Biomedical subjects

J T Pan

Publications and source records attributed to J T Pan.

At least 19 recordsLinked to original sources

PubMed1992

Low calcium/high magnesium medium increases activities of hypothalamic arcuate and suprachiasmatic neurons in brain tissue slices.

Extracellular single-unit recording was conducted in hypothalamic arcuate (ARC) and suprachiasmatic nucleus (SCN) in rat brain slices. The perifusion medium was switched from normal artificial cerebrospinal fluid (ACSF) to ACSF containing low Ca2+ and high Mg2+ to test the effect of extracellular calcium on the spontaneous activities of these neurons and their responses to some test agents. It was found that almost all of the ARC and SCN units tested increased their firing rates in low Ca2+, high Mg2+ ACSF, and exhibited more significant responses to excitatory test agents. The effects of low Ca2+, high Mg2+ ACSF were repeatable and reversible. The results suggest that extracellular Ca2+ is essential in maintaining the membrane stability of most hypothalamic neurons and most agents tested are acting postsynaptically on the unit recorded.

Action Potentials↗

PubMed1992

Neurotensin-induced activation of hypothalamic dopaminergic neurons is accompanied by a decrease in pituitary secretion of prolactin and alpha-melanocyte-stimulating hormone.

The effects of neurotensin on the activity of hypothalamic tuberoinfundibular and periventricular-hypophysial dopaminergic (DA) neurons, and on the secretion of pituitary hormones that are tonically regulated by these neurons (i.e. prolactin and alpha-melanocyte-stimulating hormone [alpha MSH], respectively) were examined in estrogen-primed ovariectomized rats. The activity of tuberoinfundibular and periventricular-hypophysial DA neurons was estimated by measuring concentrations of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the terminals of these neurons in the median eminence and intermediate lobe of the posterior pituitary, respectively. Intracerebroventricular administration of neurotensin caused a dose- and time-related increase in DOPAC concentrations in both the median eminence and intermediate lobe, and a concurrent decrease in plasma levels of prolactin and alpha MSH. These results suggest that neurotensin-induced inhibition of secretion of prolactin and alpha MSH from the pituitary may be due to the stimulatory action of this neuropeptide on the release of dopamine from tuberoinfundibular and periventricular-hypophysial neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Effects of ketanserin on DOI-, MCPP- and TRH-induced prolactin secretion in estrogen-treated rats.

The effects of ketanserin (Ket), a serotonin (5-HT2) receptor antagonist, on DOI- and mCPP-, two 5-HT agonists, and TRH-induced PRL secretion were studied. Adult female Sprague-Dawley rats ovariectomized for two weeks and treated with a long-acting estrogen, polyestradiol phosphate for one week were used. Drug administration and serial blood sampling were accomplished through indwelling intraatrial catheters which were implanted two days before the experiment. Both DOI (0.5 mg/kg BW) and mCPP (1 mg/kg BW) stimulated prolactin secretion within 10 min after iv injection and the effects were diminished by 30 min. In animals pretreated with Ket (5 mg/kg BW, sc), the effect of DOI was blocked, while that of mCPP was augmented. Co-administration of Ket (1 mg/kg BW, iv) with DOI or mCPP produced similar effect. Pretreatment with Ket, similar to sulpiride (Sulp), a dopamine antagonist, potentiated the TRH-induced prolactin secretion. Co-administration of Ket and Sulp further potentiated the TRH action. It is concluded that Ket not only acts as a 5-HT2 receptor antagonist that blocks the action of DOI, but may also act on dopamine receptor(s) with lower sensitivity to Sulp.

Amphetamines↗

PubMed1991

The study of serum apoprotein levels as indicators for the severity of angiographically assessed coronary artery disease.

Serum apoprotein A-I (Apo A-I) and B (Apo-B) concentrations were determined in 40 subjects undergoing coronary angiography for past myocardial infarction and angina pectoris, and the authors studied the relationship between the apoprotein concentrations and the severity of coronary artery disease (CAD). During this study, serum total cholesterol, triglyceride, and high-density lipoprotein, low-density lipoprotein, and very low density lipoprotein cholesterol concentrations were determined to control analysis. The results showed that the decrease in serum Apo A-I levels was the best indicator distinguishing CAD from non-coronary artery disease; the Apo B/Apo A-I ratio had the most consistent association with the severity of CAD as assessed by angiography; Apo B/Apo A-I values ranging from 0.98 to 1.00 might be considered critical values for early CAD.

