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Amygdaloid kindled seizures induce weight gain that reflects left hemisphere dominance in rats.

The present study sought to determine the effects of kindled seizures generated from the left and right amygdala upon weight gain in rat. Seventy-five female Sprague-Dawley rats were implanted with electrodes in basal amygdala of the left and right hemispheres. A kindling paradigm was employed in which electrical stimulation was applied once per day for 30 days after Stage 5 seizures. An electrode was implanted into the basal amygdala of the control rats but no stimulation was applied. All rats were weighed daily during the course of the experiment and changes in weight during this period were recorded for all rats. The results demonstrated that kindling from either the left or right amygdala induced significant increases in weight gain relative to the control rats. However, kindling from the left basal amygdala induced increases in body weight that were four times greater than control rats and two times greater than the rats kindled from the right side of the basal amygdala. Likewise, serum leptin levels, which were highly correlated with weight gain, also showed significantly greater increases in left amygdaloid kindled rats relative to rats kindled from the right amygdala and control rats. These findings demonstrate that basal amygdaloid kindling induces significant increases in weight gain and that the magnitude of these effects is linked to the dominance of the left hemisphere.

Amygdala↗

Unit responses evoked in the amygdala and striatum by electrical stimulation of the medial geniculate body.

Unit activity was recorded from cells and cell clusters in the amygdala and striatum in response to electrical stimulation of the medial geniculate body (MGB) in rats anesthetized with chloral hydrate. Responses were mostly excitatory and were evoked against a relatively silent background (i.e., the units seldom fired between stimuli). The shortest latency responses were recorded in the caudate putamen (CPU), lateral amygdaloid nucleus (AL), and amygdalostriatal transition area (AST). Longer latency responses were obtained from neurons in the basolateral (ABL), basomedial (ABM), and central (ACE) nuclei of the amygdala. Moreover, while responses were evoked in AL, AST, and CPU with 300-500 microA stimuli delivered once every 10 sec, more intense and higher-frequency stimuli were required to obtain responses in ABL, ABM, and ACE. These findings are consistent with anatomical tracing studies showing that AL, AST, and CPU receive direct projections from the MGB and related acoustic processing areas of the thalamus but that ACE, ABL, and ABM do not.

Amygdala↗

Distribution and pharmacology of alanine-serine-cysteine transporter 1 (asc-1) in rodent brain.

A polyclonal antibody against the Na+-independent alanine-serine-cysteine transporter 1 (asc-1) was raised and the specificity of the antibody verified by Western blots performed on membranes prepared from HEK293 cells transiently transfected with the cloned murine asc-1. The antibody was then used to localize the transporter in the brain of two rodent species by using immunohistochemistry at the light and electron microscopical level. asc-1-immunoreactivity (asc-1-ir) was widely distributed throughout the mouse and rat brain. Areas with high levels of asc-1-ir included hypothalamus, the medial septal area, globus pallidus, entopeduncular nucleus, cingulate and retrosplenial cortices. Moderate asc-1-ir was observed in several areas including layers III and V of the neocortex, thalamus, nucleus accumbens, caudate putamen, bed nucleus of stria terminalis, all amygdaloid nuclei, hippocampus (CA1-CA3 and hilus of the dentate gyrus), as well as several brainstem nuclei. asc-1-ir was observed as punctuate staining consistent with varicosities matching neuronal cell bodies and dendritic fields. At the ultrastructural level, asc-1-ir was mainly confined to presynaptic terminals. Immunostaining in either glial cell bodies or perivascular sites was not observed and white matter was completely devoid of asc-1-ir. Furthermore, the pharmacology of the Na+-independent uptake site for [3H]d-serine in rat brain synaptosomal P2 fractions was compared with the substrate specificity of the cloned human asc-1 transporter and a high degree of correlation was demonstrated. We conclude that asc-1-ir is widespread in the brain and limited to neuronal structures and that asc-1 may contribute to synaptic clearance of d-serine in brain.

