Preoptic Stimulation Research Articles

Brown adipose tissue thermogenesis evoked by medial preoptic stimulation is mediated via the ventromedial hypothalamic nucleus.

Experiments were designed to determine if a functional ventromedial hypothalamic nucleus was required for the activation of brown adipose tissue thermogenesis evoked by medial preoptic stimulation. Male, urethane-anesthetized Long--Evans rats, maintained at 37 degrees C, had temperatures (thermistor probes for gastrocnemius, Tm; intrascapular brown adipose tissue, TIBAT; colonic, Tc; and tail, Tt), gastrocnemius electromyogram activity (via stainless steel recording electrodes), and systemic blood pressure and heart rate (via a femoral arterial catheter) measured before and after a series of unilateral medial preoptic electrical stimulations (monophasic 0.5-ms pulses of 300 microA at 50 Hz for 30 s). Measurements were made (i) after an initial control medial preoptic electrical stimulation, (ii) after medial preoptic stimulation was applied 1 min following an intracranial injection of 300 nL of sterile saline or buffered 2% Lidocaine into the ipsilateral posterior hypothalamic nucleus or the ipsilateral ventromedial hypothalamic nucleus, and (iii) after recovery medial preoptic stimulation 45 min after Lidocaine was injected into the ventromedial hypothalamic nucleus. TIBAT and blood pressure rose significantly (p < 0.05) above the corresponding prestimulation control values with all protocols, except when Lidocaine was injected into the ventro-medial hypothalamic nucleus prior to medial preoptic stimulation. Shivering (electromyogram) activity was not evoked following medial preoptic stimulation and Tm and Tt did not significantly change from the corresponding prestimulation values. A recovery medial preoptic stimulation 45 min after Lidocaine treatment of the ventromedial hypothalamic nucleus again evoked significant increases in TIBAT above the core temperature, similar to the rise in TIBAT seen after the first control medial preoptic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Delta-9-tetrahydrocannabinol attenuates luteinizing hormone release induced by electrochemical stimulation of the medial preoptic area.

Despite diverse pharmacological actions, drugs commonly used for blocking ovulation in the rat have not been observed to exert differential effects on the LH response to preoptic stimulation, thus suggesting blocking action above the final hypothalamic GnRH pathway. To determine if ovulatory blockade by delta-9-tetrahydrocannabinol (THC) is consistent with that scheme, LH surges evoked by preoptic stimulation were contrasted with those elicited during blockade by atropine (ATR), a classic ovulation-blocking agent with which other drugs have been compared. THC (10 mg/kg) or ATR (350 mg/kg) treatment before the proestrous critical period uniformly blocked LH release and ovulation in sham-stimulated rats. Preoptic stimulation evoked LH surges after both drug treatments (p less than 0.001), peak levels increasing with the intensity of stimulation (p less than 0.05). However, both maximum LH concentration (p less than 0.05) and total integrated LH release (p less than 0.01) were lower in THC-blocked rats. Inspection of the oviducts revealed no difference in the incidence of ovulation or the number of ova discharged. The reduced LH response during THC blockade was not attributable to variation in the extent or locus of histologically determined stimulation sites. These results distinguish THC from ATR and, by extension, other blocking drugs that do not overtly affect the LH response to preoptic stimulation. Thus, ovulatory blockade by THC may involve a different mechanism, which likely includes inhibitory action within the preoptic-to-tuberal GnRH pathway.