Adult↗

PubMed1991

Neuroendocrine control of prolactin secretion: the role of the serotonergic system.

The secretion of prolactin (PRL) falls into distinct patterns in mammals. Suckling, stress, cervical stimulation and estrogen all stimulate PRL secretion. The estrogen-induced afternoon PRL surge is circadian in nature and is regulated by the central serotonergic system. Interruption of the serotonergic system by all means blocks the PRL surge. As for the site and mechanism of 5-HT action, it has been shown that 5-HT has no direct effect on the anterior pituitary and its action on PRL secretion may be dissociated from its peripheral cardiovascular effect. Its action may not involve the central dopaminergic system or interaction with the central opioid system. However, it may be stimulating a yet unidentified PRL-releasing factor during specific time in the afternoon of estrogen-treated rats.

Animals↗

PubMed1990

Paradoxical effects of oxytocin and vasopressin on basal prolactin secretion and the estrogen-induced prolactin surge.

The roles of oxytocin (OT) and vasopressin (AVP) on both basal and estrogen-induced prolactin (PRL) secretion were examined. Adult female Sprague-Dawley rats that were ovariectomized for 3 weeks and received estrogen treatment for 1 week were used. Intravenous administration of hormones and serial blood sampling were accomplished through indwelling intraatrial catheters which were implanted two days before. Plasma PRL levels were measured by radioimmunoassay. Oxytocin at a dose of 20 micrograms/rat stimulated a moderate PRL release in the morning and lower doses (5 and 10 micrograms) were without effect. Vasopressin was most effective at a dose of 5 micrograms/rat in stimulating PRL release, while consecutive injections of higher doses (10 and 20 micrograms) were less effective. In contrast, TRH, ranging from 1 to 8 micrograms/rat, induced a dose-dependent increases in PRL secretion. Using the effective dosages determined from the morning studies, repeated injections of either OT, AVP or their specific antagonists MPOMeOVT [( 1-(beta-mercapto-beta, beta-cyclopentamethylene propanoic acid), 2-(O-methyl)tyrosine, 8-ornithine]-vasotocin) and d (CH2)5Tyr(Me)AVP ([1-(beta-mercapto-beta, beta-cyclo-pentamethylene propionic acid), 2-(O-methyl)tyrosine, 8-arginine]-vasopressin), were given hourly between 1300 to 1800 h and blood samples were obtained hourly from 1100 to 1900 h. It was found that either OT or AVP significantly reduced the afternoon PRL surge, while their antagonists were not as effective. When OT or AVP were administered together with their specific antagonists, the inhibitory effects of either hormone on PRL surge were reversed. Thus it is concluded that both OT and AVP assume a non-specific stress-like effect on PRL release, in which basal secretion is stimulated and surge secretion is inhibited.

Animals↗

PubMed1990

Dopamine antagonism does not potentiate the effects of oxytocin and vasopressin on prolactin secretion.

The roles of oxytocin and vasopressin on prolactin secretion were studied. Adult female Sprague-Dawley rats ovariectomized for two weeks and treated with a long-acting estrogen, polyestradiol phosphate for one week were used. Hormone administration and serial blood sampling were accomplished through indwelling intra-atrial catheters which were implanted two days before the experiment. Both oxytocin (20 micrograms/rat) and vasopressin (5 micrograms/rat) stimulated prolactin secretion within 10 min after injection and the effects were diminished by 30 min. In animals pretreated with a small dose of dopamine antagonist, sulpiride (1 microgram/rat), the effect of TRH on prolactin secretion was repeatedly shown to be potentiated. Same pretreatments with two different time intervals (30 and 60 min) between sulpiride and oxytocin/vasopressin administration, however, had no effect on oxytocin- or vasopressin-stimulated prolactin secretion. A vasopressin analog, 1-deamino-[D-Arg8]-vasopressin (dDAVP), with antidiuretic but no vasopressor activity was also used in the study. It was found that unlike vasopressin, dDAVP had no effect on prolactin secretion. In conclusion, both oxytocin and vasopressin can have a stimulatory effect on prolactin secretion when given in vivo. Unlike TRH, however, the action of oxytocin or vasopressin was not augmented by pretreatments of dopamine antagonist. The action of vasopressin on prolactin secretion may be a side effect of its vasopressor activity.

