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PubMed1987

Selective enhancement of shock avoidance responding elicited by GABA blockade in the posterior hypothalamus of rats.

Recent studies have shown that blockade of gamma-aminobutyric acid (GABA) in the posterior hypothalamus in anesthetized rats elicits cardio-respiratory stimulation similar to that seen in emotional defense reactions and, in conscious rats, locomotor arousal suggesting a flight response. The present study was conducted in order to test the hypothesis that the behavioral effects elicited by GABA blockade in the posterior hypothalamus were the results of disinhibiting a mechanism whose activation selectively enhances reactivity to aversive stimuli. Male rats were trained on a Sidman shock avoidance schedule (RS20:SS10) as well as a food-reinforced approach schedule (VI 1). Under anesthesia, guide cannulae were stereotaxically implanted bilaterally in the posterior hypothalamus at sites where microinjection of the GABA antagonist, bicuculline methiodide (BMI) 25 ng, increased heart rate. After recovery, rats were tested in both the avoidance and VI 1 schedules after hypothalamic microinjection of saline, BMI 25 ng, and the GABA agonist, muscimol 25 ng. Microinjection of BMI significantly increased the avoidance responses but had no effect on the approach responses. Muscimol decreased both the avoidance and approach responses. When microinjected into the lateral hypothalamic area, BMI had no effect on the response rates in either schedule while muscimol decreased the approach responding only. Therefore, GABA blockade at the discrete area of the posterior hypothalamic nucleus appears to elicit a selective enhancement of avoidance responses. These results suggest that an endogenous GABAergic system in the posterior hypothalamus may tonically inhibit a constellation of autonomic, locomotor and motivational responses that are necessary for some types of defense reaction.

Animals↗
PubMed1988

Microinjection of GABA antagonists into the posterior hypothalamus elicits locomotor activity and a cardiorespiratory activation.

It is well known that electrical stimulation of an area (subthalamic locomotor region, STLR) of the posterior hypothalamus evokes locomotion as well as increases in cardiorespiratory activity. Uncertainty exists over whether these responses are due to stimulation of STLR neurons or to activation of fibers of passage originating outside this area. The purpose of the present study was to determine if stimulation of STLR neurons alone would elicit the cardiorespiratory and locomotor responses. Neurons were stimulated by microinjections of gamma-aminobutyric acid (GABA) antagonists (picrotoxin and bicuculline) into the posterior hypothalamus of anesthetized cats. Both picrotoxin and bicuculline produced increases in arterial pressure, heart rate and minute ventilation which were accompanied by locomotor movements of the limbs. Increases in arterial pressure, heart rate and phrenic nerve activity were also caused by picrotoxin microinjections in paralyzed, ventilated cats. Microinjections of GABA or a GABA agonist (muscimol) reversed all of these responses. In contrast, microinjection of GABA or muscimol into the STLR without a prior antagonist injection had only small, transient effects upon cardiorespiratory activity. However, microinjection of muscimol prevented the responses to a subsequent injection of bicuculline. These results indicate that: (1) stimulation of cell bodies alone in the subthalamic locomotor region of the hypothalamus produces all the cardiorespiratory and locomotor responses evoked by electrical stimulation; (2) the responses evoked by picrotoxin and bicuculline are due to an interaction with GABA receptors and (3) a GABAergic mechanism exerts a tonic depressive influence over the cardiorespiratory and locomotor systems by an action in the posterior hypothalamus.

Animals↗
PubMed1988

The antihypertensive effect of ethylcholine aziridinium (AF64A), a cholinergic neurotoxin, in spontaneously hypertensive rats, following administration into the posterior hypothalamus.