Morphine but not Naloxone Enhances Luteinizing Hormone‐Releasing Hormone Neuronal Responsiveness to Norepinephrine

Some axon terminals of hypothalamic opiate neurons directly synapse on luteinizing hormone-releasing hormone (LHRH) neurons. To determine whether such synaptic connections affect LHRH neuronal activity, we have examined the profiles and concentrations of LH released in response to intracerebroventricular (icv) norepinephrine (NE, 45 μg) infusions alone or following medial preoptic area (MPOA) electrochemical stimulation (ECS) in estrogen-treated ovariectomized rats. Similar studies were performed in rats treated with naloxone (5 mg/kg ip) or morphine (20 mg/kg sc) given 15 min prior to MPOA-ECS or 30 min prior to icv NE. Naloxone neither augmented nor suppressed the LH response obtained with NE alone. MPOA-ECS evoked a significant increase in plasma LH. When the preoptic area was stimulated (0 min) and NE was infused at 30 min, a significant amplification of LH release occurred. Prior treatment of rats (-15 min) with naloxone had no effect on LH responses elicited by either preoptic stimulation alone or combined with icv NE. In the second study, morphine was given sc and had no effect on basal plasma LH levels. However, when morphine was given (-15 min) and icv NE infusions were made (30 min), the rise in plasma LH induced by NE was significantly enhanced. Preoptic ECS (0 min) evoked a rise in plasma LH and this response was also enhanced by morphine pretreatment. The major effect on LH release occurred when sc morphine injections (-15 min) were combined with MPOA-ECS (0 min) followed by icv NE (30 min). In these rats, a remarkable and highly significant release of LH occurred which reached peak levels even greater than those observed during spontaneous LH surges (2,392 versus 16 to 1,800 ng/ml). Since morphine has profound effects on the serotonergic system, in the third series of studies, morphine was infused into the dorsal raphe nucleus (DRN) and LH responses to MPOA-ECS or icv NE alone or following combined ECS + NE were examined. DRN morphine did not affect basal LH release but it produced a rapid and highly significant rise in plasma prolactin. When DRN morphine was given (-15 min) and NE was infused icv (30 min), there was marked amplification in LH release compared to those values observed after only NE. However, there were no appreciable differences in LH values obtained after sc versus DRN morphine injections in response to NE. Similarly, the amplification of LH release which occurred following DRN morphine (-15 min) + MPOA-ECS (0 min) was not different from that obtained after sc morphine. In the final group of rats, DRN morphine was given (-15 min), the preoptic area was stimulated (0 min) and NE was infused (30 min). Following this treatment, plasma LH release was also markedly enhanced and did not differ appreciably (except at 60 and 120 min) from the levels of LH released after sc morphine. Prolactin concentrations rose slowly after icv NE to reach peak levels 75 min after treatment. Combinations of morphine + MPOA-ECS without or with NE neither augmented nor suppressed the high prolactin concentrations achieved after only DRN morphine infusions. We conclude from these data that: 1) those opiate neuronal terminals which synapse directly on LHRH neurons do not affect LHRH neuronal responsiveness to either NE, to MPOA-ECS or to combined preoptic stimulation+ NE, and 2) morphine has profound effects on LHRH neuronal responsiveness to both NE, to MPOA-ECS and, in particular, to combined ECS + NE. Since amplification of LH release occurs after treatment of rats with morphine either by sc injections or DRN infusions, the augmented LH and prolactin responses observed are most likely due to the morphine-induced release of serotonin and not to direct morphine effects on LHRH neurons.

Increases in adrenolumbar venous flow and epinephrine secretion elicited by preoptic and hypothalamic stimulation in the cat.

Seventy-five sites were electrically stimulated within the preoptic and hypothalamic areas of anesthetized cats (n = 16). Adrenolumbar venous blood flow, secretion of epinephrine and norepinephrine, heart rate and mean arterial blood pressure were measured at baseline and following a standard stimulus (0.6 mA for 30 s) at each site. The most frequent adrenal medullary response to central stimulation was an increase in the secretion of both catecholamines (ng/min) greater than 10% of the baseline mean. Seventeen sites (23%) increased adrenolumbar venous flow greater than 12% above the mean baseline flow rate. This group of sites also evoked significantly greater increases in the secretion of epinephrine, and in mean arterial blood pressure and heart rate. These data support the hypothesis that secreted catecholamines, especially epinephrine, may act locally to increase blood flow through the adrenal medulla.

