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PubMed1992

Facilitation of sexual behavior shortly after electrolytic lesion of the medial preoptic area: what does it mean?

To analyze the behavioral effects of an unphysiological manipulation of the medial preoptic area (MPOA), sexually experienced male rats received small bilateral electrolytic lesions within this area. Thirty-five percent of the lesioned animals showed a drastic facilitation of sexual behavior when tested 3 h after lesion. The number of intromissions, ejaculation latency, and postejaculatory interval were drastically reduced. The mean number of ejaculations was significantly higher in lesioned animals that displayed the behavior in comparison both to an intact group and a sham-lesioned group. Neither the size of the lesion nor its exact location could be correlated with the facilitation of sexual behavior. However, animals that showed facilitation tended to have the lesion located in the ventral part of the MPOA. Lesions rostral or dorsal to the MPOA were ineffective. It is suggested that the small electrolytic lesions in the MPOA produced iron deposits that stimulated the remaining intact preoptic region, resulting in the drastic facilitation of sexual behavior. The results of the present study support the hypothesis suggesting that the MPOA is involved in the mechanisms related to the initiation and execution of sexual behavior.

Animals↗
PubMed1994

Pentobarbital sodium inhibits the release of noradrenaline in the medial preoptic area in the rat.

The effect of pentobarbital sodium (PB) on noradrenaline (NA) release in the medial preoptic area was studied in ovariectomized rats by a microdialysis method coupled to HPLC. Dialyzates were collected at 6-min intervals before and after the injection in freely moving rats. PB injected i.p. at a dose of 35 mg/kg caused a marked, approximately 40-50% decrease in NA release, which became evident 50 min after the injection and lasted for another 60 min during which the observation was performed. The results suggest that the anesthetic effect of barbiturates is related to the reduction in NA release in the brain.

Animals↗
PubMed1982

Effects of ibotenic acid-induced neuronal degeneration in the medial preoptic area and the lateral hypothalamic area on sexual behavior in the male rat.

It is well known that electrolytic lesions in the medial preoptic area (MPOA) and the lateral hypothalamic area (LHA) seriously impair masculine sexual behavior in the rat. We here report that bilateral infusions of the neurotoxin, ibotenic acid (IBO), in the MPOA were as effective as electrolytic lesions in eliminating copulation whereas no behavioral effects were detected following similar infusions in the LHA. Histological examination of MPOA and LHA following IBO exposure revealed extensive degeneration of neuronal cell bodies with little evidence of non-specific damage. Also, immunohistochemical studies suggested that the serotonergic innervation of the MPOA remained largely intact in spite of IBO treatment; similarly, the damage inflicted by IBO in LHA on tyrosine hydroxylase-immunoreactive fibers in the medial forebrain bundle was insignificant. These data suggest that: (i) the functional integrity of MPOA nerve cell bodies is necessary for the expression of sexual behavior, and (ii) disruption of mating produced by electrolytic LHA lesions is due to disruption of medial forebrain bundle fiber systems. Behavioral observations of non-copulating males suggested that the MPOA injury did not interfere with all aspects of their sexual interaction with the estrous female; rather, they appeared specifically unable to perform the reflexive pelvic thrust pattern normally associated with mounting. We here report, however, that the ability to perform mounts with pelvic thrusts was temporarily restored in the vast majority of MPOA-injured males by the i.p. administration of the ergot derivative, lisuride. About 50% of these MPOA-damaged males even ejaculated, often after a low number of intromissions and short ejaculation latencies. On the other hand, injections of naloxone (an opiate receptor antagonist) failed to activate mounting in MPOA-lesioned or castrated rats. On the basis of these findings the possible ways in which steroid hormone-sensitive brain areas might interact with monoamine-containing pathways are discussed.U

Animals↗
PubMed1987

Time-course and steroid specificity of aromatase induction in rat hypothalamus-preoptic area.