Alanine↗

Quantitative autoradiographic localization of [3H]imipramine binding sites in the brain of the rat: relationship to ascending 5-hydroxytryptamine neuron systems.

Quantitative autoradiography shows that there is a close relationship between [3H]imipramine binding sites and the distribution of 5-hydroxytryptamine (5-HT) neurons in the rat brain. High labeling is observed in the midbrain raphe nuclei, the areas of the dopamine cell groups of the substantia nigra and of the ventral tegmental area of Tsai, the ventral amygdaloid nucleus, the midline thalamic area, and parts of the hypothalmus. Thus, antidepressant drugs that have high affinity for [3H]imipramine binding sites can exert an influence at the 5-HT cell body as well as at the 5-HT nerve terminal level. The present results underline the possibility that the 5-HT and dopamine hypotheses for the mechanism of action of antidepressant drugs are not mutually exclusive, because both 5-HT and dopamine neurons can be regulated by large numbers of [3H]imipramine binding sites.

Animals↗

Role of the amygdaloid nuclei in the modulation of tonic immobility in guinea pigs.

Tonic immobility (TI) is thought to represent the terminal reaction in the chain of antipredatory responses involved in maintaining survival. TI is an inhibitory behavioral response in which the animal presents a significant decrease in body activity and responsiveness to the environment induced by some form of physical restraint. This response is induced in the laboratory by inversion of the animal and brief postural contention of its movements. In nature, the TI response may be triggered by some threatening or predatory stimulus, indicating the physical contact between 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 amygdala regions on TI modulation in guinea pigs. Microinjection of carbachol (0.5 microg/0.2 microL) into the central (CEA), basolateral (BLA), and lateral posterior (LPA) nuclei of the amygdala promoted a reduction in the duration of TI episodes. Pretreatment with atropine (0.5 microg/0.2 microL) showed that the action of carbachol is mediated by muscarinic receptors.

Amygdala↗

Reduced resistance to progressive extinction in senescent rats: a neuroanatomical and behavioral study.

The behavior of senescent rats and mature-young rats was compared in a learning task which consisted of the acquisition of a visual discrimination task, its reversal, the induction of a progressively increasing extinction, relearning and, finally, a complete extinction training. It was found that young and old rats were statistically indistinguishable during all parts of the task, except the progressively increasing extinction. Here, the senescent animals made a significantly higher number of errors than the mature-young ones. Neuroanatomically, ventricular dilation, commissural changes and neuronal loss were observed in senescent rats. The significantly reduced number of neurons in the medial nucleus of the amygdala in old rats compared to young was not directly related to the changed behavior in the progressively increasing extinction part of the visual discrimination task. Based on the anatomical connections of the amygdala and its possible functions in learning and memory, the hypothesis is made that the medial amygdaloid nucleus is involved in the learning of changing response-reinforcement contingencies.

Age Factors↗

Cortical and subcortical argyrophilic grains characterize a disease associated with adult onset dementia.

Unusual cytoskeleton abnormalities were found in the brains of 28 individuals afflicted with adult onset dementia. Most conspicuous were small spindle-shaped argyrophilic grains loosely scattered throughout the neuropil. Additionally, coiled bodies of silver-stained filaments were encountered, mainly located within the white matter close to the cortical grey matter. Argyrophilic grains and coiled bodies contained dense accumulations of straight filaments with a diameter of about 9 nm. The argyrophilic grains were found in abundance within sector CA1 of the Ammon's horn and layer Pre-beta of the entorhinal region. A slightly less dense scattering of the grains occurred in layer IIIab of the adjoining temporal isocortex, insular cortex and orbitofrontal cortex. The basolateral amygdaloid complex and the hypothalamic lateral tuberal nucleus were the most affected subcortical structures. Deeper brain stem nuclei merely showed a sparse number of grains or were devoid of them. Eighty brains of demented individuals were examined. Forty-eight of them showed the features of Alzheimer's disease and four showed the features of Pick's disease. Twenty-eight cases revealed the abnormalities under consideration. Ten showed exclusively argyrophilic grains and coiled bodies, while 16 also had neuritic plaques, neurofibrillary tangles, and neuropil threads. One of the 28 cases was associated with Parkinson's disease and one showed features of both Parkinson's and Alzheimer's disease. Twenty brains of non-demented individuals of about the same age and devoid or almost devoid of Alzheimer changes were used as controls. None of the control brains showed the presence of argyrophilic grains and coiled bodies. These changes, therefore, are considered the morphological substrate of an unknown disease associated with adult onset dementia.

