Plasma Prolactin Release Research Articles

Effect of milking behavior on circulatory hormones and milk production in lactating Murrah buffaloes

The effect of milking temperament on plasma hormones, metabolites, milk yield and composition in lactating Murrah buffaloes was studied. Animals were selected from the institute herd and grouped as docile and nervous buffaloes, based on temperament score before and during milking. Blood sampling times were; before milking (-20 min.), after concentrate intake, after teat massage, during milking and 20 min. post- milking. Plasma prolactin (PRL), growth hormone (GH) and cortisol (CORT) concentrations were measured by enzyme-immunoassay procedures. Milk yields of individual buffaloes were recorded and milk composition (fat, protein, lactose, SNF, SCC) determined. Milk yield was significantly lower (P<0.05) in nervous buffaloes in comparison to docile buffaloes. Mean fat, protein, lactose and SNF varied non-significantly between the groups. Milk SCC and plasma NEFA concentration was more (P<0.05) in nervous buffaloes than in docile buffaloes. Milking temperament significantly influenced plasma PRL (P<0.01) and CORT release (P<0.05) but GH was unaffected. Concentrate feeding prior to milking induced release of plasma PRL and CORT without affecting GH and oxytocin levels. Teat stimulus further enhanced release of PRL, oxytocin and CORT hormone in both the groups. Plasma PRL, cortisol, oxytocin and GH varied significantly (P<0.01) before, during and after milking (P<0.01). Basal PRL, GH and CORT were attained 20 minutes after the completion of milking in both the groups. The results show that the behavior of buffaloes at milking influenced release of galactopoietic hormones (PRL, CORT, GH and oxytocin), milk yield and SCC, while milk fat, protein, lactose and SNF remain unaffected.

Hormone release, milk production and composition in Murrah buffaloes milked by hand and machine

Lactating Murrah buffaloes selected from the institute herd were categorized as hand and machine milking group. Blood samples were collected before milking, after concentrate feeding and teat message, during milking, and after completion of milking. Plasma prolactin (PRL), growth hormone (GH) and cortisol (CORT) concentrations were measured. Mean milk fat, protein, lactose and SNF content varied non-significantly between the groups. Milk somatic cell count (SCC), plasma glucose and NEFA concentration was more (P< 0.05) in machine milking group than in hand milking group. Both hand and machine milking operation significantly released plasma PRL (P< 0.01), CORT (P< 0.05) and GH (P< 0.01) hormone. Feeding of concentrate mixture resulted in a significant release in PRL and CORT hormone and their concentration increased further after teat message. Plasma PRL, CORT and GH varied significantly (P< 0.01) before, during and after milking (P< 0.01), and levels were normal 20-minutes post-milking in both the groups. It was concluded that feeding of concentrate mixture, teat message and milking operations either by hand or machine significantly stimulate release of plasma PRL, CORT and GH hormone in Murrah buffaloes.

Role of salsolinol in the regulation of pituitary prolactin and peripheral dopamine release.

(R)-Salsolinol (SAL), a dopamine (DA)-related tetrahydroisoquinoline, has been found in extracts of the neuro-intermediate lobes (NIL) of pituitary glands and in the median eminence of the hypothalamus obtained from intact male rats and from ovariectomized and lactating female rats. Moreover, analysis of SAL concentrations in NIL revealed parallel increases with plasma prolactin (PRL) in lactating rats exposed to a brief (10 min) suckling stimulus after 4-h separation. SAL is sufficiently potent in vivo to account for the massive discharge of PRL that occurs after physiological stimuli (i.e. suckling). At the same time, it was without effect on the secretion of other pituitary hormones. It has been also shown that another isoquinoline derivative, 1-methyldihydroisoquinoline (1MeDIQ), which is a structural analogue of SAL, can dose-dependently inhibit the in-vivo PRL-releasing effect of SAL. Moreover, 1MeDIQ can inhibit the elevation of plasma PRL induced by physiological stimuli, for example suckling, or in different stressful situations also. 1MeDIQ also has a psycho-stimulant action, which is fairly similar to the effect of amphetamine, i.e. it induces an increase in plasma catecholamine concentrations. It is clear from these data that this newly discovered endogenous compound could be involved in regulation of pituitary PRL secretion. It has also been observed that SAL is present in peripheral, sympathetically innervated organs, for example the atrium, spleen, liver, ovaries, vas deferens, and salivary gland. Furthermore, SAL treatment of rats results in dose-dependent and time-dependent depletion of the DA content of the organs listed above without having any effect on the concentration of norepinephrine. More importantly, this effect of SAL can be completely prevented by amphetamine and by 1MeDIQ pretreatment. It is clear there is a mutual interaction between SAL, 1MeDIQ, and amphetamine or alcohol, not only on PRL release; their interaction with catecholamine "synthesis/metabolism" of sympathetic nerve terminals is also obvious.