Neural substrates for photic control of elasmobranch sexual development and behavior

Brain regions where photic stimuli and reproductive systems may interact in controlling both sexual development and reproductive behavior are considered in detail. Retinal input to the preoptic area and photic stimulation of pineal neural and endocrine systems appear to be major pathways for synchronization of reproductive development with environmental conditions. Both systems most likely influence gonadotropin-releasing hormone (GnRH) production and release and the feedback control of these processes via steroid-concentrating cells. In adult elasmo-branchs, perceptions of visual stimuli are potentially important in certain aspects of mating, e.g., mate recognition and analysis of courtship displays, and the neural substrates for the perceptions are most likely conditioned by the hormonal status of the animal. Breeding fish may thus have visual mechanisms affected by synaptic input from GnRH and steroid-concentrating neurons. The central nucleus of the telencephalon (CN) provides high-level visual integration in elasmobranchs. Preoptic, terminal nerve, and perhaps midbrain reticular areas are suggested origins for hormone-related CN afferents. The optic tectum contains GnRH-immunoreactive fibers in a variety of species. Thus, GnRH modulation of visual function probably occurs at this level. Visual centers of the midbrain tegmentum are near both GnRH-immunoreactive and sex-steroid-concentrating neurons. Sensory-hormonal integrative activity within the tegmental units could provide outputs for modulation of activity in both higher visual (e.g., the CN) and lower sex-related sensorimotor systems (e.g., spinal clasper control pathways) through ascending and descending pathways, respectively.

Effects of drugs which modify catecholamine activity on amplification of LH release induced by locus coeruleus electrical stimulation

Norepinephrine may be the neurotransmitter responsible for triggering the surge release of luteinizing hormone (LH) in proestrous and steroid-treated ovariectomized rats. In a previous study, we electrically stimulated (ES) the locus coeruleus (LC), a norepinephrine cell body region from which some axons project to the hypothalamus. These studies were performed in estradiol-treated rats in which the medial preoptic nucleus (MPN) initially had been electrochemically stimulated (ECS) to partially depolarize luteinizing hormone-releasing hormone (LH-RH) neurons. We observed that LC-ES markedly amplified the amount of LH released after preoptic-ECS. The purpose of the present study was to determine if these amplifying effects of LC-ES were due to the release of a catecholamine and if so which neurotransmitter was involved in this response. All rats in this study were ovariectomized and 7 days later (day 0) they were treated with estradiol for 2 days (day 2). On day 2, all animals were anesthetized with chloral hydrate. In control rats, the MPN was electrochemically stimulated (100 μA/60 s DC) and 30 min later the LC was electrically stimulated for 15 min. MPN-ECS significantly increased plasma concentrations of LH and LC-ES markedly amplified these plasma LH levels. Thereafter, 3 studies were performed and the following drugs were given: (1) α-methyl- p-tyrosine (MPT, 300 mg/kg i.p.); (2) phenoxybenzamine (PX, 15 mg/kg i.p.) and (3) propranolol (PROP, 15 mg/kg i.p.). MPT and PROP were administered 15 min prior to MPN-ECS and PX was given 90 min before MPN-ECS. None of these drugs affected the amount of LH released after preoptic stimulation. In contrast, both MPT and PX completely suppressed the augmenting action of LC-ES on LH secretion. The effects of PROP were equivocal and the interpretation of this data depends upon which statistical test was applied. These data suggest that LC-ES induces the release of NE and it is this neurotransmitter, acting via alpha adrenoreceptors, which ultimately amplifies LH secretion.