Aged↗

[Animal experiment studies on the neurohumoral control of female puberty. 2. Studies on the influence of amygdala and of the hippocampus on sex maturation].

Immature female rats were bilaterally lesioned in the rostral or caudal part of the mediocortical amygdala (MCA) or in the ventral hippocampus (VHPC) at 21 days of age. In a second experiment, simultaneous lesioning of the MCA or VHPC and the medial preoptic area or hypothalamic ventromedial-arcuate region was performed in 21-day-old rats. Finally, discrete lesions were placed into the anterior or posterior parts of the medial (MAN) or cortical amygdaloid nuclei ath 21, 26 or 32 days of age. The effects of the different treatments on the onset of puberty were evaluated by recording the age at vaginal opening and first ovulation, the body weight on the day of vaginal opening, and the subsequent ovarian or vaginal cyclicity. The following conclusions may be drawn from the findings obtained: 1. At three weeks of age, the MCA exerts a gonadotropininhibiting function that is localized in the anterior part of the MAN. This activity is not demonstrable in older females. 2. The MAN, particularly its posterior part, may play an important role in the prepuberal maturation of the maturation of the neurohormonal ovulatory mechanisms that takes place in female rats during the fourth week of life. 3. The VHPC may be involved in the control of female sexual development mainly by its growth-stimulating activity. The results suggest an essential role of the subcortical limbic system in female sexual maturation and offer an explanation of contradictory findings on the gonadotrophin-controlling function of the MCA before puberty.

Amygdala↗

The distribution of immunoreactive alpha-neo-endorphin in the central nervous system of the rat.

Using a specific radioimmunoassay, we have found that immunoreactive (ir) alpha-neo-endorphin has a widespread and unique distribution in the rat brain and spinal cord. The highest concentration in brain is in the substantia nigra (1692.1 fmol/mg of protein). Very high concentrations of ir-alpha- neo-endorphin (greater than 500 fmol/mg of protein) are also found in the lateral preoptic nucleus, dentate gyrus, parabrachial nuclei, nucleus accumbens, globus pallidus, median eminence, and anterior hypothalamic nucleus. Relatively high concentrations of ir-alpha-neo-endorphin (250 to 500 fmol/mg of protein) are present in the bed nucleus of the stria terminalis, paraventricular nucleus, nucleus of the solitary tract, dorsomedial nucleus, central amygdaloid nucleus, periaqueductal gray matter, suprachiasmatic nucleus, periventricular nucleus, hippocampus, prepositus hypoglossal nucleus, arcuate nucleus, ventromedial nucleus, medial preoptic nucleus, zona incerta, dorsal premamillary nucleus, medial forebrain bundle (hypothalamic and preoptic), nucleus of the diagonal band, locus ceruleus, lateral septal nucleus, and nucleus ambiguus . Moderate levels (100 to 250 fmol/mg of protein) are found in the posterior hypothalamic nucleus, ventral premamillary nucleus, dorsal raphe nucleus, motor hypoglossal nucleus, caudate-putamen, periventricular thalamic nucleus, subcommissural organ, sensory trigeminal nucleus, perifornical nucleus, area postrema, supraoptic nucleus, cuneate nucleus, medial amygdaloid nucleus, and organum vasculosum laminae terminalis. Low concentrations of ir-alpha-neo-endorphin (less than 100 fmol/mg of protein) are found in many cortical structures, claustrum, thalamic nuclei, habenular nuclei, lateral geniculate body, red nucleus, superior and inferior colliculi, paramedian reticular nucleus, pontine nuclei, superior olive, vestibular nuclei, motor facial nucleus, gigantocellular reticular nucleus, and subfornical organ.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Familial progressive supranuclear palsy.

