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PubMedDate not supplied

Important roles of N-methyl-D-aspartate receptors in expression of amygdaloid-kindled seizure demonstrated by intraperitoneal administration of L-aspartate in dimethyl sulfoxide.

Intraperitoneally (i.p.) administered L-aspartate (Asp) (20 mmol/kg) produced no behavioral or EEG change in nonkindled rats. Nonkindled rats that received 18, 19, or 20 mmol/kg Asp, dissolved in 10 or 15% dimethylsulfoxide (DMSO), i.p. developed masticatory movement, head nodding, and myoclonic jerks of the limbs, followed by wild running and subsequent tonic extension of the whole body. In contrast to the effects in nonkindled rats, i.p. injection of Asp 20 mmol/kg in 15% DMSO in amygdala-kindled rats precipitated electroclinical generalized seizures identical to kindled ones. When the kindled amygdala was pretreated with 2-amino-7-phosphonoheptanoic acid (2-APH), a potent and specific antagonist of N-methyl-D-aspartate (NMDA) receptors, the Asp/DMSO-induced generalized convulsion identical to kindled amygdala seizure was suppressed. 2-APH treatment of the contralateral amygdala was without such suppression. The results suggest that (a) Asp is ineffective when given alone (when given with DMSO, however, Asp evokes generalized seizures identical to kindled ones in amygdala-kindled rats, while it induces a qualitatively different generalized seizure in nonkindled rats; (b) NMDA receptors of the kindled amygdala play an important role in activation of the transsynaptic neurocircuit underlying the expression of kindled amygdala seizure; and (c) DMSO is useful in assessing potential central effects of compounds that do not readily penetrate the blood-brain barrier (BBB).

Amygdala↗
PubMed2006

Chronic social stress in the visible burrow system modulates stress-related gene expression in the bed nucleus of the stria terminalis.

Prolonged social subjugation produces physiological indices of chronic stress in rats. In the current study, we examined the impact of social stress on glutamic acid decarboxylase (GAD) isoforms, corticotropin-releasing hormone (CRH) and vasopressin mRNA expression in forebrain stress circuitry, using the visible burrow system model of dominance-subordination. Subordinate male rats develop behavioral and neuroendocrine changes consistent with exposure to chronic stress, including marked loss of body weight and elevation of basal plasma corticosterone relative to dominant rats. Forebrain GAD65, GAD67, CRH and vasopressin mRNA expression in central stress-regulatory circuits were examined by in situ hybridization. Elevated CRH mRNA was observed in the oval nucleus of the bed nucleus of the stria terminalis (BST) of subordinate males. In contrast, GAD67 expression was decreased in the interfascicular nucleus of the BST in both the subordinate and dominant rats compared to non-burrow control rats. No changes in CRH, GAD or vasopressin were observed in amygdaloid nuclei, other BST nuclei or in the hypothalamic paraventricular nucleus. Collectively, these data suggest that exposure to the visible burrow system attenuates BST GAD expression regardless of social status, whereas the enhanced physiological responses to social stress seen in subordinates may be associated with enhanced CRH expression in the oval nucleus of the BST.

Adrenal Glands↗
PubMed2002

Parvalbumin neuron circuits and microglia in three dopamine-poor cortical regions remain sensitive to amphetamine exposure in the absence of hyperthermia, seizure and stroke.

The dopamine-releasing and depleting substance amphetamine (AMPH) can make cortical neurons susceptible to damage, and the prevention of hyperthermia, seizures and stroke is thought to block these effects. Here we report a 2-day AMPH treatment paradigm which affected only interneurons in three cortical regions with average or below-average dopamine input. AMPH (six escalating doses/day ranging from 5 to 30 mg/kg for 2 days) was given at 17-18 degrees C ambient temperature (T) to adult male rats. During the 2-day AMPH treatment, peak body T stayed below 38.9 degrees C in 40% of the AMPH treated rats. In 60% of the rats, deliberate cooling suppressed (<39.5 degrees C) or minimized (<40.0 degrees C) hyperthermia. Escalation of stereotypes to seizure-like behaviors was rare and post-mortem morphological signs of stroke were absent. Neurons labeled with the anionic, neurodegeneration-marker dye Fluoro-Jade (F-J) were seen 1 day after dosing, peaked 3 days later, but were barely detectable 14 days after dosing. Only nonpyramidal neurons in layer IV of the somatosensory barrel cortex and in layer II of the piriform cortex and posterolateral cortical amygdaloid nucleus were labeled with Fluoro-Jade. Isolectin B-labeled activated microglia were only detected in their neighborhood. F-J labeled neurons were extremely rare in cortical regions rich in dopamine (e.g. cingulate cortex), and were absent in cortical regions with no dopamine (e.g. visual cortex). Parvalbumin was seen in some Fluoro-Jade-labeled neurons and parvalbumin immunostaining in local axon plexuses intensified. This AMPH paradigm affected fewer cortical regions, and caused smaller reduction in striatal tyrosine hydroxylase (TH) immunoreactivity than previous 1-day AMPH regimens generating seizures or severe (above 40 degrees C) hyperthermia. Correlation between peak or mean body T and the extent of neurodegeneration or microgliosis was below statistical significance. Astrogliosis (elevated levels of the astroglia-marker, glial fibrillary acidic protein (GFAP)) was detected in many brain regions. In the striatum and midbrain, F-J labeled neurons and activated microglia were absent, but astrogliosis, decreased TH immunolabel, and swollen TH fibers were detected. In sum, after this AMPH treatment, cortical pyramidal neurons were spared, but astrogliosis was brain-wide and some interneurons and microglia in three cortical regions with average or below-average dopamine input remained sensitive to AMPH exposure.