Animals↗

PubMed1990

Increased plasma prolactin levels in ovariectomized thyroidectomized rats treated with estrogen.

It is well established that TRH exerts a stimulatory effect on the secretion of both TSH and PRL. Clinically, hyperprolactinemia is usually present in hypothyroid women, but not men. In experimental studies, results vary because of the sexes, and treatments of animals differ. The purpose of this study was to further investigate the physiological control of PRL secretion in hypothyroid female rats. Adult female Sprague-Dawley rats that were surgically ovariectomized (OVX) and/or thyroidectomized (Tx) for 2 weeks were used. Serial blood samples were collected through indwelling intraatrial catheters, and plasma PRL and TSH levels were measured by RIA. We found that OVX + Tx and polyestradiol phosphate (PEP; 0.1 mg/rat, sc)-treated rats exhibited significantly higher basal PRL and TSH levels and afternoon surge PRL levels than sham Tx rats with the same treatments. On the other hand, if OVX + Tx rats were not treated with estrogen, their plasma PRL levels were not significantly different from those in sham Tx controls. If challenged with TRH (1 microgram/rat, iv), significantly higher PRL responses were found in OVX + Tx + PEP rats than in sham Tx rats. The contents of TRH in the median eminence of Tx rats, however, were not different from those in sham Tx rats. When challenged with domperidone (10 micrograms/rat, iv), a dopamine antagonist, no difference in PRL increments was found in the two groups of animals. Treatment with CB154, a potent dopamine agonist, did not eliminate the difference in basal PRL levels between the two groups. Pretreatment with a smaller dose of domperidone (1 microgram/rat), however, enhanced the PRL-releasing effect of TRH more in Tx than in sham Tx rats. When T4 (2 or 10 micrograms/100 g BW.day for 21 days) was replaced in Tx rats starting the second day after Tx, both basal and TRH-stimulated PRL secretion were significantly decreased in a dose-dependent manner. In conclusion, the increased PRL levels in OVX + Tx + PEP rats may be due to increased responsiveness of the anterior pituitary gland to TRH, and not to a decreased responsiveness to dopamine. In addition, the elevation of plasma PRL in OVX + Tx + PEP rats is negatively correlated with plasma levels of thyroid hormone.

Animals↗

PubMed1990

Serotonin-stimulated prolactin secretion may not involve the dopaminergic system.

The possible involvement of the dopaminergic system in the serotonin (5-HT)-stimulated prolactin (PRL) secretion was tested in this study. Adult female rats were ovariectomized for two weeks and treated with estrogen (polyestradiol phosphate, 0.1 mg/rat, sc) for 6 days before use. They either received pretreatment with alpha-methyl-p-tyrosine (250 mg/kg BW, ip), a dopamine (DA) synthesis inhibitor, or two DA antagonists, domperidone and haloperidol (0.1 mg/kg BW, iv) before receiving 5-HT (1 mg/kg BW, iv) or quipazine (1 mg/kg BW, iv), a 5-HT agonist. Blockade of DA synthesis or antagonism of DA action invariably induced elevated plasma PRL levels. 5-HT or quipazine, however, could still induce significant PRL secretion on top of the increased PRL levels. Minor difference was found between the action of domperidone and that of haloperidol. In conclusion, the dopaminergic system may not be involved in the action of 5-HT to stimulate PRL secretion.

Animals↗

PubMed1990

Extracellular single-unit studies of suprachiasmatic neurons in brain slices. Effects of serotonin, dopamine, carbachol and LHRH.