Prolactin release and response to vasoactive intestinal peptide in an opportunistic breeder, the zebra finch ( Taeniopygia guttata)

Zebra finches in arid regions of Australia are opportunistic breeders that time their breeding cycles to coincide with nonseasonal rainfall. Hormonal profiles associated with reproductive behaviors may differ from those observed in seasonal breeders because these birds need to be reproductively competent on short notice. This study measured plasma prolactin (PRL) levels in nonbreeding and breeding zebra finches and in birds with and without prior reproductive experience. We also investigated the change in plasma PRL following injection with vasoactive intestinal peptide (VIP), the avian PRL-releasing hormone. PRL was lowest in non-paired birds, increased after pair bonds had formed, and was highest in incubating birds. No differences in PRL levels were found between males and females in these biparental care-givers. A single injection of VIP resulted in a rapid increase in plasma PRL in nonbreeding zebra finches, while PRL remained unchanged in incubating birds. When escalating doses of VIP were administered, nonbreeders responded with a maximal response in PRL release, but PRL levels in breeders remained unchanged following even the highest VIP dose. Among nonbreeders, inexperienced birds had significantly lower PRL levels than birds that had successfully reared a clutch, but both groups responded with an equally robust increase in PRL following a VIP challenge. This pattern differs from that observed in most photosensitive species in which only during a breeding cycle do birds secrete significant levels of PRL in response to exogenous VIP. Zebra finches, even when not actively breeding, must maintain competent pituitary lactotrophs that can secrete PRL at maximal rates. This is part of the suite of characters enabling these birds to respond to favorable breeding conditions at any time.

Plasma prolactin concentration increases after hypercapnia acidosis.

Responses of plasma prolactin (PRL) concentration to alterations in carbon dioxide pressure ( pCO(2)) induced by 4 min of rebreathing out of a bag with 6 l gas initially containing a concentration of 93% O(2) and 7% CO(2) (hypercapnia hyperoxia; HH) and 4 min of voluntary hyperventilation (VH) at a respiratory rate of 28 - 32 per minute were investigated in ten males. During rebreathing in HH, an augmentation of pCO(2) from 40.2 +/- 2.1 to 63.7 +/- 5.4 mmHg and a decrease of pH from 7.4 +/- 0.02 to 7.32 +/- 0.04 were found in capillary blood (p < 0.01). Neither breathing frequency (BF) nor plasma PRL changed during this period. After two minutes of post-rebreathing, pCO(2) and pH returned to basal values. BF increased from 2 min of rebreathing (12.4 +/- 1.9 breath/min) until 11 min of recovery period (18.1 +/- 4.9 breath/min) (p < 0.01), while plasma PRL increased from end of rebreathing (11.59 +/- 1.49 ng/dl) to 11 min of recovery period (13.63 +/- 1.97 ng/dl) (p < 0.01). In VH, hyperventilation decreased pCO (2) from 39.91 +/- 2.62 to 21.73 +/- 2.59 mmHg (p < 0.01) and increased pH from 7.39 +/- 0.04 to 7.58 +/- 0.04 (p < 0.01) in capillary blood. After four minutes of recovery from hyperventilation, pH and pCO(2) were back to their basal values. No changes in plasma PRL were found throughout VH. This present pilot study's new finding is that plasma PRL increases after hypercapnia acidosis. This indicates that acidosis-induced central chemoreflex function increases phrenic nerve activity based on serotonergic modulation, leading to an augmentation of BF. As serotonin is also the main PRL-releasing factor, this might have had the collateral effect of causing PRL release and delayed appearance in the peripheral circulation.

