Tuberohypophyseal Dopamine Research Articles

Melatonin increases the in situ activity of tyrosine hydroxylase in the mediobasal hypothalamus of male syrian hamsters

The effects of daily late afternoon injections of melatonin on the in situ activity of tyrosine hydroxylase (TH) were examined in the median eminence/arcuate region of the mediobasal hypothalamus (MBH) and the neurointermediate lobe (NIL) of the male Syrian hamster. TH activity was determined in tissue extracts by measuring the accumulation of L-DOPA following administration of the dopa decarboxylase inhibitor, NSD-1015. After 9 weeks of melatonin treatment, highly significant increases in the activity of MBH TH were demonstrated over a 24 hr period, compared to saline-treated controls. Melatonin-induced elevations in TH occurred concomitantly with decreases in tuberoinfundibular dopamine (TIDA) and tuberohypophyseal dopamine (THDA) concentrations. Similar findings were observed in castrated hamsters, indicating that the melatonin-induced increase in TH was not secondary to melatonin-induced changes in circulating levels of gonadal hormones. These data led to the interpretation that melatonin treatment elevated TIDA synthesis either through a direct action on the arcuate nuclei or on neurons impinging on these nuclei.

Photoperiod effects on neurohypophyseal and tuberoinfundibular dopamine metabolism in the male hamster.

Exposure of golden hamsters to a short photoperiod (< 12.5 h light/day) leads to suppression of gonadal function secondary to reduced gonadotropin and PRL secretion. PRL secretion is decreased despite a reduction of tuberoinfundibular dopaminergic activity. In the present study, the ability of photoperiod to affect tuberohypophyseal dopamine (DA) turnover was evaluated in long day (LD; 16 h of light, 8 h of darkness) and short day (SD; 8 h of light, 16 h of darkness) male hamsters. Exposure to SD led to decreases in testicular weight within 10 weeks and decreases in plasma PRL levels within 1 week. DA turnover in the neurointermediate lobe of the pituitary, as estimated by measuring the depletion of DA 60 min after tyrosine hydroxylase inhibition with alpha-methyl-p-tyrosine (250 mg/kg), was significantly elevated 1 and 4 weeks after transfer to SD, but returned by 10 weeks to the levels seen in LD animals. After 14 days of SD exposure an enhanced lactotroph sensitivity to DA was demonstrated and may also have contributed to suppression of PRL levels. Similarly to the findings of previous studies, DA turnover in the median eminence was depressed in animals housed in SD. The DA content of the anterior pituitary was not significantly affected by photoperiod. The data from this study suggest that decreases in PRL secretion associated with the transfer of hamsters from LD to SD conditions are at least in part caused by an increase in DA turnover by neurohypophyseal neurons. However, the involvement of other PRL-inhibiting or -stimulating factors in mediating the effects of photoperiod on PRL secretion cannot be ruled out.

Region-related Fos expression in hypothalamic dopaminergic neurons of rats by intraperitoneal administration of an endogenous satiety substance, 2-buten-4-olide

An effect of 2-buten-4-olide (2-B4O), an endogenous satiety substance, on hypothalamic dopamine neurons of rats was studied by double-label immunohistochemistry for c-Fos and tyrosine hydroxylase (TH). Intraperitoneal administration of 2-B4O induced Fos-like immunoreactivity in TH-immunoreactive neurons in the periventricular area and paraventricular nucleus but not in the arcuate nucleus. Thus, the present results suggest that tuberohypophysial dopamine neurons are regulated under the influence of endogenous 2-B4O.

Effects of the enkephalin analog ( d-Met 2 Pro 5)-enkephalinamide on α-melanocyte-stimulating hormone secretion

We used the met-enkephalin analog ( d-Met 2, Pro 5)-enkephalinamide (DMPEA) to investigate enkephalinergic control of α-melanocyte-stimulating hormone (α-MSH) secretion. Systemic (s.c.) administration of DMPEA elevated plasma titers of α-MSH in a dose- and time-related manner. Pretreatment with the opiate antagonist naltrexone had no effect on basal plasma levels of α-MSH but blocked DMPEA-induced α-MSH release. Treatment with a dose of naltrexone sufficient to block DMPEA-induced secretion of α-MSH had no effect on stress-induced secretion of α-MSH. Although pretreatment with the dopamine receptor agonist apomorphine prevented DMPEA-induced α-MSH secretion, DMPEA had no effect on the synthetic activity of tuberohypophysial dopamine neurons as gauged by measuring the accumulation of 3,4-dihydroxyphenylalanine in the neurointermediate lobe (NIL) following administration of NSD-1015. In vitro treatment of isolated NILs with DMPEA resulted in a significant increase in α-MSH release. Naltrexone completely blocked the stimulatory effects of DMPEA on α-MSH release in vitro. Our results indicate that DMPEA stimulates α-MSH secretion by acting directly through opiate receptors at the level of the NIL.

