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PubMed1990

Pro-gonadotropin-releasing hormone (ProGnRH) and GnRH content in the preoptic area and the basal hypothalamus of anterior medial preoptic nucleus/suprachiasmatic nucleus-lesioned persistent estrous rats.

The content of GnRH and its precursor peptide were quantified in female rats bearing lesions in the anterior medial preoptic nucleus (AMPO) and the suprachiasmatic nucleus (SCN), and the effects of the lesions on the synthetic activity of the GnRH neurons were evaluated. Electrolytic lesions which induced persistent estrous (PE), or irregular estrous cycles, were produced by passing 5-10 microA of direct current into the AMPO or the SCN of female rats which exhibited regular 4 days estrous cycles before the lesions. Approximately 5 weeks after lesion placement, blood samples were withdrawn from catheterized, freely moving animals and plasma LH, PRL, estrogen, and progesterone were determined by RIA. The preovulatory surges of LH and PRL were eliminated in AMPO- or SCN-lesioned PE rats. Moreover, the LH surge was eliminated and the PRL surge significantly attenuated after estrogen and progesterone treatment of rats bearing complete lesions, irrespective of the presence of ovaries. Irregular cycling animals with incomplete AMPO or SCN lesions, exhibited attenuated LH surge and PRL surge similar to proestrous controls. In one incidence this occurred spontaneously, and could also be induced by sequential estrogen and progesterone injections. After ovariectomy, plasma LH levels were significantly lower in the lesioned animals as compared to sham operated rats (P less than 0.05). Similar secretory patterns of LH and PRL were obtained from a second series of sham-operated rats during the different stages of the estrous cycle or from AMPO- or SCN-lesioned rats during persistent estrus. After 2 months the animals were killed between 0830 and 0930 h, and the preoptic area and the basal hypothalamus were microdissected from the brain sections. After extraction and purification, proGnRH and GnRH levels were measured by RIA. ProGnRH levels in the preoptic area were significantly reduced in AMPO- or in SCN-lesioned rats, compared to proestrous controls (P less than 0.01). In contrast, GnRH levels in either area did not differ in AMPO- or in SCN-lesioned animals compared to sham-operated, proestrous controls. Therefore, lesions of the AMPO or the SCN produce PE and reduce proGnRH without reducing GnRH levels. These data would suggest that the AMPO and the SCN participate in the control of the estrous cycle and are necessary for preovulatory surges of PRL and LH to occur and that the AMPO and the SCN form part of the neural circuit that regulates GnRH synthesis and/or release.

Animals↗
PubMed1976

Efferents from medial basal forebrain and hypothalamus in the rat. I. An autoradiographic study of the medial preoptic area.

Efferent projections from the medial and periventricular preoptic area, bed nucleus of the stria terminalis and nuclei of the diagonal band were traced using tritiated amino acid autoradiography in albino rats. Medial and periventricular preoptic area efferents were not restricted to short-axon projections. Ascending projections from the medial preoptic area (mPOA) were traced through the diagonal band into the septum. Descending mPOA axons coursed in the medial parts of the medial forebrain bundle. Projections to most hypothalamic nuclei, including the arcuate nucleus and median eminence, were observed. In the midbrain, mPOA efferents were distributed in the central grey, raphe nuclei, ventral tegmental area and reticular formation. Projections from the mPOA were also observed to the amygdala through the stria terminalis, to the lateral habenula through the stria medullaris, and to the periventricular thalamus. Axons of the most medial and periventricular preoptic area (pvPOA) neurons had a distribution similar to more lateral mPOA neurons but their longest-axoned projections were weaker. The pvPOA did not send axons through the stria medullaris but did project more heavily than the more lateral mPOA to the arcuate nucleus and median eminence. Projections from the bed nucleus of the stria terminalis (nST) were in most respects similar to those from the medial preoptic area, with the major addition of a projection to the accessory olfactory bulb. The nuclei of the diagonal band of Broca (nDBB) gave a different pattern of projections than mPOA or nST, projecting, for instance, to the medial septum and hippocampus. Descending nDBB efferents ran in the ventral portion of the medial forebrain bundle. Among hypothalamic cell groups, only the medial mammillary nuclei received nDBB projections. nDBB efferents also distributed in the medial and lateral habenular nuclei and the mediodorsal thalamic nucleus.