Amphetamine↗
PubMed1981

Extrageniculate projections to the visual cortex in the macaque monkey: an HRP study.

Extrageniculate projections to the visual cortex were examined in the macaque monkeys by the horseradish peroxidase (HRP) method. Extrageniculate neurons sending fibers to the visual cortex were found in the lateral and inferior pulvinar nuclei, paracentral thalamic nucleus, claustrum, basal nucleus of Meynert, lateral part of the basal amygdaloid nucleus, lateral hypothalamus, locus coeruleus, and dorsomedial and midline regions of the pontine tegmentum.

Animals↗
PubMed2003

Studies on the neuroanatomical basis for stress-induced oestrogen-potentiated suppression of reproductive function: evidence against direct corticotropin-releasing hormone projections to the vicinity of luteinizing hormone-releasing hormone cell bodies in female rats.

Various studies implicate corticotropin-releasing hormone (CRH) as a mediator for the inhibitory effects of stress on reproduction. This study was designed to elucidate the underlying neuroanatomy. The retrograde tracer cholera toxin was picospritzed into the vicinity of the luteinizing hormone-releasing hormone (LHRH) perikarya. CRH neurones were examined for the tracer in the medial preoptic nucleus (MPO), bed nucleus of the stria terminalis (BST), paraventricular nucleus (PVN), central amygdaloid nucleus (CeM), parabrachial nucleus (PB) and additional locations. Retrograde label was not detected in CRH neurones at any of these sites; nevertheless, in the MPO and PB, abundant retrogradely-labelled perikarya intermingled with CRH neurones. In the BST, CeM and PVN, sites containing major CRH cell populations, retrogradely-labelled cells were scarce or absent; however, retrograde labelling was found in adjacent regions: lateral septum, medial amygdaloid nucleus and areas bordering the PVN. Double-label in situ hybridization for the mRNAs for LHRH and the CRH type-1 receptor (CRH-R1) identified the receptor transcript at sites rostral and lateral to the LHRH neurones (in the vertical and horizontal limbs of the diagonal band) but not in the LHRH neurones. Given the ability of oestrogen to potentiate stress-induced suppression of LH release, the identification of CRH neurones immunoreactive for oestrogen receptor (ER) alpha in the MPO and for ER beta in the caudal PVN may be significant. In this context, it is also noteworthy that CRH neurones within the MPO and PB which are, respectively, immunopositive and immunonegative for ER alpha, lie within the vicinity of retrogradely-labelled cells. The present findings suggest that the means by which CRH may mediate inhibitory effects of stressors on LH release do not involve direct CRH projections to LHRH neurones; the indirect means for such regulation, and the sites at which oestrogen may potentiate the inhibitory response, remain to be established.

Animals↗
PubMed1995

Nigral and extranigral pathology in Parkinson's disease.

This article reviews data on the internal organization, neuronal types, and interconnections of limbic and motor components of the human brain, and the specific lesions which a few of them undergo during the course of Parkinson's disease (neuronal loss associated with the development of Lewy bodies and Lewy neurites). The severe involvement of nigral neuromelanin-laden projection cells has received particular attention during the past decades. This lesion interferes with normal function of the striatum and probably contributes to many of the motor dysfunctions characteristically occurring in Parkinson's disease. The similarly severe involvement of several areas and nuclei outside of the substantia nigra has often escaped notice. However, the pathology of Parkinson's disease cannot be completely described unless changes in these extranigral areas are taken into account. Interpretation of the characteristic lesional pattern is facilitated by combining schemata of both the limbic and motor systems. This approach reveals a key role by the amygdala and related structures in extranigral pathology. Severe lesions occur in the central amygdaloid nucleus, in nuclei projecting to the cerebral cortex in a non-specific manner, and in nuclei regulating endocrine and autonomic functions. It is suggested that extranigral lesions contribute to the development of behavioral changes and autonomic dysfunction.

