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PubMed2003

Intraperitoneal injection of ghrelin induces Fos expression in the paraventricular nucleus of the hypothalamus in rats.

Ghrelin is a 28-amino acid peptide hormone secreted from the stomach that acts as a gut-brain peptide with potent stimulatory effects on food intake. The aim of the present study was to investigate the effects of peripheral ghrelin (1 and 10 nmol/rat) injected intraperitoneally (i.p.) on food intake and neuronal activity in the hypothalamus and brain stem, as assessed by c-Fos-like-immunoreactivity (c-FLI), using a confocal laser scanning microscope (cLSM) as a sensitive microscopic technique to detect c-FLI-positive neurons. Cumulative food intake was significantly increased 5.3- and 3.7-fold for the 4-h period after i.p. injection of ghrelin at both doses. The number of c-FLI-positive neurons in the paraventricular nucleus of the hypothalamus (PVN) was significantly increased after peripheral administration of ghrelin (1 nmol i.p.; median: 41.8) compared with i.p. saline (median: 17.5). As described before, c-fos expression was increased in the arcuate nucleus of the hypothalamus (ARC). In the nucleus of the solitary tract (NTS) or the area postrema (AP), there was no significant change in the density of c-FLI-positive neurons. Our data suggest that an activation of the arcuate-paraventricular axis may be part of the brain circuits involved in the orexigenic effect of peripheral ghrelin.

Animals↗
PubMed2006

An NMDA receptor-dependent hydroxyl radical pathway in the rabbit hypothalamus may mediate lipopolysaccharide fever.

The aim of this study was to investigate the effects of antioxidants (e.g. alpha-lipoic acid and N-acetyl-L-cysteine) as well as N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. MK-801 and LY235959) on the changes of both core temperature and hypothalamic levels of 2,3-dihydroxybenzoic acid (2,3-DHBA) induced by systemic administration of lipopolysaccharide (LPS) in rabbits. The measurements of 2,3-DHBA were used as an index of the intrahypothalamic levels of hydroxyl radicals. Intravenous administration of LPS (2-10 microg/kg) elicited a biphasic febrile response, with the core temperature maxima at 80 and 200 min post-injection. Each core temperature rise was accompanied by a distinct wave of cellular concentrations of 2,3-DHBA in the hypothalamus. The rise in both the core temperature and hypothalamic 2,3-DHBA could be induced by direct injection of glutamate (100-400 microg in 10 microl/rabbit) into the cerebroventricular fluid system. Either the early or the late phase of fever rise and increased hypothalamic levels of 2,3-DHBA following systemic injection of LPS were significantly antagonized by pretreatment with injection of alpha-lipoic acid (5-60 mg/kg, i.v.), N-acetyl-L-cysteine (2-20 mg/kg, i.v.), MK-801 (0.1-1 mg/kg, i.m.), or LY235959 (0.1-1 mg/kg, i.v.) 1 h before LPS injection. The increased levels of prostaglandin E(2) in the hypothalamus induced by LPS could be suppressed by alpha-lipoic acid or N-acetyl-L-cysteine pretreatment. These findings suggest that an NMDA receptor-dependent hydroxyl radical pathway in the hypothalamus of rabbit brain may mediate both the early and late phases of the fever induced by LPS.

Acetylcysteine↗
PubMed2005

Olfactory preference and Fos expression in the accessory olfactory system of male rats with bilateral lesions of the medial preoptic area/anterior hypothalamus.

In the present study we evaluated if a medial preoptic area/anterior hypothalamus lesion affects the olfactory preference toward soiled bedding from receptive females in comparison to bedding from anestrous females or clean bedding. In the second part of the study we evaluated the accessory olfactory system response to estrous bedding with Fos immunoreactivity to determine if the preoptic lesions modify the processing of sexually relevant olfactory cues. Before medial preoptic area/anterior hypothalamus lesions, male rats spent more time investigating estrous bedding as opposed to anestrous or clean bedding. After the lesion, subjects showed no preference between estrous and anestrous bedding; that is, males spent the same amount of time investigating both types of bedding. These two odors were investigated more than clean bedding. Increments in Fos immunoreactivity neurons were seen in structures of the accessory olfactory system after exposure to soiled estrous bedding [granular layer of the accessory olfactory bulb, anterior-dorsal medial amygdala, posterior-dorsal medial amygdala, bed nucleus of the stria terminalis]. These results suggest that bilateral destruction of the medial preoptic area/anterior hypothalamus modify male olfactory preference in such a way that subjects spend the same time smelling and investigating bedding from estrous and anestrous females. This change in olfactory preference is not associated with alterations in the processing of sexually relevant olfactory cues by the accessory olfactory system.