Decreased Plasma Prolactin Release in Euthymic Lithium-Treated Women with Bipolar Disorder

In order to evaluate the effect of treatment with citalopram (CIT) and lithium (Li) on hormone levels in women with bipolar disorder, morning plasma prolactin (PRL) and cortisol (CORT) were measured in 14 nonmedicated depressed patients, 13 depressed patients responding to CIT treatment, 17 euthymic patients on long-term Li treatment, and 11 healthy controls. Plasma PRL values in the Li group were significantly lower than those of the three other groups, suggesting a net inhibitory impact of augmentative effects of Li on dopaminergic activity and serotonergic neurotransmission in the central nervous system. Plasma CORT values in nonmedicated depressed patients were significantly higher than those of healthy controls, indicating hyperactivity of the hypothalamic-pituitary-adrenal system in depression, which appears to be a state-dependent phenomenon, and is normalized upon successful treatment with Li and CIT.

Neuroendocrine serotonergic and dopaminergic responsivity in male schizophrenic patients during treatment with neuroleptics and after switch to risperidone.

The pharmacological profile of risperidone is that of an atypical neuroleptic regarding its serotonin 5-HT2A and dopamine D2 receptor blocking properties. Treatment with risperidone, though, results in considerably elevated plasma prolactin (PRL) levels which are not observed with other atypical neuroleptics, such as clozapine, indicating a differentiated action on receptors that are involved in PRL release, mainly dopaminergic and serotonergic. To assess the responsivity of serotonergic and dopaminergic receptors during treatment with neuroleptics and after switch to risperidone, using neuroendocrine paradigms. Two neuroendocrine challenge tests, measuring the PRL increases induced by acute administration of serotonergic (clomipramine, 25 mg i.v.) and dopaminergic (haloperidol, 5 mg i.m.) drugs were performed in 13 male schizophrenic patients during treatment with typical neuroleptics and, later, after 6 weeks of treatment with risperidone. The tests were also performed in a group of nine healthy male volunteers. PRL was estimated in blood samples taken every 15 min for 1 h for clomipramine and every 30 min for 2 h for haloperidol. Psychopathology was assessed using the Brief Psychiatric Rating Scale (BPRS). During treatment with neuroleptics (mean dose 1354 mg chlorpromazine equivalents, range 300-2400 mg), i.m. haloperidol caused significant elevations in plasma PRL, which were totally abolished after 6 weeks treatment with risperidone (mean dose 12.1 mg/day, range 8-16 mg/day), indicating complete D2 receptor blockade. In contrast, the PRL increases obtained after clomipramine administration during neuroleptic treatment were preserved after treatment with risperidone. Both PRL response patterns to clomipramine were similar to that of healthy controls. BPRS score was 50.2+/-9.3 points during neuroleptic treatment and was reduced after risperidone to 30.1+/-6.6 points, i.e., 40% in the mean. During treatment with typical neuroleptics, the PRL responses to clomipramine are normal, and they are preserved after switch to risperidone in doses that cause complete dopamine receptor blockade. Risperidone, a dopamine and 5-HT receptor blocker, does not affect 5-HT receptors that are involved in the PRL release by the 5-HT uptake blocker clomipramine, indicating a different behavior than other atypical neuroleptics such as clozapine or olanzapine, for which a reduction of the PRL release induced by serotonergic agents like fenfluramine or mCPP has been reported. A conclusive identification of the 5-HT receptor subtypes that are involved in this different action cannot be identified at present, but it should be taken into account that risperidone differs from clozapine, showing higher affinity for 5-HT2A than 5-HT2C receptors and lacking the marked affinity of clozapine to 5-HT1A receptors.

Effects of Δ 9-THC on VIP-induced prolactin secretion in anterior pituitary cultures: evidence for the presence of functional cannabinoid CB 1 receptors in pituitary cells