Suprachiasmatic nucleus (SCN) is the major rhythm generating center in the central nervous system. Extracellular single-unit activities of the SCN neurons were recorded in brain tissue slices either from ovariectomized (OVX) rats or from OVX rats treated with estrogen (polyestradiol phosphate, PEP, 0.1 mg/rat, sc). Neuronal responses to luteinizing hormone-releasing hormone (LHRH) and various neurotransmitters, i.e., serotonin (5-HT), dopamine (DA) and carbachol (Carb, an acetylcholine agonist) were tested. A total of 137 units were recorded from OVX and 81 from OVX + PEP rats. The steady state firing rates of SCN neurons were between 0-9 spikes/sec in OVX and 0-23 in OVX + PEP group. Among them, most fired irregularly (86.9% in OVX and 71.6% in OVX + PEP rats), and a few fired regularly (10.2% and 25.9%, respectively). Few silent units were detected (2.9% and 2.5%, respectively). It seems that estrogen treatment somewhat increased the percentage of regular firing units. As for the agents tested in this study, LHRH by itself had no significant effect on the SCN neuronal activity; 5-HT affected more than 40% of the units, with about equal number of excitation (16.8%) and inhibition (24.4%), while Carb inhibited nearly half of the units tested (49.5%), excited only a few (10.3%). All the actions of these three agents were not significantly affected by in vivo estrogen pretreatment. Dopamine, however, excited more units (50%) in OVX than in OVX + PEP group (27.1%). Although LHRH had no direct effect by itself, it exerted a significant modulatory role on the actions of the other three agents. It either potentiated (42.9%) or inhibited (53.6%) the action of 5-HT, and it significantly potentiated the action of Carb (57.1%). For the action of DA, LHRH had a more significant potentiation effect on OVX + PEP than in OVX rats. (40.9% vs. 12.5%), while the inhibitory effect was the same. In conclusion, 5-HT, DA and Carb all exert significant effects on SCN neuronal activities. LHRH can have a modulatory role upon the action of 5-HT, DA and Carb, and estrogen pretreatment specifically affects that of DA in the SCN.

Animals↗

PubMed1989

Differential effects of prazosin and yohimbine on fentanyl-induced muscular rigidity in rats.

Whereas muscular rigidity is a well-known phenomenon that is related to anesthesia induced by large doses of narcotic drugs, the precise underlying mechanism(s) remain to be fully elucidated. This study investigated the possible role of noradrenergic neurotransmission and the participation of alpha-adrenoceptors in this phenomenon. Male Sprague-Dawley rats, under ketamine-induced anesthesia (120 mg/kg, i.p.) and with proper control of respiration, body temperature and end-tidal CO2 were used. Intravenous administration of fentanyl (100 micrograms/kg) consistently caused a significant increase in the electromyographic (EMG) activity, recorded from both gastrocnemius and abdominal rectus muscles. This implied muscular rigidity was markedly antagonized by pretreatment with the specific alpha 1-adrenoceptor blocker, prazosin (50 or 250 micrograms/kg, i.v.). This antagonism occurred in spite of a high level of fentanyl in the plasma, as determined by radioimmunoassay. The specific alpha 2-adrenoceptor blocker, yohimbine (1.15 or 2.3 mg/kg, i.v.), on the other hand, not only failed to prevent fentanyl-induced activation of the EMG, but actually potentiated the response. It is concluded that noradrenergic neurotransmission, possibly originating from the locus coeruleus, may participate in the elicitation of muscular rigidity by fentanyl. Furthermore, this process may involve an excitatory action through alpha 1-, and an inhibitory action through alpha 2-adrenoceptors, in the spinal cord.

Animals↗

PubMed1989

Effect of transient dopamine antagonism on thyrotropin-releasing hormone-induced prolactin secretion in the serotonin-blocked, estrogen-treated ovariectomized rats.

Recent studies showed that a brief interruption of dopamine (DA) action markedly increased the thyrotropin-releasing hormone (TRH)-stimulated prolactin (PRL) release. It is thus of interest to delineate whether the estrogen-induced afternoon PRL surge involves the same mechanism. Long-term ovariectomized rats pretreated with polyestradiol phosphate (PEP, 0.1 mg/rat s.c.) for 6 days were used in this study. They also received either p-chlorophenylalanine (PCPA, 250 mg/kg i.p.) or ketanserin (Ket, 10 mg/kg i.p.), two serotonergic drugs known to inhibit the estrogen-induced afternoon PRL surge. Then the animals were either treated with a DA antagonist, domperidone (Domp, 0.01 mg/rat i.v.), or vehicle at 16.00 h on the sampling day. Ten minutes later, the ones receiving Domp were injected with a DA agonist, 2-bromo-alpha-ergocryptine (CB154, 0.5 mg/rat i.v.), followed 50 min later by the administration of TRH (1 microgram/rat i.v.). Plasma samples taken through indwelling intraatrial catheters were assayed for PRL by radioimmunoassay. The estrogen-induced afternoon PRL surges were completely blocked in both PCPA- and Ket-treated animals. A significant PRL surge with similar amplitude, however, was induced by either Domp or TRH, although pretreatment with Domp did not cause any potentiating effect on the action of TRH. On the other hand, Domp induced only a small rise of PRL secretion and TRH was totally ineffective in rats untreated with PEP. It is concluded that both DA antagonism and TRH stimulation can induce significant PRL release in the afternoon of estrogen-treated, serotonin-blocked rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Age-related differences in the spontaneous and thyrotropin-releasing hormone-stimulated release of prolactin and thyrotropin in ovariectomized rats.