Animals↗
PubMed2005

Sexually dimorphic gene expression in the hypothalamus, pituitary gland, and cortex.

We examined sex differences in the transcriptomes of hypothalamus, pituitary gland, and cortex of male and female mice using serial analysis of gene expression. In total 940,669 tags were sequenced. In hypothalamus, 3 transcripts are differentially expressed by gender, including growth hormone (neuromodulation) and 3beta-hydroxysteroid dehydrogenase-1 (steroidogenesis). In pituitary gland, 43 transcripts are differentially expressed, including RAS guanyl-releasing protein 2 (cell signaling), ornithine transporter (mitochondrial transport), H3 histone family 3B (chromatin structure), heterogeneous nuclear ribonucleoprotein U (chromatin remodeling), NADH dehydrogenase (mitochondrial oxidative phosphorylation), neuronatin (cell differentiation), and ribosomal protein S27a (protein metabolism). EST X (inactive)-specific transcript antisense is expressed at a higher level in the three female organs, whereas growth hormone and NADH dehydrogenase are expressed at higher levels in female cortex. Thus, the current study has characterized key sexual dimorphisms in the transcriptomes of the hypothalamus, pituitary, and cortex.

Animals↗
PubMed2000

Tonic inhibition of food intake during inactive phase is reversed by the injection of the melanocortin receptor antagonist into the paraventricular nucleus of the hypothalamus and central amygdala of the rat.

Melanocortins inhibit food intake and melanocortin 4 receptor (MC(4)R) antagonists stimulate feeding behaviour. These effects may occur due to stimulation or blockade of MC(4) receptors in the hypothalamus. To test the validity of this hypothesis, a cyclic peptide, the MC(4)R selective antagonist HS014 (20, 100 and 500 pmol), or vehicle, was injected unilaterally into the paraventricular nucleus of the hypothalamus (PVN). As MC receptors are expressed also in extrahypothalamic sites involved in the regulation of feeding behaviour, HS014 was injected bilaterally into the vicinity of the central nucleus of the amygdala (CA) and the nucleus accumbens region (Acc). All doses of HS014 induced a dose-dependent increase in food intake when injected into the PVN. Intra-amygdalar injections of HS014 (50 and 250 pmol/side) also stimulated food intake, whereas a 10-pmol dose was inactive. Local microinjections of HS014 into the Acc failed to stimulate feeding. These data suggest that endogenous melanocortin receptor agonists exert a tonic inhibitory influence on food consumption by stimulating MC(4) receptors in the hypothalamus and amygdala.

Amygdala↗
PubMed2002

Chemical stimulation of the dorsomedial hypothalamus evokes non-shivering thermogenesis in anesthetized rats.

Disinhibition of neurons in the dorsomedial hypothalamus (DMH) by microinjection of the GABA(A) receptor antagonist bicuculline methiodide (BMI) elicits a range of autonomic and endocrine changes resembling those seen in experimental paradigms for emotional stress. Stress in rats is also known to provoke increases in body temperature resulting in part from sympathetically mediated activation of brown fat. The purpose of the present study was to examine the effect of microinjection of BMI into the DMH on core body temperature and temperature of brown fat in rats. In anesthetized preparations, microinjection of BMI 10 pmol/50 nl into the DMH and adjoining posterior hypothalamus elicited marked and rapid increases in temperature in interscapular brown adipose tissue (IBAT) and lesser delayed elevations in rectal temperature. Similar injections into the paraventricular nucleus or ventromedial hypothalamus had no effect on either parameter. Peak increases in IBAT were significantly correlated with both peak increases in core temperature and maximal increases in heart rate that accompanied these changes, and all of these effects were abolished by systemic treatment with propranolol 1 mg/kg. In conscious rats instrumented for telemetry, microinjection of BMI 10 pmol/100 nl into the DMH evoked marked increases in core temperature as well as heart rate, locomotor activity, and plasma ACTH. The increase in core temperature occurred with a delayed time course similar to that seen in anesthetized preparations. These results indicate that activation of neurons in the DMH provokes increases in body temperature resulting in large part from sympathoadrenally-mediated activation of brown fat.