Locus coeruleus (LC) stimulation augments LHRH release induced by medial preoptic stimulation. Evidence that the major LC stimulatory component enters contralaterally into the hypothalamus

Previous studies by others suggest that mid- and hindbrain noradrenergic projections to the hypothalamus may be stimulatory or inhibitory to luteinizing hormone releasing hormone (LHRH) release depending upon the steroid environment of the rat. In the present study we reevaluated the effects of electrical stimulation of the locus coeruleus (LC) in estrogen-primed ovariectomized (OVX) rats anesthetized with chloral hydrate. This anesthetic agent blocked the spontaneous luteinizing hormone (LH) surges which normally occur in estrogen-treated OVX rats. In such rats, bilateral LC electrical stimulation was ineffective in altering basal LH concentrations. Thereafter, we evaluated the effects of LC electrical stimulation on patterns and concentrations of plasma LH induced by electrochemical stimulation (ECS) of the medial preoptic nuclei (MPN). Bilateral MPN-ECS induced a significant rise in plasma LH. When the LC was bilaterally stimulated for 15 min beginning 30 min after MPN stimulation, peak LH concentrations were significantly augmented and remained elevated throughout the experiment. To learn more of how LC noradrenergic projections reach regions of the hypothalamus which contain LHRH neurons, the right MPN in a group of rats was unilaterally ECS and 30 min later the right LC was unilaterally stimulated for 15 min. Plasma LH levels increased after MPN activation but no further rise or fall in LH occurred after ipsilateral LC stimulation. In the final group of rats, the right MPN was unilaterally electrochemically stimulated and this was followed 30 min later by contralateral electrical stimulation of the left LC. In these animals, peak plasma LH concentrations were significantly elevated above those obtained after only unilateral MPN stimulation. These data demonstrated that LC stimulation augments LH release but only after preliminary depolarization of LHRH neurons by ECS. Moreover, the stimulatory noradrenergic projections from LC decussate to enter contralateral hypothalamic regions containing LHRH neurons.

Hypothalamic control of nocireceptive and other neurons in the marginal layer of the dorsal horn of the medulla (trigeminal nucleus caudalis) in the rat.

The effect of electrical stimulation of the preoptic area of the hypothalamus on the discharge of neurones in the marginal layer (lamina I) of the trigeminal nucleus caudalis was studied in the anaesthetised rat. There was a powerful suppression of the discharge evoked by noxious thermal stimuli in 49/49 specific nociceptor driven (nocireceptive) neurones. The inhibitory effect increased with graded increases in the intensity of preoptic stimulation. Stimulation, however, produced only a small reduction in the discharge of 14/17 cold receptive neurones. Thresholds for producing suppression of cold receptive neurones were generally higher than those for nocireceptive neurones. There was no effect on the activity of 12/12 low threshold mechanoreceptive neurones. The inhibitory action generated on the activity of nocireceptive neurones was reduced by electrolytic lesions in the nucleus raphe magnus (NRM) or the nucleus paragigantocellularis lateralis (PGCL) or the dorsolateral and ventrolateral periaqueductal gray matter (PAG). Lesions made in the ventral or dorsal aspect of PAG were, however, ineffective in reducing the suppression. It is suggested that the powerful descending inhibitory control of nociceptive transmission in the trigeminal nucleus caudalis is one of the neuronal mechanisms mediating analgesia from the preoptic area of the hypothalamus.

Effects of long- and short-term gonadectomy on the hypothalamo-hypophysial (LH-releasing hormone-LH) system in oestrogen-treated male and female rats.

Considerable differences have previously been found in the hypothalamo-hypophysial responsiveness to oestrogen, depending upon the time between gonad removal and exposure to oestrogen. In the present study a detailed analysis was made of some of the differences which may exist in pituitary LH-releasing hormone (LHRH) receptors and the amount of LH released in response to electrochemical depolarization of the medial preoptic area after 2 or 7 days of oestradiol treatment of long- and short-term gonadectomized male and female rats. The pituitary glands of long-term gonadectomized males and females secreted more LH in response to two pulse injections of LHRH than did short-term gonadectomized rats. The amount of LH released on day 2, however, was equivalent to that secreted after 7 days of oestradiol treatment. Moreover, long-term gonadectomized males and females had equivalent LHRH receptor concentrations, which were greater than those of short-term gonadectomized animals. Peak serum LH concentrations observed after preoptic stimulation were equivalent in short- and long-term castrated rats after 2 days of oestrogen exposure. Serum LH concentrations following preoptic stimulation in short-term gonadectomized males and females were significantly greater on day 7 than on day 2 of oestradiol treatment, whereas in long-term gonadectomized animals the stimulated release of LH was equivalent both in magnitude and time of peak release on both days.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential changes in the mechanisms controlling luteinizing hormone and prolactin secretion in middle-aged female rats.