The aim of this study was to ascertain whether drug-induced cholinergic hypofunction in the posterior hypothalamus would affect the development and the maintenance of hypertension in hypertensive rats. Spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats were treated with AF64A, a neurotoxin which can irreversibly inhibit cholinergic transmission in vivo. AF64A or saline was injected bilaterally into the posterior hypothalamus of rats of two age groups: normotensive one month-old rats whose blood pressure was subsequently measured at the age of three months and hypertensive three month-old rats, whose blood pressure was measured four weeks later. In both age groups there was a significant fall in mean arterial blood pressure in SHR but not WKY rats. In SHR injected at the age of one month, there was a fall of at least 15.9 mm Hg, while in the rats injected at the age of three months there was a fall of 14.3 mm Hg. Heart rate in either strain was not affected. When AF64A was injected into the anterior hypothalamus of one month-old SHR, no antihypertensive effect was observed in these rats at the age of three months. These results show that cholinergic stimulation in the posterior hypothalamus may play a role in both the development and maintenance of hypertension in SHR.

Animals↗
PubMed1983

Corticoliberin-immunoreactive cell bodies localised in two distinct areas of the sheep hypothalamus.

The localisation of corticoliberin producing neurones in the sheep hypothalamus was attempted with an antiserum directed against synthetic ovine CRF by the indirect immunofluorescence procedure. Synthetic ovine corticoliberin-immunoreactive fibres were detected, in order of decreasing importance, in the external median eminence, in the caudal neural lobe around capillaries, at the boundary of the neural and intermediate lobe, around the anterior commissure, in the paraventricular nuclei and in the posterior hypothalamus and midbrain, suggesting that synthetic ovine corticoliberin-related substances act not only on anterior pituitary tissue, but also on the intermediate lobe, on central neurones and on peripheral target organs. Two groups of cell bodies reacted to the anti-synthetic ovine corticoliberin antiserum. The first group was located in the paraventricular nuclei and consisted of 15-20 microns diameter cell bodies with a granular cytoplasm. The second group was located mainly in the dorsolateral caudal hypothalamus, and the cell bodies were smaller (10-15 microns) and had a smooth cytoplasm. No cell bodies were detected in the basal hypothalamus). Synthetic ovine corticoliberin-immunoreactive structures did not contain immunoreactive neurophysin. The synthetic ovine corticoliberin-immunoreaction in the paraventricular neurones was abolished by preincubating the antiserum with synthetic ovine corticoliberin but not with sauvagine or several other peptides. The immunoreaction in the posterior hypothalamic groups was abolished by preincubating the synthetic ovine corticoliberin antiserum with both synthetic ovine corticoliberin and sauvagine, but not with other peptides. The results suggest that the immunoreaction was specific for synthetic ovine corticoliberin in the paraventricular but not posterior hypothalamic region. The relative contribution of both areas to synthetic ovine corticoliberin-like peptides containing nerve terminals of the median eminence remains to be established.

Animals↗
PubMed1989

Long-lasting insomnia induced by preoptic neuron lesions and its transient reversal by muscimol injection into the posterior hypothalamus in the cat.

In order to analyse the role of the anterior hypothalamus in the regulation of the sleep-waking cycle we made bilateral neuronal lesions at different levels of the anterior hypothalamus in cats, by means of microinjections of a cell-specific neurotoxin:ibotenic acid. These lesions resulted in severe insomnia in eight cats. This insomnia was characterized by a large decrease or even disappearance of paradoxical sleep and deep slow wave sleep and, to a lesser extent, by a decrease of light slow wave sleep, for 2-3 weeks. In the other five animals, we observed a large reduction of deep slow wave sleep (0-40% of control level), but a less intensive decrease of time spent in paradoxical sleep (50-75% of control level) and no marked effect on light slow wave sleep. During the first 3-6 postoperative days we also noticed hyperthermia in all cats; thereafter, the animals presented only a slight increase in brain temperature which did not appear to trigger the sleep impairment. Histological analysis of the different lesions revealed that the insomnia could be attributed to neuronal cell body destruction in the mediobasal part of the anterior hypothalamus covering; the medial preoptic area and a narrow portion of the lateral preoptic area as well as a restricted part of the anterior hypothalamic nucleus. In order to investigate the putative role of the posterior hypothalamic structures in the mechanism of insomnia after lesion of the mediobasal preoptic area neurons we injected an agonist of GABA into the ventrolateral part of the posterior hypothalamus to locally depress the neuronal activity. The bilateral intracerebral microinjection of muscimol (0.5-5 micrograms) induced a transient intensive hypersomnia (slow wave sleep and paradoxical sleep). These findings indicate that neuronal cell loss in the mediobasal preoptic area induced a long lasting insomnia. Thus, it may be hypothesized that the integrity of this structure is necessary for sleep appearance. Finally, our data are in keeping with an intrahypothalamic regulation of the sleep-waking cycle.