Adipose Tissue, Brown↗
PubMed1999

Hypothalamus, anterior pituitary and adrenal gland involvement in the activation of adrenocorticotropin and corticosterone secretion by gastrin-releasing peptide.

This study was designed to investigate the contribution of the hypothalamus, anterior pituitary and adrenal gland in the increase of adrenocorticotropin (ACTH) and corticosterone secretion induced by gastrin-releasing peptide (GRP) on in vitro isolated hypothalamus, pituitary and adrenal gland. Furthermore, we have examined in dispersed anterior pituitary cells whether the ACTH release induced by GRP is a Ca2+-dependent process. Moderate concentrations of GRP (1 and 10 nM) were able to increase the release of corticotropin-releasing factor (CRF)-like material in the medium of isolated hypothalami, whereas higher concentrations (100 and 1000 nM) were needed to elevate ACTH and corticosterone secretion in pituitary and adrenal quarters, respectively. The competitive and specific GRP receptor antagonist (Leu13-psi-CH2NH-Leu14) bombesin (10, 100 and 1000 nM) was without effect on basal secretion of CRF-like material, ACTH and corticosterone in isolated hypothalami, pituitary and adrenal quarters respectively. However, this antagonist (100 nM) completely blocked the stimulatory effects of GRP (100 nM) on bioactive CRF, ACTH and corticosterone release. In addition, in dispersed anterior pituitary cells which medium contained Ca2+ (1.5 mM), GRP stimulated the secretion of ACTH, but was without effect when the concentration of Ca2+ in the medium was lower (200 nM). These results suggest that: (1) the hypothalamus, anterior pituitary and adrenal gland seem to contribute to the elevation of ACTH and corticosterone secretion induced by GRP by a mechanism mediated through GRP receptors and (2) the stimulation of ACTH by GRP in the anterior pituitary appears to be dependent upon the presence of physiological concentrations of extracellular Ca2+.

Adrenocorticotropic Hormone↗
PubMed2002

Inhibition of protein kinase C but not protein kinase A attenuates morphine withdrawal excitation of rat hypothalamus-pituitary-adrenal axis.

Our previous studies have shown an enhanced activity of the hypothalamus-pituitary-adrenocortical axis response in rats withdrawn from morphine, which results from an increase in the hypothalamic paraventricular nucleus noradrenergic activity that is dependent on alpha-adrenoceptor activation. The first objective of this work was to examine the effect of protein kinase A (PKA) and protein kinase C (PKC) inhibitors on morphine withdrawal-induced changes in corticosterone release (an index of the hypothalamus-pituitary-adrenocortical axis activity) and in catecholaminergic turnover in the paraventricular nucleus. Plasma corticosterone levels as well as the concentration of noradrenaline, 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in the paraventricular nucleus were determined. The second purpose of the study was to assess whether kinase inhibitors, administered continuously through s.c. osmotic minipumps, get into the brain. Chronic pretreatment for 7 days with the selective PKA inhibitor N-(2'guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004) concomitantly with morphine did not affect the increase in corticosterone release observed after naloxone-precipitated morphine withdrawal. However, pretreatment with the selective PKC inhibitor, calphostin-C significantly antagonized the corticosterone hypersecretion in morphine-withdrawn rats. Neither HA-1004 nor calphostin-C co-administered with morphine for 7 days did modify the morphine withdrawal-induced increase in noradrenaline turnover. Pretreatment with HA-1004 inhibits the increase in dopamine turnover during morphine withdrawal, whereas calphostin-C did not affect the DOPAC/dopamine ratio. Our results might indicate that expression of morphine dependence for hypothalamus-pituitary-adrenocortical axis hyperactivity involves PKC but not PKA signaling mechanisms. It is suggested that in rats PKC may be up-regulated during morphine dependence. High-performance liquid chromatography (HPLC) analysis of hypothalamic tissue from rats perfused with kinase inhibitors demonstrates that both calphostin-C and HA-1004 can cross the blood-brain barrier when administered peripherally.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Cholinergic and GABAergic modulation of self-stimulation of lateral hypothalamus and ventral tegmentum: effects of carbachol, atropine, bicuculline, and picrotoxin.