Serum luteinizing hormone (LH) and prolactin (PRL) concentrations were measured in young (3-4 month old) and middle-aged (10-12 month old) intact female rats on proestrus, in ovariectomized rats after two estrogen injections (estradiol benzoate; EB, 10 micrograms/100 g body weight, s.c.) or after preoptic stimulation in EB-primed ovariectomized rats. Only animals showing regular 4-day estrous cycles were selected for the experiment. The magnitude of proestrous LH surge was significantly smaller in middle-aged than in young rats. Two BE injections, at noon on Days 0 and 3, in ovariectomized middle-aged rats failed to induce surges in LH secretion on Day 4 whereas the same treatment produced LH surges in ovariectomized young rats. The preoptic electrochemical stimulation (50 microA for 60 sec) produced a prompt rise in serum LH levels in ovariectomized EB-primed young but not in middle aged rats. The preoptic stimulation with a larger current (200 microA) induced LH secretin in middle-aged rats. In none of these situations serum PRL concentrations were different between young and middle-age rats. These results suggest differential aging rates in the preoptic mechanisms governing LH and PRL secretion in the rat. The function of the preoptic ovulatory center in responding to the estrogen positive feedback action and inducing LH secretion may become impaired and independent of the PRL control mechanism, even before the regular estrous cycle terminates.

Nucleus accumbens and preoptic area stimulation: tuberoinfundibular single unit responses, modulation of electrical activity and gonadotrophin secretion.

Single unit activity was recorded from tuberoinfundibular neurones in urethane-anaesthetized pro-oestrous rats. Responses following single shock (0.2 Hz) stimulation of the preoptic area/anterior hypothalamus (PO/AH) or nucleus accumbens (ACB) were recorded and computed for 137 single units. More cells were shown, by antidromic activation, to project to ACB (4 of 77) than to PO/AH (1 of 60). Fewer units were responsive to stimulation of ACB (p less than 0.02), those that were responsive showing a longer latency to the onset of response compared to that following PO/AH stimulation. Significantly (p less than 0.02) more slowly firing cells were found in the group of animals tested with stimulation of PO/AH. Delivery of high frequency stimulation to PO/AH resulted in a 21/2 fold increase in plasma luteinizing hormone (LH) levels (p less than 0.05), whereas ACB-stimulated and control animals showed no increases in plasma LH concentrations. During delivery of the high frequency stimulation only one cell in the ACB group of animals was orthodromically affected (out of five tested). However, in the PO/AH group, five of the seven cells tested showed either excitation or inhibition during stimulation. The possibility that the functional connections demonstrated between ACB and the endocrine hypothalamus are involved in the expression of 'higher' brain functions, recognised during changing endocrine states, is discussed.

Activation of central warm-sensitive neurons and the tail vasomotor response in rats during brain and scrotal thermal stimulation.

The effects of preoptic and hypothalamic thermal stimulation on tail skin temperature were observed at different scrotal temperatures. The threshold hypothalamic temperature for tail vasodilation at a scrotal temperature of 40 degrees C was significantly lower than that at a scrotal temperature of either 25 degrees C or 33 degrees C. The effects of scrotal thermal stimulation on tail skin vasodilated by higher hypothalamic temperatures were observed. Cooling the scrotum from 42 to 30 degrees C invariably caused a rapid fall in tail temperature, whereas scrotal cooling from 30 to 25 degrees C did not cause any significant change. Cooling of either the left or right half of the scrotum caused a similar fall in tail temperature. The temperature characteristics of the preoptic hypothalamic thermo-sensitive neurons were determined at scrotal temperatures of 32, 36 and 26 degrees C. The firing rate of warm-sensitive neurons at a given hypothalamic temperature was highest at a scrotal temperature of 36 degrees C, while that of cold-sensitive neurons was lowest at that temperature. The scrotal temperature range over which the number of neurons activated by scrotal warming increased rapidly was between 36 and 39 degrees C when hypothalamic temperature was held at 36-37 degrees C.