Animals↗
PubMed1988

A GABAergic mechanism in the posterior hypothalamus modulates baroreflex bradycardia.

Several laboratories have shown that electrical stimulation in the posterior hypothalamus inhibits the baroreceptor reflex. However, the results of these studies are difficult to interpret since it is not known if the attenuation of the baroreflex results from activation of axons of passage or from stimulation of hypothalamic cell bodies. The purpose of this study was to determine the effects of chemical stimulation of posterior hypothalamic neurons upon the baroreflex. Arterial baroreceptors were activated by increasing the pressure in an isolated carotid sinus in anesthetized cats and by an increased arterial pressure following intravenous injection of phenylephrine in both anesthetized cats and rats. The baroreceptor reflex was evaluated before and after a GABA antagonist (picrotoxin) was microinjected into the posterior hypothalamus. The bradycardia, but not the depressor response, elicited by increasing carotid sinus pressure was attenuated after unilateral microinjections of picrotoxin into the posterior hypothalamus. In addition, the heart rate response to a phenylephrine-evoked rise in arterial pressure was reduced after picrotoxin was microinjected in both the cats and the rats. Microinjection of a GABA agonist (muscimol) into the same hypothalamic site returned resting heart rate and arterial pressure to levels seen prior to picrotoxin. These results show that the depression of the bradycardia produced by hypothalamic stimulation results from activation of cell bodies in the posterior hypothalamus. This hypothalamic effect upon the baroreflex bradycardia may involve a GABAergic mechanism.

Animals↗
PubMed1993

Augmented neuronal activity in the hypothalamus of spontaneously hypertensive rats.

Previous studies indicate a tonic GABAergic inhibitory mechanism in the posterior hypothalamus (PH) contributes to modulating cardiovascular activity. Blockade of GABA receptors on neurons in this area elicits an increase in sympathetic discharge, arterial pressure, and heart rate. It has been proposed that a deficit in this inhibitory system may be responsible for the elevated pressure in the spontaneously hypertensive rat (SHR). The purpose of this study was to determine if the spontaneous neuronal activity in the posterior hypothalamus of spontaneously hypertensive rats differs from that of age-matched normotensive Wistar-Kyoto rats (WKY). Single unit, extracellular recordings of posterior hypothalamic neurons were performed on both in vivo and in vitro preparations. The spontaneous firing rate of posterior hypothalamic neurons in the anesthetized adult SHR was significantly higher (3.66 +/- 0.55 Hz) compared to that of the anesthetized adult WKY rat (2.11 +/- 0.29 Hz). Moreover, more of the neurons in the anesthetized SHR (38%) had a bursting discharge pattern than in the WKY (16%). In order to exclude inputs from peripheral receptors or other brain areas, an in vitro preparation was used. Neurons from both young and adult SHRs also had an increased spontaneous discharge rate and higher percentage of burster-type cells in the posterior hypothalamus compared to neurons from age-matched WKYs in the brain slice preparation. Both the in vivo and in vitro findings support the possibility that an elevated neuronal activity in the posterior hypothalamus, a known pressor area, of the SHR contributes to the development and/or maintenance of hypertension in this animal model.