Peripheral administration of cannabinoid CB 1 receptor agonists to laboratory rats induce a brief rise in plasma prolactin (PRL) levels followed by a prolonged decrease in PRL secretion from the pituitary. While the inhibitory component of this biphasic response depends on the cannabinoid-induced activation of dopamine release from hypothalamic terminals located in the median eminence, the neurobiological mechanisms underlying the activation phase of PRL release remains to be explained. In the present study the possible direct effect of the cannabinoid receptor agonist Δ 9-Tetrahydrocannabinol (THC) on prolactin secretion and cAMP accumulation was examined in anterior pituitary cultures. THC (0.1 and 1 μM) increased cAMP levels, and induced PRL release (1 and 10 μ). THC did not affect vasoactive intestinal peptide (VIP, 0.5 μM) induced cAMP accumulation in pituitary cultures, showing additive effects at THC 1 μM concentration. However, THC did prevent VIP-dependent increases in prolactin secretion. These results indicate that THC, through a direct pituitary action, activates both the synthesis of cAMP and PRL release and interferes with intracellular mechanisms involved in PRL secretion by VIP. These actions could be mediated through cannabinoid CB 1 receptors which were found to be present in anterior pituitary cells, including lactotrophs, as revealed by immunocytochemistry with a specific polyclonal antibody raised against the CB 1 receptor protein.

Exogenous Oxytocin Attenuates Suckling-Induced Prolactin Release but Not Maternal or Infant Behavior in Lactating Rats

The influence of exogenous oxytocin (OT) on maternal and infant behavior over 60 min of suckling, which followed 6 h of isolation, was investigated on Day 12 of lactation in rats. Mothers administered 1 IU of OT or saline through an indwelling atrial catheter and their litters indicated a similar nursing and suckling pattern, which was estimated by the crouching time of the mothers and the number of stretch reactions performed by the litters during a suckling period. To assess the alteration of the suckling intensity by OT administration, the plasma prolactin (PRL) level was determined by an Nb 2 lymphoma cell bioassay. In the control group, the plasma PRL level increased and reached a peak at 45 min after the onset of suckling in 60% of the animals. The suckling-induced PRL release was completely inhibited and/or markedly delayed by OT administration. The difference in body weight of the litters before and after a suckling period was estimated as an index of the amount of milk suckled by the litters. There was no difference in the amount of milk between the control and OT-treated groups during a 60-min suckling period. However, it was significantly greater in the OT-treated group during the first 20 min of the suckling period. These results indicate that a dose of OT is a factor in the attenuation of the intensity of suckling done by the pups, whereas the nursing and suckling behavior is not influenced by OT administration.

Stressors, Including Social Conflict, Decrease Plasma Prolactin in Male Golden Hamsters

Following exposure to a stressor, plasma prolactin (PRL) rises in most species. The purpose of the present study was to examine the effect of social conflict or of footshock stress on PRL responsiveness in male Syrian hamsters. Contrary to expectations, PRL was significantly lower in subordinate hamsters than in their dominant opponents or in controls following one, five, or nine exposures to social conflict. Similarly, PRL was reduced in hamsters subjected to a mild footshock stressor. By contrast, adrenocorticotropin, another stress-responsive hormone, was elevated following exposure to each of these stressors. We also demonstrate that PRL release is inhibited by dopamine as it is in other species by showing that there is a dose-dependent increase in PRL release following treatment with the dopamine receptor blocker, domperidone.

Prolactin secretion in lactating rats following chronic alcohol exposure: Provocative tests with secretagogues

This study was done to examine the mechanism of action of alcohol in inhibiting suckling-induced prolactin release in the lactating rat. Alcohol (0.0, 1.0 or 2.0 g/kg body weight) was administered daily for 8 days from day 5 to 12 of lactation via an indwelling atrial catheter, implanted on day 3 of lactation. Following the administration of the initial alcohol dose, infusion was continued at rates required to maintain the blood alcohol levels (BALs) for four hours every day. Prolactin responses to sulpiride and TRH were tested on day 12. Alcohol administration for 8 days and maintaining the blood alcohol levels for four hours daily did not affect the basal or sulpiride and TRH-stimulated plasma prolactin release. Since the prolactin releasing capacity of pituitary lactotropes of the lactating rat is not compromised following chronic alcohol exposure, we conclude that alcohol does not act at the anterior pituitary level to inhibit the suckling induced prolactin release but probably acts by other mechanisms: either via the hypothalamic and/or higher central nervous system or by disrupting the neural impulse transmission, engendered at the nipples in response to suckling.

Prolactin secretion during sleep in obstructive sleep apnoea patients.

