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Combination unilateral amygdaloid and ventromedial hypothalamic lesions: evidence for a feeding pathway.

Previous studies have reported hyperphagia and obesity in female rats with bilateral lesions of the most posterodorsal part of the amygdala. In rats with unilateral posterodorsal amygdaloid lesions, a dense pattern of anterograde degeneration appears in the ipsilateral ventromedial hypothalamus, but not the contralateral nucleus. In the present study, female rats with unilateral ventromedial hypothalamic lesions or sham lesions were given either sham lesions or unilateral lesions of the posterodorsal amygdala (PDA) 20 days later. Unilateral lesions of the ventromedial hypothalamus resulted in hyperphagia and excessive weight gain. Subsequent amygdaloid lesions that were contralateral to the initial hypothalamic lesions resulted in hyperphagia and additional excessive weight gains, but amygdaloid lesions ipsilateral to the initial hypothalamic lesions did not. It is concluded that the effects of the two lesions on body weight are not additive and that the PDA and ventromedial hypothalamus are part of the same ipsilateral pathway regulating feeding behavior and body weight regulation.

Amygdala↗

Expression of ARVCF in the human ganglionic eminence during fetal development.

ARVCF (armadillo repeat gene deleted in velocardiofacial syndrome) is a recently characterized member of the catenin p120 (ctn) subfamily of the armadillo repeat proteins. It is involved in modulation of cell-cell adhesion essential to many developmental processes including cellular rearrangement and migration. In the present study, by using specific immunohistochemical methods, strongly ARVCF-immunoreactive cells in a high packing density were found in the human ganglionic eminence (GE), a telencephalic structure which gives rise to precursor neurons of the striatum, the amygdala and the basal nucleus of Meynert. From 20 to 25 weeks of gestation, stripes of immunoreactive cells were found to extend from both the superior part of the GE towards the intermediate zone of the neocortex and from the inferior part of the GE either towards the amygdaloid complex or more laterally towards the intermediate zone. Bands of ARVCF-positive cells were also identified in the gangliothalamic body, a transient target for the migrating neurons from the GE to the thalamus. Double immunolabelling with ARVCF and calretinin antibodies, which mark the GE neurons migrating towards the cerebral cortex, revealed that a majority of ARVCF-positive neurons at the periphery of the GE and the cellular extensions from the GE also expressed calretinin. Our results implicate a very close association of ARVCF with migrating neurons from the GE.

Armadillo Domain Proteins↗

Direct synaptic connections of axons from superior colliculus with identified thalamo-amygdaloid projection neurons in the rat: possible substrates of a subcortical visual pathway to the amygdala.

The aim of the present study was to identify synaptic contacts from axons originating in the superior colliculus with thalamic neurons projecting to the lateral nucleus of the amygdala. Axons from the superior colliculus were traced with the anterograde tracers Phaseolus vulgaris leucoagglutinin or the biotinylated and fluorescent dextran amine "Miniruby." Thalamo-amygdaloid projection neurons were identified with the retrograde tracer Fluoro-Gold. Injections of Fluoro-Gold into the lateral nucleus of the amygdala labeled neurons in nuclei of the posterior thalamus which surround the medial geniculate body, viz. the suprageniculate nucleus, the medial division of the medial geniculate body, the posterior intralaminar nucleus, and the peripeduncular nucleus. Anterogradely labeled axons from the superior colliculus terminated in the same regions of the thalamus. Tecto-thalamic axons originating from superficial collicular layers were found predominantly in the suprageniculate nucleus, whereas axons from deep collicular layers were detected in equal density in all thalamic nuclei surrounding the medial geniculate body. Double-labeling experiments revealed an overlap of projection areas in the above-mentioned thalamic nuclei. Electron microscopy of areas of overlap confirmed synaptic contacts of anterogradely labeled presynaptic profiles originating in the superficial layers of the superior colliculus with retrogradely labeled postsynaptic profiles of thalamo-amygdaloid projection neurons. These connections may represent a subcortical pathway for visual information transfer to the amygdala.