Aging↗
PubMed1994

A three-dimensional reconstruction of the human hypothalamus.

A previous three-dimensional reconstruction of the rat hypothalamus revealed an organization of nuclei into three major clusters. This clustering may relate to the presence of three hypothalamic anlagen in the embryo and to a restriction of marker proteins and transcription factors to specific regions of the hypothalamus during development. To see if a similar clustering was apparent in the human hypothalamus, a reconstruction of the hypothalamus from a male cadaver was prepared. The reconstruction showed a clustering of nuclei into three anterior-posterior groups. With reference to the well-defined human supraoptic nucleus, the suprachiasmatic and lateral mammillary nuclei were proportionately smaller in this single human specimen than would be expected from data in the rat. A high degree of homology between hypothalamic structures in the rat and human were generally observed.

Animals↗
PubMed1997

Participation of the medial and anterior hypothalamus in the modulation of tonic immobility in guinea pigs.

Tonic immobility (TI) is an inhibitory behavioral response during which the animal presents profound physical inactivity and a relative lack of response to the environment. This response is induced in the laboratory by postural inversion of the animal and brief postural contention of its movements. In nature, the response occurs when there is physical contact between prey and predator. In this case, the physical inactivity of the prey may prevent the continuation of the attack. The neural substrate of this response is not well known and the objective of the present study was to investigate the effect of cholinergic stimulation of hypothalamic regions on TI modulation in guinea pigs (Cavia porcellus). Microinjection of carbachol (1.0 microg/0.2 microL) into the anterior hypothalamus promoted an increase in the duration of TI episodes. Microinjection of carbachol into the ventro- and dorsomedial hypothalamus, however, promoted a reduced duration of TI episodes. Pretreatment with atropine (0.5 microg/0.2 microL) showed that the action of carbachol is mediated by muscarinic receptors in the anterior and ventromedial hypothalamus but not in the dorsomedial hypothalamus. The results suggest that the hypothalamic regions may play different roles in the organization of defensive behavioral responses such as TI.

Animals↗
PubMed1991

Locomotor sites mapped with low current stimulation in intact and kainic acid damaged hypothalamus of anesthetized rats.

To determine whether local neurons mediated the locomotor effects of electrical stimulation of the lateral hypothalamus, kainic acid injections (0.5-1.25 micrograms), intended to destroy neural somata as opposed to fibers of passage, were made unilaterally in the tuberal-posterior hypothalamus of 22 rats. The area of lesion and its contralateral homolog were mapped for locomotor stepping sites in Nembutal-anesthetized rats mounted in a stereotaxic apparatus such that locomotor stepping rotated a wheel. Stimulation (25 and 50 microA, 50 Hz, 0.5-ms cathodal pulses, 10-s trains) was delivered through 50-80 microns glass pipettes filled with 2 M saline. Contralateral to the lesion, locomotor stepping sites were common in the perifornical lateral and medial hypothalamus and less dense in the zona incerta. On the side of the kainic-acid lesion, locomotor sites were generally absent in the central part of the damaged area. If they did appear within the area of lesion, they tended to be near the border with intact tissue. In a few cases, locomotor stepping sites were found centrally located in the lesion amidst widespread loss of somata. In four rats, additional maps of anterior locomotor regions in the preoptic area ipsilateral to the lesion suggested that their descending fibers were largely spared by the kainic lesions. Local neurons appear to be major contributors to the locomotion elicited by electrical stimulation of the lateral hypothalamus, but fibers of passage may also participate.

Anesthesia↗
PubMed2003

Different electroclinical manifestations of the epilepsy associated with hamartomas connecting to the middle or posterior hypothalamus.