This study aimed at investigating the effects of modulators of acetylcholine-muscarinic (ACh-M) and GABAA.B-receptors in the lateral hypothalamus and ventral tegmentum on the electrical self-stimulation evoked from these regions. In each Wistar rat, a bipolar electrode and an ipsilateral insulated cannula-cum-electrode were implanted chronically in the right hemisphere. There were two placement combinations: 1. Bipolar electrode in lateral hypothalamus-medial forebrain bundle (LH-MFB) and cannulacum-electrode in ventral tegmental area-substantia nigra (VTA-SN) or 2, bipolar electrode in VTA-SN and cannula-cum-electrode in LH-MFB. The stimulation parameters were kept at a level to obtain 50% of the maximum possible asymptotic intracranial self-stimulation (ICSS) rates (M50) from each site. Carbachol injected into VTA-SN increased the ICSS responding rate of VTA-SN as well as, indirectly, that of LH-MFB, and atropine injections had an opposite effect. Similar injections of these ligands into LH-MFB again had facilitatory and inhibitory effects on its ICSS: however, there was no indirect effect on the ICSS of VTA-SN. Bicuculline injection into VTA-SN had no effect on either its ICSS or that of LH-MFB. On the other hand, bicuculline injected into LH-MFB decreased its ICSS and, indirectly, the ICSS of VTA-SN in a dose-dependent manner. In contrast, intra VTA-SN injections of picrotoxin decreased its ICSS and, indirectly, ICSS of LH-MFB. Similar injections into LH-MFB had no effect on the ICSS of VTA-SN. The results suggest that ICSS of VTA-SN is Ach-M receptor mediated and, also, this mediation influences the ICSS of LH-MFB. On the contrary, changes in ICSS of LH-MFB following Ach-M receptor ligands do not influence the ICSS of VTA-SN. The direct effects of GABA-receptor antagonists have shown disassociation because ICSS of LH-MFB was more sensitive to bicuculline, whereas the ICSS of VTA-SN was more sensitive to picrotoxin. Thus, the cholinergic and GABAergic mechanisms of the self-stimulation of lateral hypothalamus and ventral tegmentum are different.

Animals↗
PubMed1997

Exploring the expression of the melanin-concentrating hormone messenger RNA in the rat lateral hypothalamus after goldthioglucose injection.

Melanin-concentrating hormone (MCH) is expressed in a large neuronal population of the rat lateral hypothalamus. This area is known to be implicated in the regulation of thirst and hunger and to contain glucose-sensitive cells. In the present study, we investigated the effects of goldthioglucose (GTG), a toxic form of glucose, on the expression of the MCH gene in the rat lateral hypothalamus by immunocytochemistry, in situ hybridization and competitive RT-PCR. We observed that the MCH immunoreactivity and the level of MCH mRNA were not changed after intraperitoneal GTG injection (0.35 mg/g body weight). These results together with previous data suggest that the glucose-sensitive cells of the lateral hypothalamus are different from the MCH neurons and remain to be identified.

Animals↗
PubMed1998

Organization of inputs to the dorsomedial nucleus of the hypothalamus: a reexamination with Fluorogold and PHAL in the rat.