Progressive supranuclear palsy (PSP) is a degenerative neurological disease not typically associated with a family history. Two siblings developed identical clinical features consisting of supranuclear vertical ophthalmoplegia, bradykinesia, rigidity, gait disturbance, and dementia. There was no history of encephalitis or of exposure to known chemicals. L-dopa and dopamine agonist therapy were minimally effective. Autopsy of 1 patient revealed the typical pathological findings of PSP: severe neuronal loss with neurofibrillary tangles (NFTs) in the substantia nigra, subthalamic nucleus, and locus ceruleus. Prominent neurofibrillary degeneration of the amygdaloid nucleus and hippocampus was also observed. Scattered neurofibrillary tangles were seen in the cerebral cortices. Cerebellar degeneration was characterized by a loss of neurons in the dentate nucleus associated with neurofibrillary tangles. Lewy bodies and cortical neuritic plaques were notably absent. The existence of a rare familial form of PSP is supported by these 2 siblings.

Aged↗

Sex-steroid receptor mechanism related to neuronal aromatase and the stigmoid body.

Recent immunohistochemical analyses of rat brains have established the presence of neuronal aromatase and stigmoid body in interfaces of a sex-steroid/brain axis. Aromatase P450-immunoreactive (AROM-I) neurons, which are present only during embryonic Day 16 to postnatal Day 2 (E16-P2), are found in the anterior medial preoptic nucleus, the periventricular preoptic nucleus, and the ventromedial hypothalamic nucleus. The largest AROM-I cell-group localized in the medial preoptico-amygdaloid neuronal arc (mPO-AM) shows a peak during E18-P2 and gradually diminishes after the perinatal days (but still retains the immunoreactivity in adults). In adults, other groups of AROM-I neurons emerge in the lateral septum, the central amygdaloid nucleus, and the bed nucleus of the stria terminalis. Male-predominant sex difference for aromatase expression has been detected at least in the young-to-adult mPO-AM, reflecting sexually distinct endocrine and behavioral responses in the rat reproductive functions. These results suggest the presence of distinct brain-aromatases with different regulatory systems. Neuronal aromatase may modulate development of sexual dimorphism in neonates and activation of reproductive functions in adults. The stigmoid bodies, marked by placental aromatase-associated antigen X-P2 (PAX) antiserum, are also frequent in the sex-steroid targets of rat brains and intimately coexist with estrogen receptors in the mPO-AM of young females. The neuronal inclusion, suspected as a RNA/protein conglomerate, appears to be induced by the decrease of androgen and/or the increase of estrogen, especially as a result of subneuronal aromatic switching into the estrogenous state. The neuronal aromatase and stigmoid body may play important roles in the pre- and post-receptor steps of subneuronal sex-steroids actions for brain sexual differentiation or induction of reproductive functions.

Amygdala↗

Neuronal types in the basolateral amygdaloid nuclei of man.

A parcellation of the human basolateral amygdala is given on the basis of pigmentoarchitectonic analysis. Examination of Golgi preparations and deimpregnated preparations counterstained for lipofuscin pigment revealed three classes of nerve cells: Class I neurons generate a stout main dendrite from one pole of the cell body and several minor ones from the base opposite to the main process. The dendrites are covered with spines. The axon follows a straight course and gives off numerous collaterals. Class I neurons in the lateral and accessory basal nucleus contain finely granulated and widely dispersed pigment. Cells located in the basal nucleus store a large amount of pigment, concentrated at one pole of the cell body. The small class I neurons in the granular nucleus and the intercalated cell masses are marked by large vacuolated pigment granules. Class II neurons have smoothly contoured or sparsely spined dendrites. Size and shape of their cell bodies vary. They contain a large amount of course and intensely stained lipofuscin granules. Class III neurons display similar features in the Golgi preparation but their cell bodies are devoid of pigment. A frequently occurring type is a tiny cell with thin dendrites and profusely branching local axon. Each of the different classes of neurons shows a characteristic pattern of pigmentation. Therefore, Nissl preparations combined with a pigment staining technique, offer the particular advantage of distinguishing the spine-laden neurons from sparsely spined or aspinous types.