Animals↗
PubMed2003

Location of putative glutamatergic neurons projecting to the medial preoptic area of the rat hypothalamus.

The medial preoptic area is a key structure in the neural control of reproduction. Considerable evidence has accumulated indicating that glutamatergic innervation of the area plays an important role in this control. Sources of the glutamatergic input are unknown. Present investigations were aimed at studying this question. [3H]D-aspartate, which is selectively taken up by high-affinity uptake sites at presynaptic endings that use glutamate or aspartate as a transmitter, and is transported back to the cell body, was injected into the medial preoptic area. The neurons retrogradely labelled with [3H]D-aspartate were detected autoradiographically. Labelled cells were found in several telencephalic and diencephalic structures, but not in the brainstem. Within the telencephalon, labelled neurons were detected in the lateral septum, bed nucleus of the stria terminalis and amygdala. Diencephalic structures included the medial preoptic area itself, hypothalamic paraventricular, suprachiasmatic, ventromedial, arcuate, ventral premammillary, supramammillary and thalamic paraventricular nuclei. All of them are known to project to this area. The findings provide the first neuromorphological data on the location of putative glutamatergic neurons projecting to the medial preoptic area. Furthermore, they indicate that local putative glutamatergic neurons as well as several telencephalic and diencephalic structures contribute to the glutamatergic innervation of the area.

Animals↗
PubMed1994

Activation of shivering and non-shivering thermogenesis by electrical stimulation of the lateral and medial preoptic areas.

Experiments were conducted to determine if the area of stimulation within the preoptic area and/or the magnitude of the electrical stimulus applied to the preoptic region would selectively alter the evoked thermogenic responses of normothermic and hypothermic rats. Urethane anesthetized male, Long-Evans rats kept at 37 degrees C, and later cooled to 34 degrees C, were given unilateral electrical stimulation (0.5 ms pulses of 200 microA at 50 Hz for 30 and 300 s) into either the medial preoptic area (MPO) or the lateral preoptic area (LPO). Temperature changes of intrascapular brown adipose tissue, TIBATs; of gastrocnemius muscle, Tms, tail, Tts and colonic Tcs via thermistor probes were recorded before and after stimulation along with differential, multi-unit EMG activity of the gastrocnemius muscle via implanted stainless steel electrodes. The group kept at 37 degrees C and given MPO electrical stimulations evoked graded increases in TIBATs above core dependent on the duration of the electrical stimulus but shivering did not occur and Tms did not rise. When kept at 34 degrees C the MPO-stimulated group showed greater increases in TIBATs than respective responses seen when the same stimuli were applied at 37 degrees C. The group maintained at 37 degrees C and given LPO stimuli over 300 s increased Tms as shivering occurred, yet no change in TIBATs were observed. When cooled to 34 degrees C LPO stimulation (30 or 300 s duration) showed greater shivering activity. Interesting, LPO stimulation of animals maintained at 34 degrees C also caused TIBAT to increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1993

Origin of noradrenergic projections to GnRH perikarya-containing areas in the medial septum-diagonal band and preoptic area.