Possible inputs to the DMH were studied first using the fluorescent retrograde tracer Fluorogold, and identified cell groups were then injected with the anterograde tracer PHAL to examine the distribution of labeled axons in and around the DMH. From this work, we conclude that the majority of inputs to the DMH arise in the hypothalamus, although there are a few significant projections from the telencephalon and brainstem. With few exceptions, each major nucleus and area of the hypothalamus provides inputs to the DMH. Telencephalic inputs arise mainly in the ventral subiculum, infralimbic area of the prefrontal cortex, lateral septal nucleus, and bed nuclei of the stria terminalis. The majority of brainstem inputs arise in the periaqueductal gray, parabrachial nucleus, and ventrolateral medulla. In addition, it now seems clear that inputs to the DMH use only a few discrete pathways. Descending inputs course through a periventricular pathway through the hypothalamic periventricular zone, a medial pathway that follows the medial corticohypothalamic tract, and a lateral pathway traveling through medial parts of the medial forebrain bundle. Ascending inputs arrive through a midbrain periventricular pathway that travels adjacent to the cerebral aqueduct in the periaqueductal gray, and through a brainstem lateral pathway that travels through central and ventral midbrain tegmental fields and enters the hypothalamus, and then the DMH from more lateral parts of the medial forebrain bundle. The results are discussed in relation to evidence for involvement of the DMH in ingestive behavior, and diurnal and stress-induced corticosterone secretion.

Animals↗
PubMed2001

Changes in jaw reflexes by stimulation of the hypothalamus in anesthetized rabbits.

Changes in the masseteric monosynaptic reflex (MMR) and jaw-opening reflex (JOR) responses resulting from conditioning stimulation in the hypothalamus were studied in anesthetized rabbits. Stimulation of the lateral hypothalamus evoked a facilitation of the MMR and an inhibitory or facilitatory effect on the JOR. The facilitatory effect on JOR was stronger than that on the MMR. The facilitatory effective site for the JOR was in the dorsal and lateral directions as compared to the inhibitory field. The results suggest two functionally distinct regions in the lateral hypothalamus that separately project to the jaw-opening muscles.

Aggression↗
PubMed1997

Angiotensinogen and natriuretic peptide mRNAs in rat brain: localization and differential regulation by adrenal steroids in hypothalamus.

Adrenal steroids have been shown to modulate angiotensin II and natriuretic peptide systems--peptide synthesis and metabolism--in vitro. In the present study the effects of adrenal steroids on mRNA encoding the angiotensin II precursor, angiotensinogen (AOGEN), and the natriuretic peptides, atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) in the rat hypothalamus were investigated using quantitative in situ hybridization histochemistry of [35S]- and [33P]-labeled oligonucleotide probes. Adrenalectomy produced an apparent overall decrease in preproAOGEN (ppAOGEN) mRNA in presumed astrocytes in the anterior hypothalamus with significant decreases (ANOVA) measured in the medial preoptic area, the ventral region of the medical preoptic area, the paraventricular, suprachiasmatic, supraoptic, and periventricular nuclei. ppAOGEN mRNA levels were restored by both glucocorticoid (dexamethasone; 2 micrograms/ml in drinking water) and mineralocorticoid (aldosterone; 50 micrograms/kg, SC) replacement. Treatment of intact animals with dexamethasone (2 micrograms/ml in drinking water for 5 days) and aldosterone (100 micrograms/kg, SC, daily for 10 days) produced a significant increase in ppAOGEN mRNA in those hypothalamic regions affected by adrenalectomy. ppANP and ppCNP mRNA-positive neurons were successfully detected using [35S]- and [33P]-labeled probes, respectively, and were abundant in the anterior hypothalamus, particularly in the anteromedial preoptic nucleus of the medial preoptic area. In contrast to the effects on ppAOGEN mRNA, however, alterations in adrenal steroid levels did not significantly change ppANP or ppCNP mRNA levels in neurons of the anteromedial preoptic nucleus or in the arcuate nucleus. These results indicate that adrenal steroids modulate AOGEN gene transcription in vivo, consistent with previous reports of increased levels of ppAOGEN mRNA in a number of brain regions in response to acute dexamethasone treatment and reports of decreased AOGEN immunoreactivity in brain regions of adrenalectomized rats. In contrast, despite reports of modulation of hypothalamic ANP immunoreactivity following adrenalectomy and dexamethasone treatment, it would appear that adrenal steroids do not alter the transcription or stability of hypothalamic natriuretic peptides mRNA in vivo.