Similarity of luteinizing hormone surges induced by medial preoptic stimulation in female rats blocked with pentobarbital, morphine, chlorpromazine, or atropine.

Adult proestrous rats were subjected to either electrochemical or electrical stimulation of the medial preoptic area after ovulation-blocking dosage with either pentobarbital (PTBL), morphine, chlorpromazine, or atropine. For electrochemical stimulation (ECS), 233 microA anodal DC for 30 sec (7000 mu coulombs) was delivered through a unipolar stainless steel electrode. For electrical stimulation (ES), 750 microA biphasic pulse pairs at 30 Hz, on and off each 15 sec, were delivered through a coaxial platinum electrode, in four 5-min bursts equally spaced during 60 min. In PTBL-blocked rats this stimulus produced LH surges equivalent to those after continuous stimulation for 60 min. Blood was collected 60 and 90 min after ECS or after the start of ES. Mean serum LH concentrations (RIA) maximal at 90 min after ECS, were similar under the four blocking agents (1270-1486 ng/ml serum in terms of NIAMDD LH RP-1). Like-wise, after ES there were no significant differences (P greater than 0.05) among the mean LH levels at 60 min (310-571 ng/ml serum). The 90-min values showed a downward, but not significant, trend in the case of PTBL, chlorpromazine, and atropine plus PTBL. Under morphine an apparent upward trend was due largely to an animal having an especially large increase. With rare exception, full ovulation was evident at terminal laparotomy on the morning after stimulation. Thus, whichever of the several drugs was used, medical preoptic area stimulation with given parameters induced section of comparable amounts of LH. None of the drugs appears to have primary suppressive action on the preoptic-tuberal system, on the availability of LHRH or its release into the portal vessels, on the ability of the pituitary to release LH, or on the ovarian response.

Effect of dextro-amphetamine on reticulo-preoptic interactions in "encéphale isolé" cats.

Intravenous administration of a single dose of dextro-amphetamine (1 mg/kg) in the "encéphale isolé" cat significantly increased amplitude of the P50 and N110 components of the preoptic potential evoked by the stimulation of the mesencephalic reticular formation and decreased all components of the mesencephalic reticular formation potential evoked by preoptic stimulation. Concomitantly, a state of increased and persistent arousal response was found. These findings support the idea that during wakefulness there is a reticular facilitation and a preoptic inhibition.

Sex difference and senile change in hypothalamic neuronal response to electrical stimulation of the limbic system in the rat.

To get an electrophysiological basis for understanding the sexual and age-related changes in the brain mechanisms controlling gonadotropin secretion, we studied single unit responses to electrical stimulation in the preoptico-arcuate, amygdalo-preoptic and hippocampo-preoptic neural connections in the rat. Orthodromic unit responses to single pulse electrical stimulation were recorded in young mature and aged, male and female rats by post-stimulus histogram analysis. Electrical stimulation of the medial preoptic area elicited responses in one-half of the hypothalamic arcuate neurons tested in female rats while the stimulation induced responses in less than one-third of the arcuate neurons in the male. The percentage of arcuate neurons responding to preoptic stimulation did not differ between young and aged animals. Stimulation of the medial amygdala evoked responses in a larger number of preoptic neurons in young mature rats than in aged animals in both sexes. There was no sexual difference in the number of responding neurons to amygdaloid stimulation. Percentages of preoptic neurons responding to the hippocampal stimulation were greater in young females showing regular estrous cycles than in males or aged females which showed constant estrous vaginal smears. In aged females whose vaginal cycles were induced by daily treatment with progesterone, more preoptic neurons responded to stimulation of the amygdala and the hippocampus than in aged constant estrous rats. The young cycling and aged progesterone-recycling rats had similar preoptic neuronal responses to the limbic stimulation. Stimulus thresholds for inducing these arcuate and preoptic unit responses were almost equivalent among different groups of animals. This suggests that the alteration in unit responses observed was not due to a change in neuronal excitability in the sites of stimulation in different animal groups. These results indicate that there are sex differences in the synaptic functions which transmit preoptic signals to the arcuate neurons and hippocampal impulses to the preoptic neurons. It is also suggested that the amygdalo-preoptic and hippocampo-preoptic neural pathways may be functionally modified in aged rats because of the absence of estrous cycles.