We studied the time-course and steroid specificity for aromatase induction in the hypothalamus-preoptic area (HPOA) of the adult male rat. Aromatase activity (AA) was measured in tissue homogenates by using a radiometric assay that quantifies the stereospecific production of 3H2O from [1 beta-3H] androstenedione. We found that by 48 h after administration of testosterone, HPOA AA was significantly (p less than 0.01) greater than control values in castrated rats. In contrast, AA was significantly (p less than 0.01) reduced 12 h after castration, and reached its lowest levels by 4 days after castration. Several other steroids, administered in 3-cm Silastic capsules for 7 days, were tested for their capacity to induce hypothalamic AA. In addition to testosterone, only 5 alpha-dihydrotestosterone and 5 alpha-androstane-3 alpha, 17 beta-diol were effective. Neither the stereoisomers of these compounds nor several other steroids, including estradiol, progesterone, and corticosterone, were active. This profile of activity indicates that the induction of HPOA AA is androgen-specific and, together with the demonstrated time-course of induction, lends further support to the hypothesis that androgens regulate AA through a receptor mechanism and the synthesis of new protein.

Androgens↗
PubMed1987

Opioid peptides inhibit the release of noradrenaline from slices of rat medial preoptic area.

Previous circumstantial evidence suggested that endogenous opioid peptides inhibit an excitatory noradrenergic projection to the medial preoptic area (MPOA), and thereby suppress the activity of neurones containing luteinising hormone-releasing hormone and thus systemic concentrations of luteinising hormone (LH) itself. In this paper, we report that electrically stimulated release of 3H-Noradrenaline (3H-NA) from perifused slices of rat MPOA is diminished when opioid agonists are added to the incubation medium. Thus, morphine (10 microM), beta-Endorphin (1 microM) and met-Enkephalin (1 microM), but not Dynorphin A (1-8) (1 microM), caused a significant decrease in electrically stimulated 3H-NA release. The inhibition was reversed by addition of naloxone (10 microM) to the perifusion medium but 3H-NA release was unaffected by dopamine or acetylcholine (or their antagonists sulpiride and atropine, respectively), or serotonin, neurotensin, muscimol or bicuculline (the latter two being agonist and antagonist respectively for the GABA A receptor). Therefore, the experiments provide direct evidence that brain opioids modulate the noradrenergic input to MPOA neurones and support the hypothesis that this may be one mechanism for the regulation of LH secretion.

Animals↗
PubMed1998

Effects of diabetes and estradiol on norepinephrine release in female rat hypothalamus, preoptic area and cortex.

These studies determined whether diabetes and estradiol treatment altered norepinephrine (NE) release from hypothalamus, preoptic area (POA), and cortical slices from ovariectomized (OVX) female rats. Animals were sacrificed 12 days after the onset of streptozotocin-induced diabetes and 48 h following vehicle or estradiol injection. Brain slices were preloaded with 3H-NE, and release was evoked twice (S and S2) by electrical stimulation. Diabetes increased hypothalamic NE release during S1 regardless of the administration of vehicle or estradiol. Neither estradiol treatment nor diabetes alone affected NE release during S2 in the hypothalamus or POA. Estradiol treatment elevated NE release in the POA during S2 but only in diabetic animals. Moreover, estradiol elevated cortical NE release during S2 regardless of the presence or absence of disease. We also examined whether alpha2-adrenoceptor regulation of NE release was influenced by diabetes or hormone treatment. Enhancement of NE release by alpha2-adrenoceptor antagonism was evident in all 3 brain regions. However, alpha2-adrenoceptor regulation of NE release was unaffected by diabetes and hormone treatment. These findings suggest that diabetes alters NE release in the hypothalamus/POA of female rats. Additionally, this work identifies a novel action of estradiol to enhance stimulated NE release in the cortex of female rats.

Animals↗
PubMed1994

Estrous cycle-associated axosomatic synaptic plasticity upon estrogen receptive neurons in the rat preoptic area.

This study examined the hypothesis that synaptic relationships change on a daily basis in the anterior preoptic area of the intact, cycling female rat. Specifically, the anteroventral periventricular nucleus (AVPv) was chosen for analysis due to its abundant estrogen- and progesterone-receptive neurons and its critical role in the control of gonadotropin secretion. Ultrastructural analysis revealed that in the 24 h between proestrus and estrus, there was a 39% increase in axosomatic synapses upon AVPv neurons. In the subsequent 24 h to metestrus, the number of synapses decreased by 22%. Additional data showed that ovariectomy resulted in more axosomatic synapses in the AVPv relative to proestrus (46%) and metestrus (35%). Another component of the study investigated synaptic relationships on estrogen receptor-immunoreactive (ER-ir) and non-ER-ir neurons across the estrous cycle. ER-ir neurons received significantly more synaptic input at proestrus and estrus than did non-ER-ir neurons. At metestrus and following ovariectomy, no significant differences were present. The present study indicates that estrous cycle-associated synaptic plasticity occurs in the AVPv and lends further support to the critical role of this nucleus in regulation of gonadotropin secretion. Moreover, it provides the first evidence that ER- and non-ER-ir neurons are differentially innervated.