Amygdala↗

Disruption of appetite but not hunger or satiety following small lesions in the amygdala of rats.

Discretely localized lesions were made in the amygdala to examine how specifically they might alter various measures of feeding behavior in male rats. Behavioral tests included spontaneous intake and body weight regulation, reactivity to saccharin and quinine solutions, conditioned taste aversion, the feeding response to food deprivation, the response to glucose gavage, and teh response to dietary amino acid imbalance. Lesions in virtually all regions of the amygdala disrupted feeding behavior in some respect, but alterations in specific tasks were associated only with highly circumscribed brain damage. Body weight regulation, spontaneous food and water intake, and the responses to glucose gavage and long-term food deprivation were not altered by lesions in the amygdala. The results provide evidence that, in the rat, the amygdala may play a greater role in appetite than in hunger or safety. In particular, amygdaloid nuclei may participate in maintaining a negative bias in the reactivity to all appetitive stimuli.

Amygdala↗

Expression of the neuropeptide Y Y1 receptor in the CNS of rat and of wild-type and Y1 receptor knock-out mice. Focus on immunohistochemical localization.

The distribution of neuropeptide Y (NPY) Y1 receptor-like immunoreactivity (Y1R-LI) has been studied in detail in the CNS of rat using a rabbit polyclonal antibody against the C-terminal 13 amino acids of the rat receptor protein. The indirect immunofluorescence technique with tyramide signal amplification has been employed. For specificity and comparative reasons Y1 knock-out mice and wild-type controls were analyzed. The distribution of Y1R mRNA was also studied using in situ hybridization. A limited comparison between Y1R-LI and NPY-LI was carried out.A widespread and abundant distribution of Y1R-LI, predominantly in processes but also in cell bodies, was observed. In fact, Y1R-LI was found in most regions of the CNS with a similar distribution pattern between rat and wild-type mouse. This staining was specific in the sense that it was absent in adjacent sections following preadsorption of the antibody with 10(-5) M of the antigenic peptide, and that it could not be observed in sections of the Y1 KO mouse. In contrast, the staining obtained with an N-terminally directed Y1R antiserum did not disappear, strongly suggesting unspecificity. In brief, very high levels of Y1R-LI were seen in the islands of Calleja, the anterior olfactory nucleus, the molecular layer of the dentate gyrus, parts of the habenula, the interpeduncular nucleus, the mammillary body, the spinal nucleus of the trigeminal, caudal part, the paratrigeminal nucleus, and superficial layers of the dorsal horn. High levels were found in most cortical areas, many thalamic nuclei, some subnuclei of the amygdaloid complex, the hypothalamus and the nucleus of the stria terminalis, the nucleus of the solitary tract, the parabrachial nucleus, and the inferior olive. Moderate levels of Y1R-LI were detected in the cornu Ammonis and the subicular complex, many septal, some thalamic and many brainstem regions. Y1R staining of processes, often fiber and/or dot-like, and occasional cell bodies was also seen in tracts, such as the lateral lemniscus, the rubrospinal tract and the spinal tract of the trigeminal. There was in general a good overlap between Y1R-LI and NPY-LI, but some exceptions were found. Thus, some areas had NPY innervation but apparently lacked Y1Rs, whereas in other regions Y1R-LI, but no or only few NPY-positive nerve endings could be detected. Our results demonstrate that NPY signalling through the Y1R is common in the rat (and mouse) CNS. Mostly the Y1R is postsynaptic but there are also presynaptic Y1Rs. Mostly there is a good match between NPY-releasing nerve endings and Y1Rs, but 'volume transmission' may be 'needed' in some regions. Finally, the importance of using proper control experiments for immunohistochemical studies on seven-transmembrane receptors is stressed.

Animals↗

Changes of brain monoamine contents in three models of experimentally induced muricide in rats.