Adult↗

Topography of Alzheimer's neurofibrillary change distribution in myotonic dystrophy.

Histological changes that explain the mental symptoms of patients with myotonic dystrophy (MD) have not fully been demonstrated yet. Recently, the presence of Alzheimer's neurofibrillary changes (ANCs) in the brain have been reported in this disease. We studied the brain of a 61-year-old male with MD. The distribution of ANCs was investigated and mapped through careful histological examinations. The examinations disclosed that in MD, ANCs distributed along their preferential sites of the brain; a great number of ANCs were found in the parahippocampus, hippocampus, amygdaloid nucleus, fusiform gyrus, insula, and olfactory bulb, many in the nucleus basalis of Meynert, inferior temporal gyrus, hypothalamus, and brain stem, and a few in the cingulate, frontal and temporal gyri, neostriatum, and mammillary body. In the brain stem, ANCs were seen in the central gray, oculomotor nucleus, linear nucleus, substantia nigra, locus coeruleus, dorsal raphe nucleus, superior central nucleus, retriculotegmental nucleus, and reticular formation. From this result and the previous reports by others, it may be suggested that the presence of ANCs concentrated mostly in the limbic system is a regular and significant histological finding in the brain in MD. Therefore, this limbic lesion must be related to some of the mental symptoms unique to MD. In addition, diffuse and considerable neuronal atrophy and gliosis in the thalami in the absence of ANCs also may have played a causative role in some of the mental symptoms of the present case. Besides the more concentrated occurrence of ANCs within the limbic system, the minimal presence of senile plaques in the CNS may differentiate the brain in MD from that in Alzheimer-type dementia.

Adult↗

Chronic restraint stress down-regulates amygdaloid expression of polysialylated neural cell adhesion molecule.

The amygdala is a brain area which plays a decisive role in fear and anxiety. Since exposure to chronic stress can induce profound effects in emotion and cognition, plasticity in specific amygdaloid nuclei in response to prior stress has been hypothesized to account for stress-induced emotional alterations. In order to identify amygdala nuclei which may be affected under chronic stress conditions we evaluated the effects of 21-days chronic restraint stress on the expression of a molecule implicated crucially in alterations in structural plasticity: the polysialylated neural cell adhesion molecule. We found that polysialylated neural cell adhesion molecule-immunoreactivity within the amygdala, present in somata and neuronal processes, has a regional gradient with the central medial and medial amygdaloid nuclei showing the highest levels. Our results demonstrate that chronic restraint stress induced an overall reduction in polysialylated neural cell adhesion molecule-immunoreactivity in the amygdaloid complex, mainly due to a significant decrease in the central medial amygdaloid and medial amygdaloid nuclei. Our data suggest that polysialylated neural cell adhesion molecule in these nuclei may play a prominent role in functional and structural remodeling induced by stress, being a potential mechanism for cognitive and emotional modulation. Furthermore, these finding provide the first clear evidence that life experiences can regulate the expression of polysialylated neural cell adhesion molecule in the amygdaloid complex.

Amygdala↗

Neurotensin: immunohistochemical localization in rat central nervous system.

Neurotensin immunofluorescence was examined in the rat central nervous system using a well-characterized antiserum directed against this tridecapeptide. Morphological characteristics of the fluorescence indicate its association with neuronal cell bodies and processes in the brain and with cells of the anterior pituitary. Fluorescence is seen in many brain areas, with notable densities in the substantia gelatinosa zones of the spinal cord and trigeminal nucleus, central amygdaloid nucleus, anterior pituitary, median eminence, and preoptic and basal hypothalamic areas.