The purpose of the present study was to identify the sites of origin of the noradrenergic fibers that project to areas containing gonadotropin-releasing hormone (GnRH) perikarya since norepinephrine (NE) is known to influence the activity of GnRH neurons. Fluorescent retrograde tracers were used in combination with immunohistochemistry for dopamine-beta-hydroxylase (DBH) and GnRH. Small volumes of either Fluoro-gold (FG) or Fluoro-Ruby (FR) were pressure injected into areas that contain the largest number of GnRH cell bodies, i.e., the medical septum-diagonal band complex or preoptic area. Retrogradely labeled neurons were observed ipsilaterally in the following noradrenergic cell groups: A2 (in the nucleus tractus solitarii), A1 (in the ventrolateral medulla) and locus coeruleus. Approximately 8% of all DBH-positive neurons within the A2-cell group were retrogradely labeled, while 12% of DBH-ir neurons in the A1-group were double-labeled. Only a few retrogradely labeled DBH-ir neurons were observed in the locus coeruleus (< 1%). Double-labeled neurons were not organized into discrete cell groups, but were dispersed among other NE-neurons within the A2- and A1-cell groups. The highest concentrations of double-labeled neurons were located in the central one-third of both the A2 and A1 cell groups. The results suggest that most noradrenergic terminals in the region of the GnRH perikarya in the medial septum-diagonal band/rostral preoptic area originate from ipsilateral neurons in areas A1 and A2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Role of noradrenergic fibers of the preoptic area in regulating sleep.

The preoptic area (POA) has noradrenergic (NE) terminals, and this area controls sleep apart from body temperature and reproduction. The destruction of catecholaminergic (CA) terminals in the POA produced a decrease in sleep in rats. This effect was shown to be due to the destruction of NE and not dopaminergic terminals. The rats, which were hyperthermic after the destruction of CA fibers in the POA, preferred a lower ambient temperature. Though they were unable to have normal amount of sleep after lesion, it did not affect their behavioral thermoregulation. Acute total sleep deprivation for 48 h led to a significant decrease in noradrenaline, increase in the level of metabolites of monoamines, and an enhancement in the number of dendritic spines at the medial preoptic area (mPOA). Enhanced sleep pressure during sleep deprivation could have led to a higher release of noradrenaline, and an increase in dendritic spines in the mPOA. Arousal was produced by application of noradrenaline at the mPOA, whereas the alpha antagonists produced sleep in free-moving rats. This was in contrast to the increased wakefulness produced by the destruction of NE terminals. As wakefulness and sleep, respectively, were induced on local application of alpha-2 antagonist and agonists, it was suspected that the noradrenaline and alpha antagonists might have acted on the alpha-2 receptors, which are predominantly present on the pre-synaptic terminals. Sleep produced by noradrenaline, which was locally applied at the mPOA, after destroying the NE terminals, further confirmed this possibility. Hypothermia and sexual arousal produced by application of alpha- and beta-adrenergic agonists at the mPOA would have contributed towards the wakefulness induced by these drugs in normal rats. Thus, the available evidence shows that the NE fibers in the POA are involved in the induction of sleep.

Adrenergic Agonists↗
PubMed1998

Confocal laser scanning and electron-microscopic analyses of the relationship between VIP-like and GnRH-like-immunoreactive neurons in the lateral septal-preoptic area of the pigeon.

The lateral septum and the preoptic area of birds comprise neurons immunoreactive (ir) for vasoactive intestinal polypeptide (VIP) and gonadotropin-releasing hormone (GnRH). By use of immunohistochemical single- and double-labeling techniques, we have investigated the distribution and the connections of these two types of peptidergic neurons in the lateral septal-preoptic area of the pigeon at both the light- and electron-microscopic levels. An accumulation of VIP-like-ir neurons, some of which are cerebrospinal fluid-contacting neurons, is found in the area adjacent to the ventromedial walls of the lateral ventricles in the lateral septum corresponding to the medial part of the lateral septal organ. VIP-like-ir terminals are scattered throughout the lateral septal-preoptic area, which also contains GnRH-like-ir cell bodies. The number of GnRH-like-ir cell bodies in the lateral septum is smaller than that of the VIP-like-ir neurons. GnRH-like-ir cells have a simple bipolar or multipolar shape and a beaded axon that emerges from the soma or one of the proximal dendrites. Confocal laser scanning microscopy has shown VIP-like-ir terminals in close apposition to GnRH-like-ir cell bodies in the lateral septal-preoptic area. Furthermore, the electron-microscopic double-immunolabeling has revealed synaptic contacts between VIP-like-ir axon terminals and GnRH-like-ir cell bodies or dendrites. These contacts, however, do not show synaptic specializations. The present results suggest that functional interactions take place between VIP and GnRH neurons in the lateral septal-preoptic area of the pigeon and that these interactions are involved in mediating photoperiodic responses.