Monoamine levels were measured by high performance liquid chromatography with electrochemical detection in seven brain regions of three models of experimentally-induced muricide (mouse-killing behavior) in rats (bilateral olfactory bulbectomized rats: OB rats, midbrain raphe nuclei lesioned rats: Raphe rats and nucleus accumbens lesioned rats: Acc rats). Noradrenaline (NA) levels in the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH), 3,4-dihydroxyphenylacetic acid (DOPAC) levels in LH and homovanillic acid (HVA) levels in the frontal cortex (FC) were increased in all three muricide models. In LH, serotonin (5-HT) levels increased in Acc rats and the 5-hydroxyindoleacetic acid (5-HIAA)/5-HT ratio was reduced in OB rats. But in VMH an increase in NA level was not accompanied by any changes of other amines in three muricide models except for 5-HT and 5-HIAA in Raphe rats. In the mamillary body (MB), NA level was increased and 5-HIAA/5-HT ratio was decreased in both OB and Acc rats. Monoamine changes in the amygdaloid nuclei were different in three muricide models, suggesting that the role of monoamines in various nuclei of the amygdala may be different in each muricide model. The present findings suggest that both noradrenergic (LH and VMH) and serotonergic function (LH and MB) may play an important role in exhibiting muricide of OB, Raphe and Acc rats, while dopaminergic function (LH and FC) may be related rather to hyperirritability elicited in these three muricide models.

3,4-Dihydroxyphenylacetic Acid↗

Distribution and cellular localization of DARPP-32 mRNA in rat brain.

In situ hybridization histochemistry has been used to determine the regional distribution and cellular localization of DARPP-32 mRNA in the rat brain. Results support the concept that DARPP-32 is present primarily in cells expressing the dopamine D1 subtype receptor, and that DARPP-32 is not synthesized in dopamine-containing cells. Strongly labelled neuronal cell bodies were found in the caudate nucleus, nucleus accumbens, olfactory tubercle, parts of the bed nucleus of the stria terminalis, and the amygdaloid complex. In addition large amounts of DARPP-32 mRNA were visualized in the medial habenula and around the third ventricle, in ependymal cells and tanycytes, and in the cerebellar Purkinje cells. A less pronounced activity was seen in layers II-III and VI throughout the cerebral cortex. The present studies together with previous biochemical and immunocytochemical studies demonstrate that DARPP-32 gene expression is greatest primarily in D1 dopaminoceptive cells, although there are exceptions. In situ hybridization may thus be used to quantitate regulation of DARPP-32 mRNA in discrete brain regions.

Animals↗

Vagus nerve prolonged stimulation in cats: effects on epileptogenesis (amygdala electrical kindling): behavioral and electrographic changes.

PURPOSE: To analyze the effect of prolonged (daily) electrical vagus nerve stimulation (VNS) on daily amygdaloid kindling (AK) in freely moving cats. METHODS: Fifteen adult male cats were implanted in both temporal lobe amygdalae, both lateral geniculate bodies, and prefrontal cortices. A bipolar hook (5-mm separation) stainless steel electrode also was implanted in the unsectioned left vagus nerve. AK only was performed on five of the cats as a control. The remaining 10 cats were recorded under the following experimental conditions: VNS (1.2-2.0 mA, 0.5-ms pulses, 30 Hz) for 1 min along with AK (1-s train, 1-ms pulses, 60 Hz, 300-600 microA), followed by VNS alone for 1 min, four times between 11:00 a.m. and 2 p.m. At different times, VNS was arrested, and AK was continued until stage VI kindling was reached. RESULTS: The behavioral changes evoked by VNS were as follows: left miosis, blinking, licking, abdominal contractions, swallowing, and eventually yawning, meowing, upward gaze, and short head movements. Compulsive eating also was present with a variable latency. Outstanding polygraphic changes consisted of augmentation of eye movements and visual evoked potentials while the animal was awake and quiet, with immobility and upward gaze. An increase of the pontogeniculooccipital (PGO) wave density in rapid eye movement (REM) sleep also was noticeable. AK was completed (to stage VI) in the control animals without a vagus nerve implantation in 23.4+/-3.7 trials. In animals with VNS, the AK was significantly delayed, remaining for a long time in the behavioral stages I-III and showing a reduction of afterdischarge duration and frequency. Stage VI was never reached despite 50 AK trials, except when the vagus nerve electrodes were accidentally broken or vagal stimulation was intentionally arrested. Under these circumstances, 24.4+/-8.16 AK trials alone were necessary to reach stage VI of kindling. CONCLUSIONS: Our results indicate that left, electrical VNS interferes with AK epileptogenesis. This anticonvulsant effect could be related to the increase of REM sleep.

