (DYN1-8-AB) were examined on the activity of dopaminergic (DA) neurons comprising the nigrostriatal, mesolimbic, tuberoinfundibular and periventricular-hypophysial systems in the male rat brain. DA neuronal activity was estimated by measuring the concentration of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in brain (striatum, nucleus accumbens, median eminence) and pituitary regions (intermediate lobe) containing terminals of these neurons. The intracerebroventricular administration of either DYN1-17-AB or DYN1-8-AB produced a time-related increase in the activity of tuberoinfundibular and periventricular-hypophysial DA neurons, but failed to alter the activity of nigrostriatal or mesolimbic DA neurons. The ability of both DYN1-17-AB and DYN1-8-AB to enhance the activity of tuberoinfundibular and periventricular-hypophysial DA neurons was reversed by the kappa opioid agonist U-50,488. These results indicate that DYN1-17-AB and DYN1-8-AB, presumably by binding endogenous dynorphins, remove a tonic inhibitory action of these opioid peptides on tuberoinfundibular and periventricular-hypophysial DA neurons.

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

PubMed1992

Evidence that histamine-stimulated prolactin secretion is not mediated by an inhibition of tuberoinfundibular dopaminergic neurons.

The effects of histamine on prolactin secretion and the activity of tuberoinfundibular dopaminergic (DA) neurons were examined in male rats. Tuberoinfundibular DA neuronal activity was estimated in situ by measuring the metabolism [concentration of 3,4-dihydroxyphenylacetic acid (DOPAC)] and synthesis [accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of a decarboxylase inhibitor] of dopamine in the median eminence. Intracerebroventricular (icv) injection of histamine produced a dose- and time-dependent increase in plasma prolactin levels but had no effect on DOPA accumulation or DOPAC concentrations in the median eminence. These results indicate that the stimulation of prolactin secretion following icv histamine is not mediated by an inhibition of tuberoinfundibular DA neurons.

3,4-Dihydroxyphenylacetic Acid↗