Animals↗
PubMed1987

Anatomical and electrophysiological evidence for a projection from the medial preoptic area to the 'mesencephalic and subthalamic locomotor regions' in the rat.

There is considerable physiological evidence indicating that the medial preoptic area plays an important role in neural circuits mediating ingestive, thermoregulatory, and reproductive behaviors, all of which involve foraging. The current series of anatomical and electrophysiological experiments was therefore designed to characterize a direct projection from the medial preoptic area to a region in the zona incerta just dorsal to the subthalamic nucleus, which appears to lie within the 'subthalamic locomotor region', and to the pedunculopontine nucleus, which lies within the 'mesencephalic locomotor region'. First, implants of the fluorescent tracer True blue were placed in the pedunculopontine nucleus, and retrogradely labeled neurons were consistently found in dorsal regions of the medial preoptic nucleus, anteroventral preoptic nucleus, rostral tip of the medial preoptic area, lateral parts of the medial preoptic area, and median preoptic nucleus. Second, combined retrograde-immunostaining experiments indicated that a small number of galanin-stained neurons in the rostral tip of the medial preoptic area project to the pedunculopontine nucleus, whereas in nearby regions some galanin- or neurotensin-stained neurons in the lateral preoptic area, and some neurotensin-stained neurons in the substriatal gray appear to project to the pedunculopontine nucleus, as do some neurotensin- or corticotropin releasing factor (CRF)-stained cells in the bed nucleus of the stria terminalis. Third, injections of the anterograde tracer Phaseolus vulgaris leukoagglutinin (PHA-L) into various parts of the medial preoptic area all labeled axons with terminal boutons in the caudal zona incerta and pedunculopontine nucleus. Fourth, single-pulse stimuli were delivered to the zona incerta and pedunculopontine nucleus and the location of antidromically activated neurons in the medial preoptic area was mapped using extracellular recordings. Somewhat less than one-third of the cells recorded from in the medial preoptic area were antidromically activated from either site and some 14% were influenced from both sites. The application of a reciprocal collision test to a small number of neurons suggested that at least some neurons in the medial preoptic area may send collaterals to both sites. And fifth, injections of procaine into the zona incerta were shown to block the antidromic activation of medial preoptic neurons by single-pulse stimulation of the pedunculopontine nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Orexin A (hypocretin-1) application at the medial preoptic area potentiates male sexual behavior in rats.

The medial preoptic area plays an important role in the regulation of male sexual behavior in rats, and this area receives orexinergic inputs. The role of orexinergic inputs in the medial preoptic area in sexual behavior has not been studied, though they have been shown to play a role in some other physiological functions. In this study, the changes in male sexual behavior in rats were studied after local injection of orexin A (Hypocretin-1) at the medial preoptic area. The results of the study showed that orexin A application at the medial preoptic area increased sexual arousal as well as the copulatory performance. Sexual arousal is one of the physiological stimuli, which influences wakefulness. It is possible that the earlier reports showing increased wakefulness, on application of orexin A at the medial preoptic area/basal forebrain, has a contribution from sexual arousal.

Animals↗
PubMed2006

Homeostatic regulation of sleep: a role for preoptic area neurons.