Adrenal Cortex Hormones↗
PubMed2000

Activation of gamma-aminobutyric acid(A) receptors in the paraventricular nucleus of the hypothalamus reduces apomorphine-, N-methyl-D-aspartic acid- and oxytocin-induced penile erection and yawning in male rats.

The effect of muscimol and baclofen injected into the paraventricular nucleus of the hypothalamus on penile erection and yawning induced by apomorphine, oxytocin and N-methyl-D-aspartic acid (NMDA) was studied in male rats. Muscimol (20-200 ng), but not baclofen (200 ng), injected into the paraventricular nucleus of the hypothalamus 10 min before apomorphine (50 ng), oxytocin (10 ng) or NMDA (50 ng) reduced penile erection and yawning induced by the above compounds given into the paraventricular nucleus. Bicuculline (250 ng) injected into the paraventricular nucleus 5 min before muscimol (100 ng) prevented the inhibitory effect of muscimol on penile erection and yawning induced by apomorphine, oxytocin and NMDA. The present results show that gamma-aminobutyric acid (GABA) inhibits penile erection and yawning by acting on GABA(A) receptors in the paraventricular nucleus of the hypothalamus.

Animals↗
PubMed1997

Prostaglandin E receptor EP3 subtype is involved in thermal hyperalgesia through its actions in the preoptic hypothalamus and the diagonal band of Broca in rats.

The effects of microinjection of prostaglandin E2 (PGE2) (0.5 fg-500 pg/0.2 microl) into the medial part of the preoptic area (MPO) on nociception were studied using a hot-plate test in rats. The intraMPO microinjection of PGE2 only at non-pyrogenic doses (5-50 fg) reduced the paw-withdrawal latency, suggesting hyperalgesia. Maximal reduction was obtained 15 min after the injection of PGE2 at 50 fg. Subsequently, to determine which types of prostanoid receptors are involved in the hyperalgesic effect of PGE2 in the MPO, we administered PGE2 receptor agonists, i.e., 17-phenyl-omega-trinor PGE2 (an EP1 receptor agonist), butaprost (an EP2 receptor agonist) and M&B28767 (an EP3 receptor agonist) into the MPO and observed the nociceptive behavior. The intraMPO injection of M&B28767 (0.005 fg-50 pg), like that of PGE2, exhibited a U-shaped dose response characteristic, i.e., a significant decrease of the paw-withdrawal latency only at 0.05-5 fg with the maximal response at 0.5 fg. However, neither the administration of EP1 (0.5 fg-50 ng) nor EP2 (0.5 fg-500 pg) agonists had any effect on nociception. The microinjection of M&B28767 at 0.5 fg into the other parts of preoptic hypothalamus (the lateral part of the preoptic area and the median preoptic nucleus) and the diagonal band of Broca (DBB) produced hyperalgesia similar to the intraMPO-induced hyperalgesia in terms of magnitude and time course. Microinjection of M&B28767 (0.5 fg) into either the paraventricular nucleus, the ventromedial hypothalamus, the lateral hypothalamic area or the septal nucleus had no effect on nociception. These findings suggest that PGE2 at non-pyrogenic doses in the brain induces hyperalgesia, at least in part, through its actions on EP3 receptors in the preoptic hypothalamus and the DBB in rats.

Alprostadil↗
PubMed1997

Activity changes of the cat paraventricular hypothalamus during phasic respiratory events.

We monitored the spatiotemporal organization of cellular activity in the medial paraventricular hypothalamus during spontaneously-occurring periods of increased inspiratory effort followed by prolonged respiratory pauses (sigh/apnea) in the freely-behaving cat. Paraventricular hypothalamic activity was assayed by video images of light captured with a stereotaxically-placed fibre optic probe. Respiratory activity was measured through electromyographic wire electrodes placed in the diaphragm. Sigh/apnea events appeared in all behavioural states, and especially during quiet sleep. Overall paraventricular hypothalamic activity declined transiently, with the onset of decline coinciding with the beginning of the sigh inspiratory effort, reached a nadir at apnea onset 4.4+0.5 s from the beginning of the sigh, increased during the course of the apnea, and subsequently rebounded above baseline to peak at 10.9+2.5 s after sigh onset. Scattered, small areas of the imaged region were activated or depressed independently of the overall image values. The data suggest that paraventricular hypothalamic activity changes dynamically during phasic respiratory events, and may contribute to the progression of the sigh/apnea. We speculate that the medial paraventricular hypothalamus influences breathing patterns through projections to parabrachial respiratory phase-shift regions, and that longer-latency influences may also be exerted indirectly through blood pressure effects from paraventricular hypothalamic projections to medullary cardiovascular nuclei. Additionally, the paraventricular hypothalamus may convey respiratory influences from other rostral structures, such as the hippocampus.