Amygdala↗
PubMed2003

5-Hydroxytryptamine7 (5-HT7) receptor immunoreactivity-positive 'stigmoid body'-like structure in developing rat brains.

We examined the expression of 5-hydroxytryptamine(7) (5-HT(7)) receptor protein in developing and adult rats with immunohistochemical technique. In adult male rats, 5-HT(7) receptor immunoreactivity was detected in the septum, striatum, indusium griseum, tenia tecta, thalamus, hippocampus and hypothalamus in the forebrain as well as the pons and cerebellum. In brains of 1, 7, 15 and 21 days old male rats but not of adult ones, 5-HT(7) receptor immunoreactivity-positive dot-like structures were detected. The dot-like structures were visualized in hypothalamus, hippocampus, frontal cortex, brainstem and cerebellum at 1 day old male rats. In 7 days old male rats, the dot-like structures were found in the hypothalamus, medial preoptic area (MPA), bed nucleus of the stria terminalis (BST), amygdaloid nucleus and brainstem reticular formation. In 15 and 21 days old male and female rats, 5-HT(7) receptor immunoreactive dots were most clearly detected in MPA, hypothalamus, raphe pallidus, raphe magnus and brainstem reticular formation. The 5-HT(7) receptor immunoreactivity-positive dot-like structures were shown in the cytoplasm and they were less than 1 microm in diameter in 1 and 7 days old rats and became larger to 1-3 microm in 15 and 21 days old rats. From the distribution and morphologic features, the 5-HT(7) receptor immunoreactivity-positive dot-like structure found in developing rat brains is considered to be identical to a cytoplasmic inclusion named 'stigmoid body'.

Aging↗
PubMed1998

The neuronal organization of the supracapsular part of the stria terminalis in the rat: the dorsal component of the extended amygdala.

In the present normal anatomical light and electron microscopic study in the rat, histochemical (Nissl, Timm, Golgi) or immunocytochemical (microtubule-associated protein type 2, glutamate decarboxylase, glutamate receptor subunit 1, synaptophysin) stains were used to analyse neurons embedded within the stria terminalis and their associated neuropil. These cells are closely related to the bed nucleus of the stria terminalis and the centromedial amygdala, and have been termed the "supracapsular part of the bed nucleus of the stria terminalis". The largest part of this neuronal complex is located in the ventrolateral part of the stria, where it appears as a round or oval "lateral pocket" in virtually any type of light microscopic preparation because of its collection of neuronal cell bodies and dense neuropil, in addition to a lacework of unmyelinated axons. A much smaller but still distinct "medial pocket" is located in the medial corner of the stria. The large lateral subdivision of the supracapsular stria terminalis is directly continuous with the lateral bed nucleus of the stria terminalis and extends to the central amygdaloid nucleus, containing a column of neurons that is only broken up into cell clusters at the most caudal levels of the stria as it drops vertically toward the amygdala. The considerably smaller medial subdivision appears, in turn, to be directly continuous with the medial part of the bed nucleus of the stria terminalis. The medial column tapers off more rapidly than the lateral part, so that as the middle levels are approached, only small interrupted clusters of cells are seen. Solitary neurons can also be found in practically every part of the stria terminalis except among the ventrally located axons of the commissural component. Most of the neurons are small to medium in size, as viewed in transverse sections of the stria, but larger neurons are also encountered. In sections parallel to the stria, many neurons are fusiform in appearance. The dendrites are often aligned in a longitudinal fashion; many of the dendrites related to the cells in the lateral pocket are moderately to densely spined, whereas those in the medial pocket are more sparsely spined. The neuropil in both the lateral and medial pockets is characterized by boutons, bundles of unmyelinated axons, and dendrites. Based on their vesicle content, the boutons are divided into three major types: (A) round or slightly oval, agranular vesicles of uniform size; (B) pleomorphic, agranular vesicles, many of which are flattened; and (C) pleomorphic agranular vesicles, some of which are considerably larger than the ones in type B boutons. Type A boutons establish contacts with both dendritic spines and shafts, whereas types B and C usually contact dendritic shafts and sometimes somata. These synaptic components are similar to those described earlier for the central and medial amygdaloid nuclei. Overall, our results support the contention advanced in 1923 by Johnston [J. comp. Neurol. 35, 337481] that the cells accompanying the stria terminalis are interconnecting columns of a macrostructure encompassing the bed nucleus of the stria terminalis and centromedial amygdala. More recently, it has been appreciated that columns of neurons below the globus pallidus also belong to this macrostructure [Alheid G. F. et al. (1995) In The Rat Nervous System, 2nd edn, pp. 495 578, Academic, San Diego; de Olmos J. S. et al. (1985) In The Rat Nervous System, pp. 223-334, Academic, Sydney], which has been named the "extended amygdala".