The median preoptic nucleus (MnPN) and the ventrolateral preoptic area (vlPOA) contain putative sleep-regulatory neurons that exhibit elevated discharge rates during sleep compared with waking. Expression of c-Fos protein immunoreactivity (IR) in GABAergic neurons in the MnPN and the vlPOA is high in spontaneously sleeping rats and in rats undergoing recovery sleep after sleep deprivation. However, it is unclear whether c-Fos-IR in these neurons is evoked by increases in sleep pressure or by increases in sleep amount. We examined c-Fos-IR in MnPN and vlPOA neurons under experimental conditions that dissociated homeostatic sleep pressure, sleep amount, and time of day. Groups of rats with strong diurnal rhythms in sleep-wake organization were killed after (1) spontaneous sleep in the light, (2) spontaneous sleep in the dark, (3) sleep deprivation (SLD) in the light and (4) recovery sleep after SLD in the light. Numbers of GABAergic neurons expressing c-Fos-IR in the MnPN were significantly higher after SLD in the light compared with spontaneous sleep and recovery sleep in the light. In contrast, Fos-IR in vlPOA GABAergic neurons was most prevalent after spontaneous sleep and recovery sleep in the light. No light-dark differences in Fos-IR were observed in the MnPN after SLD in groups of rats with weak or absent diurnal sleep-waking rhythms. Our findings define potential roles for MnPN and vlPOA GABAergic neurons in homeostatic aspects of sleep regulation.

Animals↗
PubMed1989

AMPA, kainic acid, and N-methyl-D-aspartic acid stimulate locomotor activity after injection into the substantia innominata/lateral preoptic area.

The substantia innominata/lateral preoptic area (SI/LPO) is a subpallidal region which has been shown to regulate the hypermotility produced by drugs acting in the nucleus accumbens. Evidence has been presented that the SI/LPO contains glutamatergic nerve terminals and receptors for excitatory amino acids. The purpose of this study was to determine the effects of the activation of excitatory amino acid receptors in the SI/LPO on locomotor activity following the direct injection of excitatory amino acids into this brain site. It was found that the bilateral injection of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA), kainic acid, and N-methyl-D-aspartic acid into the SI/LPO produced marked dose-dependent stimulations of locomotor activity which resembled the effects of these agents after their injection into the nucleus accumbens. The effect, however, was bell-shaped in that at high doses, the locomotor activity values decreased from their peak values. The coinjection of gamma-glutamylaminomethylsulfonate (GAMS) with AMPA into the SI/LPO was found to inhibit the hypermotility response to AMPA at doses that were unable to produce a significant inhibition of the hypermotility responses to kainic acid or N-methyl-D-aspartic acid. The injection of 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the SI/LPO inhibited the hypermotility responses to AMPA or kainic acid while having no significant inhibitory effect on N-methyl-D-aspartic acid stimulated locomotor activity. The injection of D-alpha-aminoadipic acid into the SI/LPO produced a significant inhibition of the hypermotility response produced by N-methyl-D-aspartic acid at a dose that did not produce a significant inhibition of the hypermotility response produced by AMPA.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Aminoadipic Acid↗
PubMedDate not supplied

A direct dopaminergic control of aromatase activity in the quail preoptic area.