Animals↗
PubMed2001

The lateral hypothalamus is involved in the pathway mediating the hypotensive response to cingulate cortex-cholinergic stimulation.

1. The injection of acetylcholine (ACh) into the medial prefrontal cortex (MPFC) caused marked hypotensive response in either unanesthetized or anesthetized rats. 2. The present experiment was designed to investigate anatomical connections of the ACh injection site in the MPFC with putative autonomic-related brain nuclei, as well as their possible involvement in the mediation of the hypotensive response to ACh. 3. For the above purpose, the bidirectional neuronal tracer biotinylated dextran amine (BDA) was injected into Cg1 and Cg3 areas, within the MPFC of male Wistar rats. Five days later the animals were sacrificed and brain slices were processed and analyzed to determine neuronal projections efferent from as well afferent to the MPFC. 4. Neuronal staining was more prominent in regions ipsilateral to the BDA injection site. Prominent efferent projections of the MPFC were observed in the contralateral MPFC: ipsi- and contralateral amygdala and hypothalamus; ipsilateral septal area, diagonal band, and zona incerta. 5. Similar but not equal patterns of neuronal labeling were observed when BDA injections were performed within the two adjacent MPFC areas. BDA injections centered in the ACh injection site in the Cg3 area caused strong labeling in the septal area and diagonal band as well as an overall hypothalamic labeling. Within the hypothalamus an intense cortical projection was observed in the lateral hypothalamus (LH). BDA injections into the Cg1 area caused a more evident labeling of the amygdaloid complex. 6. Neuronal cell bodies were evident throughout the MPFC as well as in the sensory-motor cortex when BDA was injected into the LH, thus indicating a massive ipsilateral cortical projection from the Cg3 to the LH. 7. Bilateral NMDA-induced lesions within the LH caused a significant attenuation of the depressor responses to ACh injection in the MPFC, whereas unilateral lesions were marginally effective. These results indicate the involvement of the LH in the mediation of the hypotensive response to ACh injection into the MPFC as well as the bilateral distribution of the hypotensive pathway.

Acetylcholine↗
PubMed1999

Levels of dopamine beta hydroxylase immunoreactivity in the preoptic hypothalamus of the ovariectomised ewe following injection of oestrogen: evidence for increased noradrenaline release around the time of the oestrogen-induced surge in luteinizing hormone.

We have measured dopamine beta hydroxylase (DBH) immunoreactivity in the preoptic hypothalamus as an index of release of noradrenaline in the ovariectomised (OVX) ewe at the time of an oestrogen-induced surge in luteinizing hormone (LH) release. OVX ewes (n=5) were given an injection of 50 microg oestradiol benzoate (or oil), which causes a surge in the secretion of LH. Blood samples were taken and sheep were killed 16 h later. Other groups (n=3) were given oil or oestrogen and killed 6 h later. Brains were collected for immunohistochemistry and image analysis. The number of DBH-stained cells and the integrated optical density of the cells was measured throughout the A1 field of the brainstem. The DBH staining was measured in the terminal beds of the hypothalamus. There was no difference between the controls and the EB-treated OVX ewes in the number of DBH positive cells or the optical density of DBH-staining cells in the A1 field. Within the preoptic area, there was reduced (P<0.02) DBH staining in the 16 h EB-treated ewes. There was no change in the DBH staining in the paraventricular nucleus or the arcuate nucleus of the hypothalamus. These data suggest that there is release of noradrenaline in the preoptic area at the time of the E-induced GnRH/LH surge in the OVX ewe.

Animals↗