Activation of tuberoinfundibular and tuberohypophysial dopamine neurons following intracerebroventricular administration of bombesin

The effect of bombesin on the activity of dopamine (DA) neurons comprising the nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophysial systems in the male rat was determined by measuring: (1) the accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of a decarboxylase inhibitor, and (2) the concentration of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in brain (striatum, nucleus accumbens, median eminence) and pituitary regions (intermediate and neural lobes) containing terminals of these neurons. Intracerebroventricular (i.c.v.) injection of bombesin caused a dose- and time-related increase in the activity of DA neurons projecting to the median eminence and intermediate lobe of the pituitary, and a corresponding decrease in the concentrations of prolactin and α-melanocyte-stimulating hormone (αMSH) in the plasma. In contrast, doses of bombesin up to 10 ng i.c.v. failed to alter the activity of DA neurons terminating in the striatum, nucleus accumbens or neural lobe of the pituitary gland. Equimolar doses of bombesin and gastrin-releasing peptide (GRP), a bombesin-like peptide, increased the concentrations of DOPAC in the median eminence and intermediate lobe of the pituitary, suggesting that GRP-preferring receptors may be responsible for the stimulatory effects of bombesin on DA neuronal activity in these regions. The results of these studies suggest that bombesin increases the activity of tuberoinfundibular and tuberohypophysial DA neurons projecting to the median eminence and intermediate lobe of the pituitary, respectively, and thereby inhibits the secretion of prolactin and αMSH.

Activation of tuberohypophysial dopamine neurons following intracerebroventricular administration of the selective kappa opioid receptor antagonist nor-binaltorphimine

The effect of the kappa opioid receptor antagonist nor-binaltorphimine (NOR-BNI) was examined on the activity of dopamine (DA) neurons comprising the nigrostriatal, mesolimbic, and tuberohypophysial systems in the male rat. DA neuronal activity was estimated by measuring: (1) the concentration of the DA metabolite 3,4-dihydroxyphenylacetic acid and, (2) the accumulation of 3,4-dihydroxyphenylalanine after administration of a decarboxylase inhibitor in brain (striatum, nucleus accumbens) and pituitary regions (intermediate lobe, neural lobe) containing terminals of these neurons. The intracerebroventicular administration of NOR-BNI produced a dose- and time-related increase in the activity of tuberohypophysial DA neurons, but failed to alter the activity of nigrostriatal or mesolimbic DA neurons. The ability of NOR-BNI to enhance the activity of tuberohypophysial DA neurons was blocked by the kappa opioid agonist U-50,488. These results indicate that NOR-BNI, acting on kappa opioid receptors, activates tuberohypophysial DA neurons projecting to the neural and intermediate lobes of the pituitary.

Stress-induced secretion of alpha-melanocyte-stimulating hormone is accompanied by a decrease in the activity of tuberohypophysial dopaminergic neurons.

The purpose of the present study was to examine the acute effects of stress on the secretion of alpha-melanocyte-stimulating hormone (alpha MSH) and the activity of tuberohypophysial dopamine (DA) neurons in female and male rats. The activity of tuberohypophysial DA neurons was estimated by measuring the accumulation of 3,4-dihydroxyphenylalanine (DOPA) following administration of the decarboxylase inhibitor NSD 1015, and the concentrations of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the intermediate and neural lobes of the posterior pituitary. The combination of brief (2 min) ether exposure followed by 30 min of supine restraint (immobilization in the supine position) decreased the rate of DOPA accumulation in the intermediate, but not in the neural lobe of both female and male rats. Similarly, brief ether exposure followed by 10, 20 or 30 min of supine restraint increased plasma alpha MSH concentrations and decreased DOPAC concentrations in the intermediate lobe of female and male rats. In the absence of ether, tube restraint (confinement in a cylindrical acrylic tube) increased alpha MSH secretion and decreased intermediate lobe DOPAC concentrations, whereas ether in the absence of physical restraint had no effect. These results suggest that the stress-induced activation of alpha MSH secretion in both female and male rats may be due, in part, to a decrease in the activity of tuberohypophysial DA neurons in the intermediate lobe of the posterior pituitary.