Animals↗
PubMed1992

Estradiol selectively regulates alpha 1B-noradrenergic receptors in the hypothalamus and preoptic area.

We previously demonstrated that estradiol administered in vivo elevates the number of alpha 1-adrenoceptors in preoptic area (POA) and hypothalamic membranes from ovariectomized female rats and potentiates alpha 1 receptor augmentation of beta-adrenoceptor-stimulated cAMP formation in slices from these brain regions. Present studies examined (1) if estradiol selectively regulates any alpha 1-adrenoceptor subtype, and (2) which alpha 1 receptor subtype mediates the augmentation of cAMP synthesis. Hypothalamic and POA membranes from estradiol-treated rats, when compared to ovariectomized rats, had modestly (30-50%) but significantly elevated numbers of 3H-prazosin (alpha 1) binding sites. Estradiol affected neither the number of alpha 1 receptor sites in frontal cortex nor the affinity of 3H-prazosin binding in any brain region examined. Results of binding studies conducted in the presence of chlorethylclonidine, a selective, irreversible inactivator of the alpha 1B receptor subtype, indicated that the estrogen-dependent increase in total alpha 1 binding sites in POA and hypothalamic membranes was attributable to a selective, five- to sixfold increase in alpha 1B receptor number. Progesterone had no measurable effects on alpha 1 receptor binding. Blockade of alpha 1B receptors with chlorethylclonidine eliminated phenylephrine augmentation of isoproterenol-stimulated cAMP formation in slices, whereas the alpha 1A antagonist 5-methyl-urapadil did not. This suggests that the alpha 1B receptor subtype potentiates cAMP formation. Thus, the increased alpha 1 receptor augmentation of cAMP formation seen in slices from estradiol-treated rats is correlated with increased alpha 1B receptor number.

Animals↗
PubMed2005

Changes of body temperature and thermoregulatory responses of freely moving rats during GABAergic pharmacological stimulation to the preoptic area and anterior hypothalamus in several ambient temperatures.

Action of gamma-aminobutyric acid (GABA) in the preoptic area and anterior hypothalamus (PO/AH) has been implicated to regulate body temperature (T(b)). However, its precise role in thermoregulation remains unclear. Moreover, little is known about its release pattern in the PO/AH during active thermoregulation. Using microdialysis and telemetry techniques, we measured several parameters related to thermoregulation of freely moving rats during pharmacological stimulation of GABA in normal (23 degrees C), cold (5 degrees C), and hot (35 degrees C) ambient temperatures. We also measured extracellular GABA levels in the PO/AH during cold (5 degrees C) and heat (35 degrees C) exposure combined with microdialysis and high performance liquid chromatography (HPLC). Perfusion of GABA(A) agonist muscimol into the PO/AH increased T(b), which is associated with increased heart rate (HR), as an index of heat production in all ambient temperatures. Although tail skin temperature (T(tail)) as an index of heat loss increased only under normal ambient temperatures, its response was relatively delayed in comparison with HR and T(b), suggesting that the increase in T(tail) was a secondary response to increased HR and T(b). Locomotor activity also increased in all ambient temperatures, but its response was not extraordinary. Interestingly, thermoregulatory responses were different after perfusion of GABA(A) antagonist bicuculline at each ambient temperature. In normal ambient temperature conditions, perfusion of bicuculline had no effect on any parameter. However, under cold ambient temperature, the procedure induced significant hypothermia concomitant with a decrease in HR in spite of hyperactivity and increase of T(tail). It induced hyperthermia with the increase of HR but no additional change of T(tail) in hot ambient temperature conditions. Furthermore, the extracellular GABA level increased significantly during cold exposure. Its release was lower during heat exposure than in a normal environment. These results indicate that GABA in the PO/AH is an important neurotransmitter for disinhibition of heat production and inhibition of heat loss under cold ambient temperature. It is a neurotransmitter for inhibition of heat production under hot ambient temperature.

Analysis of Variance↗
PubMed1985

Comparison of the effects of different isomers of bicuculline infused in the preoptic area on male rat sexual behavior.