In the quail preoptic area (POA) anatomical and pharmacological data suggest that catecholamines may be implicated in the control of testosterone (T) aromatization into estrogens. The biochemical mechanism(s) mediating this control of the enzyme activity is (are) however unexplored. The present studies were carried out to investigate whether the catecholamines, dopamine (DA) and norepinephrine (NE) are able to directly affect aromatase activity (AA) measured during in vitro incubations of POA homogenates. AA was quantified in the POA-hypothalamus of adult male Japanese quail by measuring the tritiated water production from [1beta-3H]-androstenedione. Enzyme activity was linear as a function of the incubation time and of the protein content of homogenates. It exhibited a typical Michaelis-Menten kinetics, with an apparent Km of 2.8 nM and a Vmax of 266.6 fmol h(-1) mg wet weight(-1). AA was then measured at a substrate concentration of 25 nM in the presence of catecholamines and some of their receptor agonists or antagonists, at two concentrations, 10(-3) and 10(-6) M. Norepinephrine and prazosin (alpha1-adrenergic antagonist) had no or very limited effects on AA at both concentrations. In contrast, DA and some D1 and/or D2 receptor agonists (apomorphine[D1/D2], SKF-38393 [D1] and RU-24213 [D2]) depressed AA by 40 to 70% at the 10(-3) M concentration. One D2 receptor antagonist also produced a major inhibition of AA (sulpiride) while other antagonists either had no significant effect or only produced moderate decreases in enzyme activity (SCH-23390 [D1], spiperone [D2], pimozide [D2]) as did two DA indirect agonists, amfonelic acid and nomifensine. The inhibitory effect of the agonists was not antagonized by the less active antagonists, SCH-23390 [D1] or spiperone [D2]. Taken together these results suggest that the inhibitory effects do not involve specific binding of DA or its agonists/antagonists to dopaminergic receptors mediating changes in cAMP concentration. This conclusion is also supported by the observation that addition of dibutyryl cAMP did not change brain AA. It appears more likely that DA and dopaminergic drugs inhibit AA by a direct effect on the enzyme, as suggested by the competitive nature of DA and SKF-38393 inhibition of AA (Ki's of 59 and 84 microM, respectively). The functional significance of this effect should still be demonstrated but this mechanism may represent an important physiological pathway through which neurotransmitters could rapidly affect steroid-dependent processes such as the neural synthesis of estrogens. This would provide a mean by which environmental stimuli could affect reproductive behavior and physiology.

Animals↗
PubMed1994

Testosterone effects on neurotensin-immunoreactive cells in the quail preoptic area.

In the quail preoptic area (POA), neurotensin-immunoreactive (NT-ir) cells are mostly located in the sexually dimorphic medial preoptic nucleus (POM). They are more numerous in females than in males and, in females, their number varies during the ovulatory cycle. This suggests a control by steroids of NT expression in the POA. This idea was tested by comparing the NT-ir populations in gonadectomized males and females treated or not with testosterone. No sex differences in the NT-ir cell number was present in gonadectomized birds. Testosterone treatment increased the number of immunoreactive perikarya. This effect was anatomically specific and the increase was observed in the area caudal to the anterior commissure but not in POM itself.

Animals↗
PubMed1989

Neurons of origin and fiber trajectory of amygdalofugal projections to the medial preoptic area in Syrian hamsters.

The amygdaloid neurons of origin and the trajectory of amygdaloid fibers to the medial preoptic area of the adult male Syrian hamster were identified by using horseradish peroxidase (HRP) histochemistry. After iontophoresis of HRP into the medial preoptic area, retrogradely labeled amygdaloid neurons were located in the dorsal and caudal parts of the medial amygdaloid nucleus and throughout the amygdalohippocampal area. No amygdaloid neurons were labeled after HRP applications confined to the most rostral portion of the medial preoptic area (anterior to the body of the anterior commissure). Following more caudal medial preoptic area injections (body of the anterior commissure to the suprachiasmatic nucleus) the distribution of retrogradely labeled cells in the medial amygdaloid nucleus and the amygdalohippocampal area revealed no topographic organization of the amygdalopreoptic connections. When amygdaloid neurons were labeled, the amygdalohippocampal area contained two to five times as many HRP-filled cells as the medial amygdaloid nucleus. Retrogradely transported HRP could be followed from the medial preoptic area to the amygdala through fibers in the dorsomedial quadrant of the stria terminalis. In addition, electrolytic lesions of the stria terminalis prior to iontophoresis of HRP into the medial preoptic area prevented retrograde transport to neurons in both the dorsocaudal medial amygdaloid nucleus and the amygdalohippocampal area. These results confirm earlier observations describing the location of autoradiographically labeled efferents from the medial amygdaloid nucleus to the medial preoptic area and provide new information about the restricted region within the medial amygdaloid nucleus from which these projections arise. They also suggest that, unlike the projections from the medial amygdaloid nucleus to the bed nucleus of the stria terminalis, the efferents to the medial preoptic area travel entirely in the stria terminalis.