PURPOSE: The epilepsy associated with hypothalamic hamartomas (HHs) has typical clinical, electrophysiologic, and behavioral manifestations refractory to drug therapy and with unfavorable evolution. It is well known that only sessile lesions produce epilepsy, but no correlation has been established between the different types of sessile hamartomas and the diverse manifestations of the epilepsy. We correlate anatomic details of the hamartoma and the clinical and neurophysiologic manifestations of the associated epilepsy. METHODS: HHs of seven patients with epilepsy (ages 2- 25 years) were classified as to lateralization and connection to the anteroposterior axis of the hypothalamus by using high-resolution brain magnetic resonance imaging. We correlated the anatomic classification with the clinical and neurophysiologic manifestations of the epilepsy as evaluated in long-term (24 h) video-EEG recordings. RESULTS: HHs ranged in size from 0.4 to 2.6 cc, with complete lateralization in six of seven patients. Ictal manifestations showed good correlation with the lobar involvement of ictal/interictal EEGs. These manifestations suggest the existence of two types of cortical involvement, one associated with the temporal lobe, produced by hamartomas connected to the posterior hypothalamus (mamillary bodies), and the other associated with the frontal lobe, seen in lesions connecting to the middle hypothalamus. CONCLUSIONS: A consistent clinical and neurophysiologic pattern of either temporal or frontal lobe cortical secondary involvement was found in the patients of our series. It depends on whether the hamartoma connects to the mamillary bodies (temporal lobe cases) or whether it connects to the medial hypothalamus (frontal lobe cases).

Adolescent↗
PubMed1990

Involvement of transforming growth factor alpha in the release of luteinizing hormone-releasing hormone from the developing female hypothalamus.

Little is known about the presence of trophic factors in the hypothalamus and the role they may play in regulating the functional development of hypothalamic neurons. We have investigated the ability of epidermal growth factor (EGF) and transforming growth factor alpha (TGF-alpha) to affect the release of luteinizing hormone-releasing hormone (LHRH), the neuropeptide that controls reproductive development. We have also determined whether the genes encoding EGF and TGF-alpha are expressed in the prepubertal female hypothalamus. Northern blot analysis of poly(A)+ RNA utilizing a single-stranded EGF cDNA probe failed to reveal the presence of EGF mRNA in either the hypothalamus or the cerebral cortex at any age studied (fetal day 18 to postnatal day 36). In contrast, both a complementary RNA probe and a double-stranded TGF-alpha cDNA recognized in these regions a 4.5-kilobase (kb) mRNA species identical to TGF-alpha mRNA. The abundance of TGF-alpha mRNA was 3-4 times greater in the hypothalamus than in the cerebral cortex. Both EGF and TGF-alpha (2-100 ng/ml) elicited a dose-related increase in LHRH release from the median eminence of juvenile rats in vitro. They also enhanced prostaglandin E2 (PGE2) release. The transforming growth factors TGF-beta 1 and -beta 2 were ineffective. Only a high dose of basic fibroblast growth factor was able to increase LHRH and PGE2 release. Blockade of the EGF receptor transduction mechanism with RG 50864, a selective inhibitor of EGF receptor tyrosine kinase activity, prevented the effect of both EGF and TGF-alpha on LHRH and PGE2 release but failed to inhibit the stimulatory effect of PGE2 on LHRH release. Inhibition of prostaglandin synthesis abolished the effect of TGF-alpha on LHRH, indicating that PGE2 mediates TGF-alpha-induced LHRH release. The results indicate that the effect of EGF and TGF-alpha on LHRH release is mediated by the EGF/TGF-alpha receptor and suggest that TGF-alpha rather than EGF may be the physiological ligand for this interaction. Since in the central nervous system most EGF/TGF-alpha receptors are located on glial cells, the results also raise the possibility that--at the median eminence--TGF-alpha action may involve a glial-neuronal interaction, a mechanism by which the trophic factor first stimulates PGE2 release from glial cells, and then PGE2 elicits LHRH from the neuronal terminals.