Intracerebral infusion of (+) bicuculline methiodide, but not of its (-) isomer, in the preoptic area, stimulated masculine sexual behavior in rat as evidenced by a decrease in the number of intromissions preceding ejaculation and a shortening of the ejaculation latency and postejaculatory interval. Data suggest a role of the GABAergic system in mediating masculine sexual behavior.

Animals↗
PubMed1998

Intracranial androgenic activation of male-typical behaviours in house mice: concurrent stimulation of the medial preoptic area and medial nucleus of the amygdala.

This experiment examined whether testosterone proprionate (T) action in the medial preoptic area (MPO) would synergize with T action in the medial nucleus of the amygdala (AME) for the expression of androgen-dependent behaviors in house mice. Cannulae containing T were bilaterally implanted into the MPO, the AME, or both areas concurrently (MPO/AME) of castrated males. In addition, other castrates were implanted subcutaneously with empty Silastic capsules (BSIL) or Silastic capsules containing T (TSIL). All subjects were examined for the following androgen-dependent, male-typical behaviors: mounting, urinary scent marking, preference for female urine over male urine, preference for female over male conspecifics and ultrasonic mating vocalizations. MPO implants restored ultrasonic vocalizations and preference for females, but had little or no effect upon urine marking, mounting or preference for female urine. In contrast, AME implants were ineffective at restoring any of these male-typical behaviors. The combined MPO/AME implants were not more effective in restoring male-typical behaviors than MPO implants alone, thus providing no evidence for synergy in hormone action between these two brain areas. In general, castration (BSIL) resulted in low levels of all behaviors whereas systemic T replacement (TSIL) resulted in high levels of behavior, verifying the androgen-dependence of these behaviors. Group differences in male-typical behavior could not be accounted for by differences in general activity levels. Moreover, none of the brain-implanted groups had larger seminal vesicles than those of the BSIL. Thus, when the brain implants affected behavior, they most probably did so through their effects within the brain. Although the AME is a target for steroid hormones and is an important area for the expression of male-typical behaviors, intracranial T implants into the AME did not demonstrate a role for androgen in the AME in restoring male-typical behaviors in castrated mice.

Amygdala↗
PubMed1983

Preoptic area and substantia nigra interact in the control of maternal behavior in the rat.

This study provides evidence that the preoptic region and the substantia nigra interact in the control of maternal behavior. In the first experiment, large electrolytic lesions of the substantia nigra were found to severely disrupt maternal behavior and cause stereotyped motor activity in postpartum lactating rats. In order to test the hypothesis that the preoptic region and the substantia nigra interact in the control of maternal behavior, a second experiment employed an asymmetrical lesion design. Postpartum lactating rats that received a unilateral knife cut severing the lateral connections of the medial preoptic area and a contralateral lesion of the substantia nigra showed larger deficits in maternal behavior than either sham females or females that received a unilateral preoptic knife cut paired with an ipsilateral substantia nigra lesion. Measurements of body weights, body temperatures, and stereotyped behavior indicated that the differences in maternal behavior between the ipsilateral and contralateral groups could not be explained on the basis of nonspecific effects.

Animals↗
PubMed1995

Effect of application of gamma amino butyric acid at the medial preoptic area on sleep-wakefulness.

Intracerebral microinjections of gamma amino butyric acid were given bilaterally at the medial preoptic area (mPOA) to determine the possible role of this neurotransmitter in the genesis and regulation of sleep-wakefulness. GABA (50 micrograms/0.2 microliters) when administered through chronically implanted cannulae in free moving rats, did not produce any significant alterations in sleep-wakefulness. This may be attributed either to the non-involvement of GABA at the level of mPOA in the regulation of sleep, or to other factors like the low dose and rapid breakdown of the injected drug.

Animals↗
PubMed1993

Effects of triazolam and nifedipine injections into the medial preoptic area on sleep.

We have reported previously that microinjections of the benzodiazepine (BZ) hypnotic triazolam into the medial preoptic area (MPA) of the hypothalamus increase sleep in the rat. As a follow up to previous work, which has indicated that the dihydropyridine calcium channel blocker, nifedipine, prevents sleep induction by an intraperitoneally administered BZ, we have now coinjected nifedipine and triazolam into the MPA. It was found that nifedipine alone had no significant effects on sleep and prevented sleep induction by triazolam. There were no drug-specific effects on core temperature in any treatment condition. These data suggest that dihydropyridine-sensitive sites may be involved in the mechanism of sleep induction by BZs.