Amygdala↗

Effect of microinjection of histamine into the brain on plasma levels of epinephrine and glucose in freely moving rats.

The effect of histamine administered to the brain on the plasma levels of epinephrine, norepinephrine and glucose was investigated in freely moving rats. Histamine (10 micrograms) administered intracerebroventricularly (into the lateral ventricle) induced a hyperglycemic response with preceding increases in plasma catecholamines, especially epinephrine. When histamine (5 micrograms) was injected into three different levels of the ventricular system, the magnitude and duration of the resulting increases in plasma epinephrine and glucose were in the following rank order: the third ventricle greater than aqueduct much greater than fourth ventricle. These results suggest that the sites of action of histamine are located rostrally from the midbrain. Microinjections of histamine (1 microgram) into the hypothalamic nuclei including the medial preoptic area, paraventricular nucleus, ventromedial hypothalamic nucleus, posterior hypothalamic nucleus and mammillary body had no elevating effect on the plasma levels of epinephrine and glucose. Other brain regions, such as the lateral septum, medial amygdaloid nucleus and periaqueductal grey of the midbrain, were also excluded as possible sites of histamine action. From the present results, it seems that histamine stimulates plural sites close to the ventricular system to induce hyperglycemic responses.

Animals↗

Cardiovascular responses to chemical and electrical stimulation of amygdala in rats.

Electrical stimulation of the amygdala has been shown to produce changes in cardiovascular variables. To locate neuronal cell bodies responsible for these changes, responses of arterial pressure (AP) and heart rate (HR) to DL-homocysteate (DLH, 0.15 M, 50-100 nl) microinjected into sites in three amygdaloid nuclei were compared with responses to electrical (90-150 microA) stimulation of the same sites in 35 artificially ventilated, paralyzed, urethan-anesthetized rats. Electrical stimulation resulted in depressor responses in most sites (89%). Changes in AP were accompanied by variable changes in HR. Chemical stimulation produced significantly fewer (25%) depressor responses. Similar results were obtained with injections of 1.0 M DLH. To eliminate the influence of the anesthetic on these responses, AP was recorded in nine conscious rats while stimulating the amygdala. Changes in behavior and AP in these animals could be obtained only by electrical stimulation. These results may be interpreted to indicate either that cell bodies responsible for changes in cardiovascular variables during electrical stimulation are not located in the amygdala or that chemical and electrical stimulation affect different neuronal elements in circuits located in the same anatomic site.

Amygdala↗

Up-regulation of methionine-enkephalin-like immunoreactivity by 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment in the forebrain of the Long-Evans rat.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is considered to be one of the most toxic environmental contaminants, named dioxin. Exposure to TCDD induces a plethora of intoxication symptoms, including anorexia and hypothermia, in several mammals and human. Enkephalin, an endogenous pentapeptide, is an important neuroregulator of autonomic functions, such as food intake and body temperature. In this study, we investigated the effects of TCDD gastric administration on methionine-enkephalin (MEK) immunoreactivity in the brain of the Long-Evans rat, the species strain considered to be the most TCDD-susceptible, using immunohistochemical staining. A single dose of TCDD (dissolved in olive oil, 50 microg/kg) or olive oil alone was administrated to the rats by gavage. Compared with the vehicle-treated rat, a marked increase in the density of MEK immunoreactive cell bodies, fibers and terminals was found 2 weeks after TCDD treatment in the forebrain of the TCDD-treated rat, i.e. the central amygdaloid nucleus, field CA3 of the hippocampus, paraventricular hypothalamic nucleus, medial preoptic nucleus, interstitial nucleus of the posterior limb of the anterior commissure, lateral globus pallidus, ventral pallidum and lateral division of the bed nucleus of the stria terminalis. These results demonstrated for the first time a site-specific increased enkephalinergic activity in certain brain regions of the Long-Evans rat. It is suggested that the increased MEK immunoreactivity may act as a compensatory adaptation for the pathophysiological alterations caused by TCDD exposure.