Aging↗
PubMed1997

Reciprocal talk between the auditory thalamus and the hypothalamus: an antidromic study.

In this study we sought to validate physiologically the hypothalamus afferent projections from the auditory thalamus previously identified with tract tracing techniques in the ring dove. In total, we recorded the responses of 628 units in the nucleus ovoidalis (Ov) and its shell region to electrical stimulation applied to anterior hypothalamus and ventromedial nucleus. Ninety-six acoustic units in the shell region displayed good antidromic responses, confirming this region's axonal projections into these nuclei of the hypothalamus. Orthodromic responses (143 units) recorded in the Ov-Ov shell region suggest on the other hand reciprocal projections from the hypothalamus back to the auditory thalamus.

Afferent Pathways↗
PubMed1994

Adenylyl cyclase mRNA expression does not reflect the predominant Ca2+/calmodulin-stimulated activity in the hypothalamus.

Only three (Types I, II, V) of the six currently-described subtypes of adenylyl cyclase are prominently expressed in the rat brain. These species are differently sensitive to Ca2+, beta gamma subunits of G-proteins and protein kinase C. A knowledge of the susceptibility of the cAMP-signalling system in particular brain regions to these diverse modes of regulation can shed light on the mechanism of action of the neurotransmitters that modify neuronal activity in such regions. Cyclic AMP is extensively involved in the physiological functions of the hypothalamus. We have used in situ hybridization histochemistry with synthetic oligonucleotides to examine the expression in the rat hypothalamus of the three major brain subtypes of adenylyl cyclase-Ca2+/calmodulin-stimulable (Type I), Ca(2+)-insensitive (Type II) and Ca(2+)-inhibitable (Type V). The hypothalamus expresses high levels only of Type II mRNA, particularly in the supraoptic and paraventricular nuclei. Curiously, the strong expression of the Ca(2+)-insensitive Type II mRNA and the lack of expression of the major brain specific Type I mRNA does not correlate with the adenylyl cyclase activity, which is largely Ca2+/calmodulin stimulable in plasma membranes prepared from the hypothalamus.

Adenylyl Cyclases↗
PubMed1999

Projections of the estrogen receptor-immunoreactive ventrolateral hypothalamus to other estrogen receptor-immunoreactive sites in female guinea pig brain.

The ventrolateral hypothalamus in female guinea pigs includes an estrogen receptor dense region adjacent to the ventromedial hypothalamus. This region is reciprocally connected with other estrogen receptor-containing areas suggesting that steroid hormone receptor-containing cells may be directly linked. Phaseolus vulgaris leucoagglutinin, an anterograde tract tracer, was specifically placed in this region with the aim of labeling some projections from estrogen receptor-containing neurons. These projections were colocalized immunocytochemically with the distribution of estrogen receptor-containing cells. Dense ventrolateral hypothalamic innervation was observed in some regions also containing a high concentration of estrogen receptor-containing cells. These regions included the medial preoptic area, the bed nucleus of the stria terminalis, the ventrolateral hypothalamus anterior and posterior to the injection site, and the midbrain central gray. A low density of ventrolateral hypothalamic fibers and terminals was observed in two regions rich in estrogen receptors, the amygdala and the arcuate nucleus. In general, ventrolateral hypothalamic fibers and terminals were present in all regions where estrogen receptors were found except the medial thalamus and habenular region. Labeled terminal boutons and perineuronal baskets were found around estrogen receptor-containing cells in most regions which contained estrogen receptor-containing cells. These close appositions were suggestive of synaptic contacts, suggesting that the ventrolateral hypothalamus may influence steroid-dependent behaviors via the modulation of estrogen receptor-containing cells. Furthermore, ventrolateral hypothalamic projections may include direct connections with estrogen receptor-containing cells, suggesting the presence of a network of interconnected estradiol-sensitive neurons involved in the regulation of estradiol-dependent functions.