Importance of time-related parameters of pre-optic electrical stimulation in the release of LH in the pentobarbital-blocked pro-oestrous rat.

The effectiveness of pre-optic stimulation in overcoming the pentobarbital blockade of ovulation in the rat has long been recognized and employed in neuroendocrine investigations. Although some reports have appeared comparing certain aspects of electrical stimulation in effectiveness in releasing LH, no complete study in female rats has been reported. The present study utilized regularly cycling rats of the Charles River CD strain in which ovulation was blocked by the injection of sodium pentobarbital on the afternoon of pro-oestrus. Electrical stimulation was delivered through bipolar platinum electrodes stereotaxically positioned in the preoptic area, and LH was measured in plasma samples obtained at the onset of stimulation and 10, 20, 30, 45, 60, 80, 120 and 150 min thereafter. LH release was established in response to a baseline set of parameters: 15 HZ, 1.5 mA and 1.5 ms per phase, 30 s on/off for 60 min. Stimulations employing equi-coulombic increments of 1/3 introduced in each parameter in turn were compared in groups of 4-6 animals. Use of small increments in each parameter allowed the detection of those parameters to which the pre-optico-hypothalamo-pituitary system is most sensitive over the range studied, namely duration: of each pulse and of the overall stimulation period. This observation may be explained in terms of characteristics of the pituitary responsiveness.

Amygdala neurones: converging synaptic inputs produced by median eminence and medial preoptic area stimulations in rats.

1. Amygdaloid afferent inputs from the median eminence and the medial preoptic area were studied electrophysiologically in urethane-anaesthetized female rats.2. Stimulation of the surface of the median eminence produced orthodromic responses in about 80% of the forty-seven amygdala units tested and about 65% of the responsive cells showed an excitation.3. Stimulation of the ipsilateral medial preoptic area orthodromically excited seventeen and inhibited twenty of the forty-nine units tested.4. Stimulation of the contralateral medial preoptic area evoked orthodromic excitation in nine and inhibition in three of the twenty-two units tested. These stimuli were ineffective for producing antidromically conducted impulses in the tested units.5. Sixteen of the thirty amygdala units tested for responses to both median eminence and ipsilateral medial preoptic area stimulation responded orthodromically with either excitation or inhibition. The latency of the response to median eminence stimulation was approximately equal to that of the response to ipsilateral preoptic area stimulation in four of these sixteen units.6. A characteristic bursting discharge was observed in eleven amygdala units during and after ipsilateral preoptic area stimulation. A transitory inhibition was evoked simultaneously with the bursting discharge in some units. Seven of the eleven units were also tested for median eminence stimulation, and a transitory excitation was observed in each of these units.7. These results suggest the existence of converging synaptic inputs both from tuberoinfundibular neurones and the ipsilateral medial preoptic area to certain amygdala neurones. They also demonstrate the existence of a specific neural pathway mediating a characteristic self-sustained bursting discharge in some amygdala neurones after such stimulation.

Effects of estradiol-induced lesions of the arcuate nucleus on gonadotropin release in response to preoptic stimulation in the rat.