Effect of estradiol on the spontaneous and thyrotropin-releasing hormone (TRH)-stimulated release of prolactin (PRL) and thyrotropin (TSH) in young and aged ovariectomized (Ovx) rats was investigated. Old (22-26 months) and young (3 months) female rats were Ovx 3 weeks before use. They were injected subcutaneously with estradiol benzoate (EB, 25 micrograms/kg) or sesame oil for 3 days and were catheterized via the right jugular vein. Twenty hours after the last administration of EB, rats were injected with TRH (10 micrograms/kg) through the catheter. Blood samples were collected before and 5, 10, 20, 40 and 60 min after TRH injection. On the day following blood sampling, all rats were decapitated. The anterior pituitary glands (APs) were excised, and incubated with or without TRH (10 ng/ml) at 37 degrees C for 30 min. The basal level of PRL concentration in plasma samples was 5-fold higher in old Ovx rats than in young Ovx rats. Five min after TRH injection, the increase in plasma PRL was greater in old animals than in young animals. Plasma PRL remained higher in old animals than in young animals at 10, 20, 40 and 60 min following TRH challenge. Administration of EB to old and to young Ovx rats produced increases in both basal and TRH-stimulated secretions of PRL, but did not affect the difference in plasma PRL patterns between old and young animals. The release of PRL from APs was increased significantly in all rats after a 30-min incubation with TRH. In Ovx rats injected with oil, the basal release of PRL in vitro was increased with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMed1989

Small dose of domperidone potentiated the effects of TRH and serotonin on prolactin release in ovariectomized, estrogen-treated rats.

A transient antagonism of the dopaminergic action by using a dopamine antagonist, domperidone, plus a dopamine agonist, CB154, has been shown to potentiate the effect of thyrotropin-releasing hormone (TRH) on prolactin (PRL) secretion. In order to test whether the serotonin (5-HT)-induced PRL secretion can also be enhanced in a similar way, we used 5-HT instead of TRH in our first experiment. We found that the dose of domperidone used (10 micrograms/rat) seems to be excessive since it induced a marked and substantial increase in PRL release and the use of CB154 further masked the action of 5-HT. We used a smaller dose of domperidone (1 microgram/rat) without the CB154 and found that it induced a moderate amount of PRL release which lasted for over 1 h. Given TRH (1 microgram/rat) or 5-HT (0.3 mg/rat) 1 h later resulted in a significant increase in plasma PRL which was much higher than that induced by TRH or 5-HT alone. The potentiating effect of domperidone was even more significant for the 5-HT- than the TRH-stimulated PRL secretion. Pretreatment with 5-HT or vasoactive intestinal polypeptide (10 micrograms/rat) were without any effect in potentiating the action of TRH. In conclusion, antagonizing the dopamine action appears to enhance the stimulatory effect of TRH and 5-HT on PRL secretion.

Animals↗

PubMed1989

Fentanyl stimulates prolactin release through mu-opiate receptors, but not the serotonergic system.

Both serotonin (5-HT) and opiates exert a stimulatory effect on PRL secretion. Some evidence suggests that the action of opiates may be elicited through serotonergic neurons. We tested this hypothesis in the present study by evaluating the effect of perturbation of the serotonergic system on PRL secretion induced by fentanyl, a potent morphine-like analgesic. Female Sprague-Dawley rats ovariectomized for 3 weeks and given polyestradiol phosphate (0.1 mg/rat) for 1 week were used in the study. Fentanyl, at a dose of 20 micrograms/rat, induced significant PRL secretion that peaked at 10 min and lasted for more than 30 min. Pretreatment with naloxone (0.5 mg/kg BW, ip) did not block the acute phase of PRL secretion, but significantly lowered the PRL level at 30 min. Fentanyl at a smaller dose (5 micrograms/rat, iv) still induced significant PRL release 10, but not 30, min after injection. This effect was significantly blocked by pretreatment with the same dose of naloxone. On the other hand, whereas animals pretreated with ketanserin or LY53857 (both at a dose of 5 mg/kg BW, ip), two specific 5-HT2 receptor antagonists, had no effect on fentanyl-induced PRL secretion, the same treatment significantly blocked 5-HT-induced PRL secretion. Likewise, pretreatment with p-chlorophenylalanine (250 mg/kg BW, ip), a 5-HT synthesis inhibitor, for 2 days had no effect on the action of fentanyl, while 5-HT-induced PRL secretion was significantly augmented. We conclude that fentanyl acts through mu-opiate receptors to stimulate PRL secretion in a process that does not involve the serotonergic system.