Plasma prolactin (PRL) concentration exhibits a sleep-dependent pattern, with highest levels during sleep and lowest levels during the waking period. The syndrome of obstructive sleep apnoea (OSA) is associated with severe hypoxaemia and chronic sleep fragmentation, both of which could affect the sleep-entrained PRL rhythm. Treatment with nasal continuous positive airway pressure (CPAP) immediately restores a normal sleep structure by successful abolition of the apnoeas. In the present study, seven OSA patients underwent two night studies, once when no treatment was given and once during the first night of CPAP treatment. Sleep was recorded polygraphically in all experiments. Plasma PRL was measured at 10 min intervals and secretory rates were calculated by a deconvolution procedure. CPAP treatment greatly reduced hypoxaemia and improved sleep quality. The secretory pulse amplitude and the total amount of PRL secreted during the night remained constant regardless of whether patients were treated or not. The only difference found was a lower pulse frequency in untreated OSA patients as compared to treated patients, which may be attributed either to hypoxaemia or to sleep disturbance or to the combined action of both. Treatment may be considered to normalize PRL release by restoring pulse frequency to values similar to those observed for normal subjects.

Evidence that amplification of norepinephrine-induced LH release by morphine is indirectly due to suppression of tuberoinfundibular dopamine secretion

We previously observed that morphine markedly amplifies LH secretion following intracerebroventricular (i.c.v.) norepinehrine (NE) infusions. Based on additional evidence, we hypothesized that perhaps these morphine effects were due to suppression of tuberoinfundibular dopamine (TIDA) secretion thus allowing NE to evoke a greater release of LHRH from axon terminals in the median eminence than would otherwise occur. In the present studies, we examined whether apomorphine (a DA receptor agonist) would suppress and haloperidol (a DA receptor antagonist) would mimic these enhancing effects of morphine on NE-induced LH secretion. Estrogen-treated ovariectomized rats were used in these studies. NE, when infused i.c.v. (45 μg) evoked a modest increase in plasma LH(1.1 ± 0.2to2.2 ± 0.2ng/ml) within 15 min. When morphine sulfate (10 mg/kc s.c.) was given 15 min prior to NE, LH peak values of11 ± 2ng/ml were obtained by 60 min. Treatment of rats with apomorphine (1.5 mg/kg s.c.) at −15 min, morphine at 0 min and i.c.v. NE at 15 min resulted in a significant blunting of morphine's effect on NE-induced LH release. Moreover, in all morphine-treated rats, plasma prolactin (PRL) increased significantly within 10 min, peaked at 30 min and declined towards basal values by 90 min. Apomorphine completely blocked this morphine effect of PRL release. Haloperidol (HAL; 2.5 mg/kg s.c.) treatment had no effect on basal LH release but resulted in a significant increase in PRL which remained elevated up to 180 min. When HAL was given at 0 min and NE was infused i.c.v. at 15 min, a rapid, progressive and highly significant temporal increase in LH secretion occurred with peak values of20.4 ± 4ng/ml being reached by 90 min. Since our other recent studies have shown that i.c.v. DA infusions neither amplify nor suppress NE-induced LH release nor do they affect basal LH levels when given alone, we could not attribute morphine's action on NE release to alterations in A15 or A14 DA neuronal activity nor to increases in hypothalamic incertohypothalamic (A13) DA secretion. Rather, the suppression of TIDA (A12) neuronal activity or blockade of DA receptors by morphine or HAL, respectively, suggest that amplification of NE-induced LH release may be due to the suppression of inhibitory DA influences on the release of LHRH from axon terminals within the median eminence. The implications of these opiate actions on preovulatory LH surges are discussed.

Sexually dimorphic effects of aging on tuberoinfundibular dopaminergic neurons and lactotropes of rats