Kappa-Opioid-Receptor-Mediated Regulation of α-Melanocyte-Stimulating Hormone Secretion and Tuberohypophysial 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-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 tuberhypophysial 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 decar☐ylase 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. Taken together, these results indicate the DOPAC concentrations in the intermediate lobe and neural lobe of the posterior pituitary are a useful index of tuberohypophysial neuronal activity.

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.

Evidence for stimulatory noradrenergic and inhibitory dopaminergic regulation of oxytocin release in the lactating rat.

The present experiments tested the involvement of central catecholaminergic systems in the suckling-induced release of oxytocin (OT) during lactation in the rat. In the first experiment, female rats in midlactation were separated from their offspring for 4 h and then allowed to suckle their litters for 30 or 60 min or to remain nonsuckled. The turnover rates of norepinephrine (NE) and dopamine (DA) were calculated from the rate of decline after synthesis inhibition. Suckling decreased the turnover rate of DA in the median eminence and in the neurointermediate lobe of the pituitary gland. Suckling increased the turnover rate of NE in the rostral paraventricular and supraoptic nuclei, areas that contain most of the OT cells that project to the neural lobe of the pituitary, and in the interstitial nucleus of the stria terminalis, but not in the arcuate or caudal paraventricular nuclei, median eminence, or neurointermediate lobe. In a second experiment, midlactating females received intracerebral microinjections of the catecholamine neurotoxin 6-hydroxydopamine or of vehicle into the vicinity of the paraventricular and supraoptic nuclei 1 week before a suckling test. The release of OT was completely prevented in 6-hydroxydopamine-treated animals, and NE was significantly decreased in the paraventricular, supraoptic, and arcuate nuclei. In a third study, the increase in plasma OT in response to suckling was prevented by stimulation of DA receptors with bromocriptine, while blockade of DA receptors with domperidone significantly increased plasma OT levels in nonsuckled lactating rats. These results suggest that suckling stimulation activates the noradrenergic innervation to the rostral paraventricular nucleus and to the supraoptic nucleus, which exerts an excitatory influence on the release of OT and decreases activity of the tuberohypophyseal DA system, which provides a tonic inhibitory influence over the secretion of OT.

Effects of gonadal steroids on tuberoinfundibular and tuberohypophysial dopaminergic neuronal activity in male and female rats.

The activities of tuberoinfundibular and tuberohypophysial dopamine (DA) neurons were estimated by measuring the turnover of DA in terminals of these neurons in the median eminence and in the neural and intermediate lobes of the pituitary, respectively. The rate of DA turnover (alpha-methyltyrosine-induced decline of DA) in the median eminence was two to three times faster in females than in males, but no sexual differences in DA turnover rates were noted in the neural and intermediate lobes. Two weeks following gonadectomy the rate of DA turnover in the median eminence was increased in the male but decreased in the female. These effects were reversed by testosterone and estrogen replacement in gonadectomized males and females, respectively. Neither gonadectomy nor steroid replacement altered DA turnover in the neural or intermediate lobes of either males or females. These results indicate that estrogen stimulates and testosterone inhibits tuberoinfundibular DA neuronal activity while neither steroid affects tuberohypophysial DA neuronal activity.

Effect of neonatal prolactin deficiency on prepubertal tuberoinfundibular and tuberohypophyseal dopaminergic neuronal activity.

PRL is present in milk of lactating rats and, when ingested by the pups, can pass through the gut and enter the systemic circulation. The present study tested whether suppression of normal milk PRL intake by the pups during the early postpartum period affects the subsequent level of activity of the tuberoinfundibular dopamine (DA) system. Maternal plasma and milk PRL levels were depressed in lactating rats by daily injections of bromocriptine. Such treatment during postpartum days 2-5, but not during postpartum days 9-12, resulted in a marked suppression of DA turnover in the median eminence and an elevation of the plasma PRL concentration in the offspring when measured at 30-35 days of age. Simultaneous infusion of ovine PRL by osmotic minipump reversed the effects of neonatal bromocriptine treatment. DA turnover in the neurointermediate lobe was unaffected by any treatment. Basal plasma PRL levels in 3- to 5-day-old pups were not reduced by maternal bromocriptine treatment, indicating that bromocriptine was not secreted into the milk in sufficient amounts to depress endogenous PRL secretion in the pups. These results suggest that the normal activity of the tuberoinfundibular DA system, but not that of the tuberohypophyseal DA system, of the rat may be impaired if milk PRL levels are reduced during a critical postpartum period.