Animals↗

beta-Lipotropin: localization of cells and axons in rat brain by immunocytochemistry.

Using specific antisera to human beta-lipotropin, we have visualized cells and axons with beta-lipotropin-like immunoreactivity in rat brain and pituitary. The beta-lipotropin so localized is well delineated and contained in the cytoplasm of cells and in beaded axons. Areas of greatest beta-lipotropin content are hypothalamus (with cell bodies in the medial basal hypothalamus and arcuate regions), periventricular nucleus of the thalamus, ansa lenticularis, zona compacta of the substantia nigra, medial amygdaloid nucleus, zona incerta, periaqueductal central gray area, locus ceruleus, and a few fibers in the reticular formation. The question of the exact relationship of beta-lipotropin and methionine-enkephalin remains open, because some brain areas contain both substances and some areas contain only one or the other.

Animals↗

Neurotensin induces Fos and Zif268 expression in limbic nuclei of the rat brain.

The endogenous tridecapeptide neurotensin exerts a wide range of behavioral, electrophysiological and neurochemical effects when administered directly into the brain. These effects are thought to result from the activation of distinct populations of neurotensin receptors distributed throughout the central nervous system. We have mapped the sites of functional change in the rat brain associated with the central administration of neurotensin using the induction of the nuclear protein products of the immediate early genes c-fos and zif268 as markers of cellular activation. The administration of neurotensin into the lateral ventricle of rats produced an increase in the number of nuclei positive for Fos and Zif268 immunoreactivity in the central and basolateral nuclei of the amygdala and the paraventricular and supraoptic nuclei of the hypothalamus. Neurotensin also produced an increase in serum corticosterone concentration and decrease in body temperature. The intraperitoneal administration of SR48692, a non-peptide neurotensin receptor antagonist, blocked the neurotensin-induced corticosterone secretion and significantly reduced the number of neurotensin-induced Fos-positive and Zif268-positive neurons in the amygdaloid complex. A significant positive correlation was found between the number of Fos-positive nuclei in the central or basolateral nucleus of the amygdala and the serum corticosterone concentration. A significant positive correlation was also found between the number of Zif-positive cells in the paraventricular nucleus of the hypothalamus and change in body temperature following treatment. Our findings indicate that the central role of neurotensin in increasing serum corticosterone involves the induction of Fos in the central and basolateral nuclei of the amygdala. In contrast, the neurotensin-induced hypothermia, which was unaffected by pretreatment with SR48692, involves Zif induction in the paraventricular nucleus of the hypothalamus. These data support further the existence of central neurotensin receptor subtypes which may regulate distinct immediate early genes.

Amygdala↗

The projections of the A8, A9 and A10 dopaminergic cell bodies: evidence for a nigral-hypothalamic-median eminence dopaminergic pathway.