Amygdala↗
PubMed1980

The preoptic area of the domestic fowl. I. A Golgi study.

The preoptic area of the domestic fowl (Gallus gallus) was studied by means of the Golgi technique. At least two regions can be recognized: (i) a medial and (ii) a lateral area, clearly distinguishable laterally from the adjacent telencephalic regions. The dendritic organization of the preoptic area is quite uniform. The neurons can be classified as isodendritic elements. The magnocellular elements are few and irregularly scattered mostly in the periventricular grey of the medial preoptic area. Of relevant interest is also the observation of some bipolar and horizontal neurons in the dorsal part of the medial preoptic area, near the anterior commissure.

Animals↗
PubMed1987

Development of the preoptic area: time and site of origin, migratory routes, and settling patterns of its neurons.

Neurogenesis and morphogenesis in the rat preoptic area were examined with [3H]thymidine autoradiography. For neurogenesis, the experimental animals were the offspring of pregnant females given an injection of [3H]thymidine on two consecutive gestational days. Nine groups were exposed to [3H]thymidine on embryonic days E13-E14, E14-E15, E21-E22, respectively. On postnatal day P5, the percentage of labeled cells and the proportion of cells originating during 24-hr periods were quantified at four anteroposterior levels in the preoptic area. Throughout most of the preoptic area there is a lateral to medial neurogenetic gradient. Neurons originate between E12-E15 in the lateral preoptic area, between E13-E16 in the medial preoptic area, between E14-E17 in the medial preoptic nucleus, and between E15-E18 in the periventricular nucleus. These structures also have intrinsic dorsal to ventral neurogenetic gradients. There are two atypical structures: (1) the sexually dimorphic nucleus originates exceptionally late (E15-E19) and is located more lateral to the ventricle than older neurons; (2) in the median preoptic nucleus, where older neurons (E13-E14) are located closer to the third ventricle than younger neurons (E14-E17). For an autoradiographic study of morphogenesis, pregnant females were given a single injection of [3H]thymidine during gestation, and their embryos were removed either two hrs later (short survival) or in successive 24-hr periods (sequential survival). Short-survival autoradiography was used to locate the putative neuroepithelial sources of preoptic nuclei, and sequential survival autoradiography was used to trace the migratory waves of young neurons and their final settling locations. The preoptic neuroepithelium is located anterior to and in the front wall of the optic recess. The neuroepithelium lining the third ventricle is postulated to contain a mosaic of spatiotemporally defined neuroepithelial zones, each containing precursor cells for a specific structure. The neuroepithelial zones and the migratory waves originating from them are illustrated. Throughout most of the preoptic area, neurons migrate predominantly laterally. The older neurons in the lateral preoptic area migrate earlier and settle adjacent to the telencephalon. Younger neurons migrate in successively later waves and accumulate medially. The sexually dimorphic neurons are exceptional since they migrate past older cells to settle in the core of the medial preoptic nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1980

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.

Afferent Pathways↗
PubMed1997

Chronic gestational cocaine treatment decreases oxytocin levels in the medial preoptic area, ventral tegmental area and hippocampus in Sprague-Dawley rats.

We examined the effects of gestational cocaine treatment on oxytocin levels in the whole hippocampus (HIP), ventral tegmental area (VTA), medial preoptic area (MPOA) and amygdala (AMY) in rat dams on postpartum days (PPDs) 1 and 2. Cocaine treatment significantly reduced oxytocin levels in the MPOA within 12-16 h of delivery (PPD 1), but had no significant effect on the other brain areas. Oxytocin was significantly reduced in the HIP and VTA but not in the AMY or MPOA on PPD 2. These data provide the first evidence for the reduction of oxytocin levels in the VTA, HIP and MPOA as a result of gestational cocaine treatment.

Amygdala↗