Animals↗
PubMed1996

beta-adrenergic modulation of male sexual behavior elicited from the medial preoptic area in rats.

This study was aimed at investigating the role of the adrenergic mechanism in the medial preoptic area (mPOA) in sexual arousal and copulatory performance. Saline, norepinephrine (NE), phenoxybenzamine (PBZ) and propranolol (PROP) were injected into the mPOA in different groups of rats. NE application (3 micrograms) facilitated the male sexual behavior by increasing sexual arousal and copulatory performance. On the other hand, application of PROP and PBZ produced inhibition of male sexual behavior. Effects produced by low doses of PROP were more significant than PBZ. The results, viewed in the light of other available reports, suggest that the mPOA beta-adrenergic mechanism is important in the elaboration of male sexual behavior.

Adrenergic alpha-Agonists↗
PubMed1996

Exogenous estrogen acts differently on production of estrogen receptor in the preoptic area and the mediobasal hypothalamic nuclei in the newborn rat.

Expression of the estrogen receptor (ER) in the preoptic area (POA) and the mediobasal hypothalamus (MBH) in newborn female rats was studied by immunohistochemistry (IHC) and in situ hybridization histochemistry (ISHH). The number of ER immunoreactive (ER-IR) cells decreased and expression of ER mRNA was suppressed in the arcuate (ARH) and the ventromedial (VMH) hypothalamic nuclei by daily injections of estradiol benzoate (EB) for ten consecutive days. In contrast, in the POA, expression of ER mRNA was not suppressed by EB treatment, while the ER immunoreactivity and the number of ER-IR cells was decreased by EB treatment. Results of quantification of ER mRNA by reverse transcription-polymerase chain reaction correlated well with results from ISHH: that is, ER mRNA expression decreased in the MBH but not in the POA. Thus, estrogen affects ER gene expression differently in these two brain regions.

Animals↗
PubMedDate not supplied

Synaptology of luteinizing hormone-releasing hormone neurons in rat preoptic area.

The ultrastructural appearance of luteinizing hormone-releasing hormone (LHRH) immunoreactive elements was studied in the medial preoptic area (MPOA) of adult male Fischer 344 rats. The purpose of the study was to determine the distribution and morphology of innervation of the LHRH neuron. Although not numerous, both axo-somatic and axo-dendritic synapses were present and generally of the asymmetric (Gray's II) category. Analyses of 56 profiles of 11 separate perikarya revealed only 7 axo-somatic terminals. The synaptic input to LHRH dendrites was a fraction of that to non-identified dendrites in the same electron micrographic fields; 0.4% of LHRH dendritic membrane was in synaptic contact compared to 6.6% of nonidentified dendritic membrane. In addition to receiving an input, LHRH processes were also seen to make synapses onto non-immunoreactive elements. Close examination of this material for evidence of contact between LHRH elements revealed two clear examples of synaptic interaction and several instances of close association in which no other elements intervened.

Animals↗
PubMed1986

Multiple unit activities recorded from the medial preoptic area during copulatory behavior in freely moving male rats.

Multiple unit activities (MUAs) were recorded from the medial preoptic area (MPO) during copulatory behavior in freely moving male rats. The baseline firing rate in the male MPO was 19.6 spikes/s +/- 7.1 S.E. (n = 14), and it was increased by 36.7% when a female rat was introduced (26.8 spikes/s +/- 8.9 S.E., n = 14). The firing rate remained elevated until ejaculation. The maximum firing rate (53.5 spikes/s +/- 16.7 S.E., n = 14) was obtained specifically during pursuit-mounting behavior. This high frequency firing with pursuit-mounting behavior was, however, immediately inhibited for 8.2 s +/- 2.1 S.E. (n = 14) when mounting was followed by intromission. The firing-inhibition was further prolonged (120.9 s +/- 44.6 S.E., n = 14) when ejaculation was performed after mounting and intromission. In cases where mounting was elicited alone, a firing-inhibition was not observed and the firing rate after mounting returned to the average firing rate during copulatory behavior. These results suggest that the MPO neurons may play a major role in pursuit-mounting, intromission and ejaculation.

Action Potentials↗