Animals↗

Differential actions of corticotropin releasing factor on basolateral and central amygdaloid neurones, in vitro.

Intracellular current- and voltage-clamp recordings were obtained from basolateral (BLA) and central (ACe) neurones of the rat amygdala in vitro. The effect of superfusion of rat corticotropin releasing factor (rCRF) was examined on the ACe and BLA, nuclei with a high density of CRF-immunoreactive cell bodies and CRF receptors, respectively. rCRF (12.5-250 nM) had no effect on either resting membrane potential or input resistance in BLA neurones. In contrast, at low nanomolar concentrations rCRF (10-50 nM) caused hyperpolarisation and decreased membrane input resistance in the majority of ACe neurones. The equilibrium potential for this effect was -84 mV in the presence of tetrodotoxin (0.5 microM), suggesting that this response may be mediated by a postsynaptic increase in K+ conductance. Furthermore, rCRF consistently reduced the amplitude of, and the current mediating, the slow after hyperpolarisation following evoked action potential firing in both nuclei. This effect was concentration-dependent with an EC50 of 40 nM in BLA neurones and was insensitive to tetrodotoxin and noradrenergic antagonists. In addition, the putative CRF antagonist alpha-helical CRF9-41 (5 microM) blocked the effect of rCRF and showed partial agonist action on slow after hyperpolarisations. In BLA neurones, rCRF (50 nM) prolonged the Ca(2+)-spike evoked in the presence of tetrodotoxin and tetraethylammonium (2 mM), suggesting that the blockade of the slow after hyperpolarisation occurs subsequent to Ca2+ entry. These results suggest that rCRF has a differential effect on the membrane properties of BLA and ACe neurones possibly by activation of a heterogeneous population of CRF receptors.

Amygdala↗

Neurons containing tuberoinfundibular peptide of 39 residues project to limbic, endocrine, auditory and spinal areas in rat.

Accumulating evidence suggests that tuberoinfundibular peptide of 39 residues (TIP39) may be the endogenous ligand of the parathyroid hormone 2 receptor. The vast majority of TIP39-containing neurons are localized in two regions, the subparafascicular area at the thalamic-midbrain junction, and the medial paralemniscal nucleus in the rostral pons. In contrast to the restricted localization of TIP39-containing cell bodies, TIP39-containing fibers have a widespread distribution. TIP39 neurons were lesioned electrolytically to determine the origin of TIP39-containing fibers within different parts of the rat CNS. Following bilateral lesions of the medial subparafascicular area including the subparafascicular nucleus, TIP39-immunoreactive fibers almost completely disappeared from forebrain regions including the anterior limbic cortical areas, the shell and cone portions of the nucleus accumbens, the lateral septum, the bed nucleus of the stria terminalis, the amygdaloid nuclei, the fundus striati, the subiculum, the thalamic paraventricular nucleus, and the hypothalamic paraventricular, dorsomedial and arcuate nuclei. Unilateral lesions of the medial and the lateral subparafascicular area demonstrated that the projections are ipsilateral and that medial lesions produce higher reductions in the density of TIP39 fibers except in the amygdala and the hypothalamus. Following lesions of the medial paralemniscal nucleus, TIP39-immunoreactive fibers disappeared from the medial geniculate body, the periaqueductal gray, the deep layers of the superior colliculus, the external cortex of the inferior colliculus, the cuneiform nucleus, the nuclei of the lateral lemniscus, the lateral parabrachial nucleus, the locus coeruleus, the subcoeruleus area, the medial nucleus of the trapezoid body, the periolivary nuclei, and the spinal cord, suggesting that these regions receive TIP39-containing fibers from the medial paralemniscal nucleus, and unilateral lesions demonstrated that the projections are ipsilateral. The projections of the TIP39-containing cells in the subparafascicular area suggest their involvement in limbic and endocrine functions, while the projections of the TIP39-containing cells in the medial paralemniscal nucleus suggest their involvement in auditory and nociceptive functions.

Animals↗