Permanent alteration of peptide feedback on dopamine neurons after injection of α-melanotropin antiserum at a critical period of postnatal development

Tonic inhibition of alpha-MSH secretion by the tubero-hypophyseal dopamine (DA) neurons of the rat starts at the end of the first postnatal week, after a peak in plasma MSH at days 5 and 6. In order to obtain information on the maturation of central control, we studied the development of alpha-MSH feedback on DA neurons and the possible role of circulating peptide. The characteristic response of these DA neurons to i.p. alpha-MSH, i.e., an acute rise in cellular fluorescence intensity as determined by microfluorimetry, was not yet detected at day 4 but present at day 8. When rats were injected i.v. with antiserum to alpha-MSH on days 5 and 6 and tested as adults, their DA neurons failed to react to i.p. alpha-MSH (2-100 micrograms/kg), but they were still responsive to prolactin (600 micrograms/kg). The DA system was already unresponsive to alpha-MSH at postnatal day 8. Antiserum injection on days 11 and 12, when plasma MSH is low, did not affect the reaction of DA neurons to alpha-MSH on day 14. These developmental processes were analogous in both sexes. Injections of control serum were ineffective. Our observations indicate that the feedback reaction of DA neurons to alpha-MSH develops in conjunction with the onset of inhibitory control of MSH release. The presence of alpha-MSH during a critical period appears to be necessary for the development of the responsiveness of DA neurons to the peptide hormone.

Effects of water deprivation and administration of hypertonic saline on dopamine concentrations in posterior pituitary and vasopressin release in rats

Changes in concentrations of arginine vasopressin (AVP) in plasma and the neurointermediate lobe of the pituitary and those in dopamine (DA) in the neurointermediate lobe in rats were studied simulataneously after depriving the animals of water as well as after giving intraperitoneal (i.p.) injections of hypertonic saline (4.5% saline, 25 ml/kg of body weight). After water deprivation for 24 h, both AVP in plasma and DA in the neurointermediate lobe increased without any changes in AVP in the neurointermediate lobe. Water deprivation for 48–72 h caused further increases in both AVP in plasma and DA in the neurointermediate lobe with a significant decrease in AVP in the neurointermediate lobe. Rehydration for 24 h subsequent to 72 h of water deprivation made AVP in plasma and DA in the neurointermediate lobe return to the values of normally hydrated rats, whereas AVP in the neurointermediate lobe was still depressed. Thirty min after the i.p. injection of hypertonic saline, both AVP in plasma and DA in the neurointermediate lobe increased markedly with no change in AVP in the neurointermediate lobe. The time course of change in DA in the neurointermediate lobe was similar to that in plasma AVP when plasma osmolality was changed chronically or acutely. These results may make questionable the preconception that the tuberohypophyseal DA neurons are not involved in or regulated by early changes in vasopressin secretion.

The hypothalamohypophyseal system in vitro: Electrophysiology of the pars intermedia and evidence for both excitatory and inhibitory inputs

The purpose of this study was to better assess the function of catecholamine-containing nerve terminals in the pituitary pars intermedia lobe. Hypothalamohypophyseal explants, which included the intact mediobasal hypothalamis (MBH), median eminence, infundibular stalk and the neurointermediate lobe, were obtained from 2–3-week-old male and female albino rats. The tissue was placed in a perfusion chamber and maintained under physiological conditions for up to 12 h. A set of bipolar stimulating electrodes was positioned on the surface of the median eminence, infundibular stalk or the rostroventral arcuate nucleus of the MBH. A microelectrode recorded electrical activity in the pars intermedia gland. Two types of spontaneous action potentials were found; fast 2–4 ms duration neural fiber type spikes and slower 7–10 ms duration spikes probably derived from non-neural endocrine cells. Single-pulse electrical stimulation at all 3 sites evoked both kinds of potentials, while trains of stimuli (0.1–20 Hz) decreased or completely inhibited the basal firing rate of the slower ones. Application of the neuroleptic. l-sulpiride (0.01, 0.1 or 1.0 μmol), to the perfusion medium increased the spontaneous endocrine cell activity and blocked the stimulus-induced inhibition in the explants but had no effect on the activity in isolated pituitaries. Dopamine (0.1 μmol), which is knoqn to inhibit the secretion of pro-opiomelanocortin peptides, reversibly suppressed the spontaneous endocrine cell potentials. These observations support a hypothesis for the presence of a functional tuberohypophyseal dopamine inhibitory system and a possible, but as yet unidentifiable, excitatory system in the pars intermedia. Thus, hypothalamohypophyseal explants can be used to elucidate specific information on this type of neuroendocrine axis.

Differential regulation of tuberohypophysial dopaminergic neurons terminating in the intermediate lobe and in the neural lobe of the rat pituitary gland.