The effect of aging on plasma prolactin (PRL) levels, hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons and pituitary lactotropes was evaluated in prolactinoma-free young (5-month-old) and old (23- to 24-month-old) Long-Evans rats of either sex. The young female rats were in diestrus, the old ones in recurrent pseudo-pregnancy. The tyrosine hydroxylase (TH)-labelled neurons in the arcuate nucleus (AN) and axons in the median eminence (ME) as well as the PRL-labelled lactotropes in the pituitary gland were studied by morphometry and densitometric immunohistochemistry. Further, we investigated the secretory function of isolated lactotropes by reverse hemolytic plaque assay (RHPA) and by cell culture in comparable animal groups. Compared with young animals, the plasma PRL levels of old rats of both sexes were similar or reduced. All morphometric and densitometric measurements of the AN neurons, ME axons (except number) and pituitary lactotropes were comparable in young and old female rats. In old male rats the AN and ME measurements were mostly decreased, while the lactotropes remained almost unchanged. The RHPA generally showed a reduced PRL release from lactotropes of old animals of both sexes. The PRL release from the cultured lactotropes, on the contrary, was greatly increased in old female rats and unchanged in old male rats. Our functional and morphological data suggest that the in vivo function of lactotropes in old prolactinoma-free female and male rats does not seem to be strongly influenced by the mildly reduced TIDA neuron activity, yet emphasize the differences of the aging process in the two sexes

Thymostimulin effects on lymphoid organs in Ames dwarf mice

This work was undertaken to study the effects of thymostimulin (TP-1) on the immune function in Ames dwarf mice, and to relate these effects to PRL and/or GH deficiency in these animals. Male Ames dwarf mice implanted with pituitaries from normal mice under the kidney capsule, sham-operated dwarf mice and normal immature or adult mice were injected daily for five days with TP-1. In comparison to normal animals, sham-operated dwarf mice had markedly lower body, thymus and spleen weights, as well as a lower number of lymphocytes in the spleen and in the thymus and the natural killer (NK) activity of spleen lymphocytes. Ectopic pituitary transplants produced the expected enhancement of body weight gain and increased spleen and thymus weights, which reached the values found in normal (non-dwarf) animals. The numbers of lymphocytes in the spleen and thymus were significantly increased in pituitary-grafted dwarf mice, but the grafts did not modify the cytotoxic activity of NK spleen cells, or the number of peripheral white blood cells (PWBC). In sham-operated dwarf mice, TP-1 treatment did not modify the number of cells in the spleen and thymus, or the NK activity. In pituitary-grafted dwarf mice, treatment with TP-1 induced an increase in the number of spleen lymphocytes and in the NK activity of spleen cells without affecting the weight of lymphoid organs or the number of thymic cells. Plasma prolactin (PRL) and growth hormone (GH) levels of pituitary-grafted dwarf mice were not changed after TP-1 administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effects of δ-9-tetrahydrocannabinol on dopaminergic activity in several rat brain areas

In this work, we examined the acute effects of two doses of δ-9-tetrahydrocannabinol (THC) on several pre- and postsynaptic biochemical measures of dopaminergic activity in the striatum, limbic forebrain, and hypothalamic-anterior pituitary area of adult male rats. The exposure to a low dose of THC (0.5 mg/kg bw) decreased the number of striatal D 2 dopaminergic binding sites, but did not affect their affinity. Treatment with a higher dose of THC was ineffective. In addition, both doses decreased the number of D 1 dopaminergic binding sites in the limbic forebrain without changing their affinity. We did not find any changes in the dopamine (DA) or L-3,4-dihydroxyphenylacetic acid (DOPAC) content, or in the DOPAC/DA ratio, in either the striatum or limbic forebrain. THC treatment produced a dose-related decline in plasma prolactin (PRL) levels. Furthermore, both the basal and DA-inhibited in vitro release were PRL were reduced in animals exposed to THC in a dose-dependent manner. This inhibitory effect of THC on PRL release was accompanied by a decreased DOPAC/DA ratio in the medial basal hypothalamus that, in turn, may be a result of the fall in PRL levels rather than a direct action of the drug. These data show that acute exposure to THC can alter brain dopaminergic neurotransmission. Our results suggest that the reduction of PRL release following THC exposure, both in vivo and in vitro, might be elicited by a direct action of THC on the pituitary.

ECT-induced PRL release: A 5-HT 1A-mediated event?