Amygdala↗
PubMed1976

Selective actions of prolactin on catecholamine turnover in the hypothalamus and on serum LH and FSH.

The effects of prolactin (PRL) administration on catecholamine turnover in various brain regions of ovariectomized rats were determined by observing the decline of dopamine and norepinephrine concentrations after alpha-methyltyrosine (alphaMT) administration. PRL had no effect on the steady state concentration of dopamine in the median eminence, anterior hypothalamus and corpus striatum or on the norepinephrine concentration in the anterior hypothalamus. However, PRL selectively enhanced dopamine turnover in the median eminence and anterior hypothalamus after a latent period of 10-26 h. In addition, PRL administration significantly decreased serum concentrations of LH and FSH. These results suggest that the PRL-induced increase in activity of dopaminergic neurons in the median eminence or anterior hypothalamus may be responsible for the reduction of the post-castration rise in serum concentrations of LH and FSH.

Animals↗
PubMed1982

Methadone blocks dopamine-mediated release of gonadotropins in rat hypothalamus.

In the present study the effect of methadone (M) on gonadotropin-releasing hormone in the rat hypothalamus was investigated. The specificity of the M effect was demonstrated by injecting M (100 ng) and the M antagonist, naloxone (5 ng), into the ventromedial hypothalamus. A significant drop in the blood testosterone level (p less than 0.05) 15 min following M injection and reversal following naloxone administration suggest a decrease in synthesis or release of LHRH. To determine whether the LHRH response to dopamine (DA) is altered by M, studies were conducted in vitro and in vivo. For the in vitro study hypothalami were incubated with M (10(-7) M), DA (10(-7) M), DA plus M, and DA plus M plus naloxone. Supernatants from the incubate were used to coincubate pituitaries in order to study the effect on luteinizing hormone release. Treatment of the hypothalamus with M had no effect on basal but inhibited the DA-stimulated release of LHRH. For the in vivo study rats were pretreated with decarboxylase inhibitor (RO4-4602) followed by treatment per kilogram body weight with M (10 mg), L-dopa (1, 10, and 100 mg), L-dopa plus M, LHRH (500 ng), and M plus LHRH. M had no effect on the LHRH-induced increase in testosterone levels, whereas the L-dopa-induced increase in testosterone was blunted by M treatment. It is concluded that M blocks the DA-mediated release of gonadotropin-releasing hormone in the rat hypothalamus.

Animals↗
PubMed1992

Influences of hypothyroidism on TRH concentrations and preproTRH mRNA levels in rat hypothalamus: a simple and reliable method to detect preproTRH mRNA level.

To gain further insight into the regulation of hypothalamic TRH by thyroid hormones, we measured TRH concentration in specific hypothalamic nuclei and preproTRH mRNA levels in the anterior hypothalamus. Adult male rats were decapitated 1, 7, 14 days after thyroidectomy. Micropunches by the method of Palkovitz from seven hypothalamic nuclei and median eminence were used for measurement of TRH by radioimmunoassay. As compared with normal levels, TRH concentration significantly decreased in the median eminence and five hypothalamic nuclei including paraventricular nucleus (PVN), posterior nucleus, anterior nucleus, arcuate nucleus, and ventromedial nucleus pars lateralis, by 7 days after thyroidectomy. No significant changes were observed in dorsomedial nucleus or ventromedial nucleus pars medialis until 14 days after thyroidectomy. A rapid and simple method to detect specific mRNA for preproTRH was developed using the polymerase chain reaction and a single anterior hypothalamic section. PreproTRH mRNA levels in the anterior hypothalamus increased approximately twice 7 days after thyroidectomy. These data indicate that thyroidectomy caused a marked increase in preproTRH mRNA levels of the anterior hypothalamus, while it significantly reduced TRH concentrations not only in PVN and median eminence but also in other specific hypothalamic nuclei, suggesting that these nuclei might be involved in the thyrotropin regulation in the hypothalamus.

Animals↗