Using the microdissection method of Palkovits and a sensitive microassay for dopamine (DA) and norepinephrine (NE), the CNS projections of the nigral A8, A9 and A10 dopaminergic cell bodies have been determined in rat brain. Following bilateral electrolytic lesions of the A8-A9-A10 region, DA levels fell significantly in the following areas: dorsal septal nucleus (85%), olfactory tubercle (75%), lateral amygdaloid nucleus (75%), habenula (75%), parietal cortex (75%), cingulate cortex (70%), cerebellum (50%), thalamic paraventricular nucleus (50%), and preoptic suprachiasmatic nucleus (45%). Of particular interest was the finding of a 40% fall in the dopamine levels of the median eminence after such lesions. Concentrations of NE in these same areas following lesions of the A8-A9-A10 region were unchanged. These findings suggest that the nigral A8, A9 and A10 dopaminergic cell bodies, project diffusely to many different areas of cortex, hypothalamus, and brain stem, and, more importantly, provide evidence for a previously unsuspected dopaminergic pathway from substantia nigra to median eminence, an area intimately concerned with neuroendocrine regulation.

Animals↗

Afferent and efferent connections of the olfactory bulbs in the lizard Podarcis hispanica.

The connections of the olfactory bulbs of Podarcis hispanica were studied by tract-tracing of injected horseradish peroxidase. Restricted injections into the main olfactory bulb (MOB) resulted in bilateral terminallike labeling in the medial part of the anterior olfactory nucleus (AON) and in the rostral septum, lateral cortex, nucleus of the lateral olfactory tract, and ventrolateral amygdaloid nucleus. Bilateral retrograde labeling was found in the rostral lateral cortex and in the medial and dorsolateral AON. Ipsilaterally the dorsal cortex, nucleus of the diagonal band, lateral preoptic area, and dorsolateral amygdala showed labeled cell bodies. Retrogradely labeled cells were also found in the midbrain raphe nucleus. Results from injections into the rostral lateral cortex and lateral olfactory tract indicate that the mitral cells are the origin of the centripetal projections of the MOB. Injections in the accessory olfactory bulb (AOB) produced ipsilateral terminallike labeling of the ventral AON, bed nucleus of the accessory olfactory tract, central and ventromedial amygdaloid nuclei, medial part of the bed nucleus of the stria terminalis, and nucleus sphericus. Retrograde labeling of neurons was observed ipsilaterally in the bed nucleus of the accessory olfactory tract and stria terminalis, in the central amygdaloid nucleus, dorsal cortex, and nucleus of the diagonal band. Bilateral labeling of somata was found in the ventral AON, the nucleus sphericus (hilus), and in the mesencephalic raphe nucleus and locus coeruleus. Injections into the dorsal amygdala showed that the mitral neurons are the cells of origin of the AOB centripetal projections. Reciprocal connections are present between AOB and MOB. To our knowledge, this is the first study to address the afferent connections of the olfactory bulbs in a reptile. On the basis of the available data, a discussion is provided of the similarities and differences between the reptilian and mammalian olfactory systems, as well as of the possible functional role of the main olfactory connections in reptiles.

Afferent Pathways↗

Expression of the neuropeptide Y Y1 receptor mRNA in the human brain: an in situ hybridization study.

Using cRNA in situ hybridization, the regional distribution of mRNA encoding the human Y1 receptor was investigated in the normal human brain and compared with the autoradiographic distribution of putative Y1/[125I][Leu31,Pro34]PYY binding sites. Surprisingly, relatively high levels of Y1 receptor mRNA, distributed in a ty laminar fashion, were detected in the frontal and temporal cortices; laminae I, IV and VI were particularly enriched. The claustrum and nucleus of the medial geniculate body also revealed high levels of Y1 receptor mRNA signals. Moderate levels of specific hybridization were detected in the caudate nucleus, putamen, nucleus accumbens, amygdaloid nuclei, and arcuate and paraventricular nuclei of the hypothalamus. In all these regions, only very low levels of specific [125I][Leu31,Pro34]PYY binding were detected with the exception of the dentate gyrus of the hippocampal formation which expressed rather high levels of both the Y1 receptor mRNA and its translated protein. Accordingly, the human brain can express the Y1 receptor mRNA but this may not necessarily translate into a functional receptor as revealed by low specific binding levels observed in most regions.

Aged↗