Animals↗

PubMed1988

The serotonin 5-HT2 receptor system, but not the alpha 1-adrenergic receptor system, is involved in the estrogen-induced afternoon prolactin surge in the rat.

Ketanserin (Ket), a new serotonergic (5-HT2) antagonist, has recently been shown to block the estrogen-induced afternoon PRL surge (Endocrinology 120: 2070-2077, 1987). It is not certain, however, whether the effect of Ket was due to its serotonergic or adrenergic receptor antagonistic property. Another 5-HT2 receptor antagonist, LY53857, which possesses no alpha 1-adrenergic receptor affinity, as well as an alpha 1-adrenergic receptor antagonist, prazosin, were used in this study to further clarify the mechanism of 5-HT in the control of PRL secretion. Adult female Sprague-Dawley rats ovariectomized for 2-3 weeks and given a single injection of polyestradiol phosphate were studied 6 days later. Ket, LY53857 and prazosin were examined singly or in combination and animals were injected twice on the sampling day at 1200 and 1300h, respectively. The dosages were as follows: Ket and LY53857, 3 mg/kg BW, ip and 2 mg/kg BW, sc; prazosin, 1 mg/kg BW, ip and 0.7 mg/kg BW, sc. Blood samples were drawn from indwelling intraatrial catheters throughout the afternoon PRL surge.

Animals↗

PubMed1988

Modulatory actions of luteinizing hormone-releasing hormone on electrical activity of preoptic neurons in brain slices.

Single unit activity was recorded from 378 neurons, in two preoptic nuclei rich in luteinizing hormone-releasing hormone neurons, using in vitro brain tissue slices which were prepared form either ovariectomized or ovariectomized plus estradiol-treated rats. To test possible transmitter-like actions, agents were injected into the perfusion medium. Luteinizing hormone-releasing hormone excited 46%, inhibited 7%, and evoked biphasic responses in 2% of the 250 units tested. By comparison, two other peptides, thyrotropin-releasing hormone and cholecystokinin-octapeptide sulfated were exclusively excitatory, acting on 55 and 67% of the neurons, respectively. The response to thyrotropin-releasing hormone, cholecystokinin-octapeptide sulfated, and neurotransmitters were prompt, large, and consistent from trial to trial. In contrast, responses to luteinizing hormone-releasing hormone were usually delayed, small, and variable. Responses to the agents tested were not affected by in vivo estradiol treatment. Possible modulatory actions of luteinizing hormone-releasing hormone were tested by comparing the responses of single neurons to norepinephrine and serotonin before and after an application of luteinizing hormone-releasing hormone. In 39 and 20% of the 119 neurons tested, the norepinephrine responses were potentiated and attenuated, respectively, by luteinizing hormone-releasing hormone. In 46 serotonin-responsive neurons, 28% were potentiated and 22% attenuated. These neuromodulatory actions of luteinizing hormone-releasing hormone were specific in affecting only certain responses of certain neurons, and they were not duplicated on the same neurons by thyrotropin-releasing hormone. It appears that luteinizing hormone-releasing hormone may be a neuromodulator in the preoptic area.

Action Potentials↗

PubMed1988

The pharmacologic induction of prolactin release in the medial preoptic/suprachiasmatic nuclei-lesioned, estrogen-treated ovariectomized rat.

It has been shown that lesions of the medial preoptic/suprachiasmatic nuclei (MPO/SCN) abolish the estrogen-induced afternoon prolactin (PRL) surge. Recent studies using both dopamine antagonist and thyrotropin-releasing hormone (TRH) successfully induced an increase in plasma PRL in various animal models. The same drug approach was used in this study in the MPO/SCN lesioned rat to determine whether these areas participated in the induced PRL release. It is concluded that a significant PRL release can be induced by DA antagonism, or TRH stimulation preceded by DA antagonism in the MPO/SCN lesioned, estrogen-treated ovariectomized rat.

Animals↗