In order to characterize the properties of tuberohypophysial dopaminergic neurons which terminate in the intermediate (IL) and neural (NL) lobes of the pituitary gland a technique was developed which permitted the selective dissection of the rat pituitary into its three distinct lobes (NL, IL and anterior lobe, AL). The success of the dissection was evaluated histologically and biochemically by measuring the distribution of peptide hormones characteristic of the dissected regions. As would be predicted, prolactin was found almost exclusively in the AL, arginine-vasopressin in the NL and alpha-melanotropin in the IL. Over two-thirds of total immunoreactive beta-endorphin was located in the IL and less than 30% was found in the AL. The concentration of dopamine (DA) was greater in the IL than in the NL, but the rate of turnover of the amine was approximately the same suggesting that the basal activity of tuberohypophysial DA neurons is similar in both regions. On the other hand, the turnover of DA in the IL, but not NL, was increased following the administration of a DA antagonist (haloperidol) and decreased following a DA agonist (bromocriptine). Thus, the activity of DA neurons terminating in the IL is regulated, at least in part, by DA receptor-mediated mechanisms and in this regard these neurons resemble DA neurons terminating in the nucleus accumbens and striatum. Since DA turnover in NL was not altered by the administration of haloperidol or bromocriptine it is proposed that these neurons lack DA receptor-mediated regulatory mechanisms and thus resemble tuberoinfundibular DA neurons terminating in the median eminence.

Tuberohypophyseal and Tuberoinfundibular Dopamine Systems Exhibit Differential Sensitivity to Neonatal Monosodium Glutamate Treatment

The arcuate nucleus (AN) is the presumed origin of the dopaminergic innervation of posterior lobe of the pituitary. Posterior lobe dopamine levels were determined in rats that had been neonatally treated with monosodium glutamate (MSG) to lesion the AN. MSG-induced AN damage was confirmed neurochemically, histologically and immunocytochemically. MSG treatment resulted in a substantial loss of AN neurons and approximately a 50% loss of dopamine uptake capacity (Vmax) in the mediobasal hypothalamus. Posterior pituitary dopamine levels were not significantly altered by MSG-induced AN damage. These results suggest that MSG treatment spares the tuberohypophyseal dopamine system and that the AN may not be the sole origin of the dopaminergic innervation of the posterior pituitary.

Injection of hypertonic saline or mannitol accelerates the dehydration-induced activation of dopamine synthesis in the neurointermediate lobe of the rat hypophysis.

The rate of dopamine (DA) synthesis (DOPA accumulation after the administration of an inhibitor of aromatic L-amino acid decarboxylase) was determined in terminals of tuberohypophyseal DA neurons in the neurointermediate lobe (NIL) of the rat hypophysis at various times after the presentation of osmotic stimuli. DA synthesis in the NIL, but not in median eminence or striatum, was increased 24 h but not 4 h after an injection of hypertonic saline (5 ml 15% NaCl/kg, s.c.), provided the animals were not permitted access to water after the injection; 24 h of water deprivation per se was without effect on the rate of DA synthesis. DOPA accumulation in the NIL was also increased after an intravenous infusion of mannitol (25 ml 20% mannitol/kg) plus 24 h of water deprivation. These results suggest that the dehydration-induced activation of tuberohypophyseal DA neurons which is normally seen after 2-3 days of water deprivation can be accelerated if water deprivation is preceeded by injections of hypertonic saline or mannitol.

Type A monoamine oxidase catalyzes the intraneuronal deamination of dopamine within nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophyseal neurons in the rat.

Clorgyline (0.3-10 mg/kg, i.p.) inhibited type A monamine oxidase (5-hydroxytryptamine as substrate) but not type B monoamine oxidase (phenylethylamine as substrate) in homogenates of rat striatum and olfactory tubercle; deprenyl (0.3-3 mg/kg, i.p.) inhibited type B but not type A monoamine oxidase in these homogenates. The same doses of clorgyline increased concentrations of dopamine in striatum, and dopamine and norepinephrine in the olfactory tubercle, median eminence and posterior pituitary; they also reduced the concentrations of dihydroxyphenylacetic acid and the rate of synthesis of dopamine (DOPA accumulation after a decarboxylase inhibitor) in the same brain regions. On the other hand, the administration of deprenyl at doses that markedly inhibited type B monoamine oxidase did not alter the concentrations of dopamine, norepinephrine and dihydroxyphenylacetic acid or the rate of accumulation of DOPA in these brain regions. In addition, only clorgyline significantly lowered serum concentrations of prolactin. These results that type A monoamine oxidase catalyzes the intraneuronal deamination of dopamine within terminals of nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophyseal dopamine neurons.