Female Wistar rats treated with a single subcutaneous injection of 2 mg estradiol valerate (EV) develop gradually progressive, multifocal lesions of the arcuate nucleus. They also exhibit vaginal estrus and endocrine profiles characteristic of animals sustaining anterior hypothalamic deafferentation. In this study, EV-treated females with the arcuate lesions released significantly less LH 1 h following electrochemical stimulation of the medial preoptic area (MPOA) than did normally cycling controls in proestrus. FSH release in response to MPOA stimulation was the same for both groups. As plasma LH concentrations were not significantly different between EV-treated and control animals 1 h after the injection of a potent LHRH analog, the reduced LH response to MPOA stimulation appears to reflect a primarily hypothalamic defect. However, the EV treatment also affected pituitary responsiveness to long-term stimulation as evidenced by reduced LH responses to the LHRH analog after 2 and 3 h. No such differences were seen in the FSH response.

Sexual behavior in male rhesus monkeys elicited by electrical stimulation of preoptic and hypothalamic areas

Electrical stimulation of the preoptic area, lateral hypothalamus or dorsomedial nucleus of the hypothalamus (DMH) has produced sexual behavioral responses in 11 male rhesus monkeys. At a short latency following the onset of each train of stimulation, the stimulated males would mount estrogen-treated, receptive females. Quantitative measures of the elicited sexual behavior, in 4 males, were applied to describe differences between the effects of preoptic and DMH stimulation on male sexual performance. As compared to spontaneous sexual activity, stimulation of the DMH produced mounts of longer duration, with more thrusts per mount, higher thrusting rates and a greater number of ejaculations per test session; refractory periods between successive ejaculatory episodes were shortened as a result of stimulation-induced mounting behavior. Preoptic stimulation also induced mounts of longer than normal duration characterized by a slightly increased number of thrusts per mount. In contrast to DMH stimulus effects, however, thrusting rate was decreased significantly by preoptic stimulation and ejaculation did not occur even after multiple stimulus-induced mounts. Penile erections were elicited by stimulation of the anterior hypothalamus, ventromedial nucleus and the posterior hypothalamus in socially isolated or restrained males; however, stimulation of these same sites was ineffective for provoking sexual behavioral responses when tests were performed while the males were paired with receptive females.

Facilitation of the lordosis reflex of female rats from the ventromedial nucleus of the hypothalamus.

1. Effects of electrical stimulation of hypothalamic ventromedial nucleus (v.m.n.) on the lordosis reflex of female rats were examined in ovariectomized and oestrogen-primed animals with chronically implanted electrodes. 2. Lordosis triggered either by manual cutaneous stimulation or by male mounting, was facilitated by electrical stimulation of the v.m.n. 3 A gradual increase in lordosis performance followed a relatively long period of stimulation; never less than 15 min and usually about 1 hr of stimulation was necessary for maximum facilitation. Following the termination of stimulation, the performance returned gradually to the control level during a 5--8 hr period. 4. The optimal frequency of stimulation was between 10 and 30 Hz. Threshold for effective facilitation was, on the average, 12.5 microA. 5. Stimulation tended to induce larger facilitation when applied to the lateral side of v.m.n. 6. Pre-treatment with oestrogen was necessary to obtain facilitation by v.m.n. stimulation. The threshold dosage of oestrogen was 2.5 microgram per animal. 7. Stimulation was effective in adrenalectomized rats, in dexamethasone-primed animals, and in rats pre-treated with exogenous progesterone. Thus, adrenal prodesterone release is not required for the v.m.n. facilitation of lordosis. 8. Medial preoptic stimulation with the same parameters suppressed the lordosis reflex. 9. The v.m.n. participates in the control of lordosis by a facilitatory output. The delay before facilitation implies that the v.m.n. is not in the direct reflex-arc for the execution of lordosis. Rather, a summation or interaction process with an unusually long time course is involved.