Plasma prolactin (PRL) levels rise sharply in response to spontaneous or electrically induced seizures and although the relationship between this neuroendocrine response and the clinical effects of electmconvulsive therapy (ECT) has yet to be demonstrated, the possibility that studying this phenomenon may shed some light on the mechanism of action of ECI remains (Fink 1979, Abrams 1988). The ECTinduced PRL release is markedly reduced followir/; pretreatment with the ergot derivative m.'thysergide, a serotonin (5-HT) receptor an, ~gonist (Papakostas et al 1988, Zis et al 1989a). i lowever, the hypothesized role of 5-HT in this neuroendocrine response remains uncertain for several reasons. First, the use of ergot derivatives as 5-HT receptor antagonists to study the regulation of PRL release has been criticized on the grounds that PRL secretion is tonically inhibited by dopamine, and these compounds pessess dopamine receptor agonist properties (Lambert~ and MacLeod 1979). Second, i¢ has been shown that pretreatment with the 5-HT2 antagortist ketanseri'n and ritanserin fails to attenuate the ECT-induced PRL surge (Zis et al 1989b, Papakostas et al 1990). And third, it was re-

Plasma prolactin levels during smolting in Atlantic salmon, Salmo salar

To obtain more information on a possible involvement of prolactin during parr-smolt transformation of Atlantic salmon, Salmo salar, parr and smolt populations of the same age were sampled from February to June. A clear separation of the two populations was observed according to their size and gill (Na +K +)-ATPase activity. Comparison of plasma prolactin (PRL) levels between these two populations indicated a significant decrease from May to early July in smolts whereas, in parr, a steady increase was observed. Diel variations in plasma PRL levels at three different dates were also studied in fish undergoing smolting. Sampling fish over a 24-h period on 11 March, 5 May and 15 July did not indicate the presence of a diel rhythm in PRL release. These data support the hypothesis that the PRL decrease is associated with smolting in Atlantic salmon and that such a decrease cannot be explained by a change in diel rhythm of plasma PRL levels.

The 24-hour profile of plasma prolactin in men with major endogenous depressive illness.

Plasma prolactin (PRL) levels were measured at 15-minute intervals for 24 hours in 18 men suffering from major endogenous depressive illness and in 7 age-matched healthy men. Eleven of the 18 depressed patients were restudied during clinical remission following either electroconvulsive therapy or treatment with amitriptyline hydrochloride. During the acute phase of the illness, the unipolar depressed patients had fragmented patterns of PRL secretion with an early timing of the nocturnal secretory phase of PRL, which started, on the average, 2 hours earlier than in healthy subjects. Moreover, the amplitude of the circadian variation of PRL was reduced in these patients, with subnormal PRL levels occurring during the midsleep period. This latter abnormality was also observed in bipolar patients, who had otherwise normal PRL profiles. These lower midsleep PRL concentrations were associated with a significant increase in the amount of time spent awake during the same period. Antidepressant treatment did not consistently correct the abnormalities in the patterns of PRL release observed during the acute phase of the illness. These results indicate that early timing of nocturnal PRL secretion and damping of the nighttime PRL elevation may be found in men with endogenous depressive disorders. In contrast to disturbances of the corticotropic and somatotropic axes, these abnormalities of PRL secretion may still be present during clinical remission following antidepressant treatment.

Central actions of adenosine on pituitary secretion of prolactin, luteinizing hormone and thyrotropin.

Pituitary hormones were measured in plasma in unanesthetized male and female rats prepared with venous and ventricular cannulae following ventricular infusions of adenosine and two adenosine receptor agonists. Adenosine (10, 100, and 200 nmol) injected intraventricularly caused dose-related rises in plasma prolactin (PRL) in males; in females, only the 100- and 200-nmol doses increased PRL. Similar doses of adenosine had little effect on plasma levels of luteinizing hormone (LH) and thyrotropin (TSH) in the same animals. The adenosine receptor agonists L-N6-phenylisopropyladenosine (L-PIA) and 5'-N-ethyl-carboxamideadenosine (NECA) potently stimulated prolactin secretion at doses of 10 and 50 nmol when administered into the lateral ventricle, and at a dose of 2.5 nmol when administered into the third ventricle. The secretion of PRL was antagonized by the adenosine receptor antagonist theophylline (25 nmol), when theophylline was coadministered with NECA and L-PIA. TSH levels were reduced slightly but significantly following the 10- and 50-nmol infusions of L-PIA into the lateral ventricle. The less potent D-isomer of PIA (D-PIA) did not significantly stimulate PRL release. Coupled with studies indicating the presence of adenosine in the basal hypothalamus, our observations indicate a potential neuroendocrine role for this purine in prolactin secretion.