Amygdala↗
PubMed2006

High doses of methamphetamine that cause disruption of the blood-brain barrier in limbic regions produce extensive neuronal degeneration in mouse hippocampus.

Histological examination of brain after a single high (40 mg/kg) dose of D-methamphetamine (METH) was used to determine the relationships between blood-brain barrier (BBB) disruption, hyperthermia, intense seizure activity, and extensive degeneration that this exposure often produces. In very hyperthermic mice (body temperatures > 40.5 degrees C) exhibiting status epilepticus, increase in mouse IgG immunoreactivity (IgGIR) in the medial and ventral amygdala was observed within 90 min after METH exposure. In a few instances, where body temperature was in the 40.0 degrees C range, such IgGIR was also seen in animals that had exhibited status epilepticus. Variable increases in IgGIR, which correlated with neurodegeneration, also occurred within 12 h in the hippocampus, indicating BBB disruption in this region also. Degenerating neurons, Fluoro-Jade C (FJ-C) labeled, were first detected 4 h after METH in the amygdala and hippocampus. Extensive neurodegeneration occurred in the amygdaloid and hippocampal pyramidal cell regions in animals with marked IgGIR increase in these regions by 12 and 24 h after METH. A very rapid activation of brain microglia and/or infiltration of macrophages in regions of notable IgGIR increase with intense neurodegeneration were seen within 24 h. The phagocytosis rate of neurons in the hippocampus was so rapid that FJ-C labeling was virtually nonexistent 3 days after METH. METH did not produce IgGIR increase or neurodegeneration in the limbic regions in the absence of hyperthermia and seizures. Thus, high doses of METH can cause damage to the BBB when hyperthermia occurs, resulting in rapid and extensive hippocampal and amygdalar damage. The BBB disruption in the medial amygdala occurs first, and may well be contributing to the induction and severity of seizures, while BBB disruption in the hippocampus is likely a result of the seizures and hyperthermia. This hippocampal damage should be sufficient to compromise learning and memory.

Amphetamine-Related Disorders↗
PubMed1996

[Increase of mu opioid receptor density in rat central nervous system following formalin nociception and its enhancement by electroacupuncture].

Using receptor autoradiography it was found: (1) After formalin injection in the rat hind paw, the mu opioid receptor density was significantly increased in certain central areas related to antinociception, i.e., the caudate nucleus, nucleus accumbens, amygdaloid nucleus, periaqueductal gray, interpeduncular nucleus, nucleus raphe magnus and spinal dorsal horn. (2) In addition to most of above mentioned central areas, in rat whose noxious responses were inhibited by electroacupuncture, there was a significant increase of receptor density in the cingulate cortex, septal area, preoptic area, superior central nucleus, superior colliculus and medial geniculate body. In comparison with the rats with formalin injection alone, the receptor density in the interpeduncular nucleus, the ventrolateral part of the caudal periaqueductal gray and spinal dorsal horn of the lumbar enlargement was further increased in the rats showing electroacupuncture analgesia. The above results provide further evidence supporting the postulation that noxious stimulation is capable of activating endogenous opioid peptidergic system which is further enhanced by electroacupuncture.

Acupuncture Analgesia↗
PubMed2002

[Sporadic cerebral amyloid angiopathy presenting with dementia and prominent capillary beta-amyloid deposition: a case report].

We report a sporadic case of unusual cerebral amyloid angiopathy (CAA) with prominent capillary involvement. A 67-year-old doctor developed gait disturbance, resting tremor and rigidity. He was diagnosed to have Parkinson's disease, for which the treatment with levodopa was effective. Four years later he began to exhibit progressive cognitive decline and behavioral abnormalities consisting of hallucination and agitation. Subsequently, his condition steadily worsened and became bedridden with severe dementia, and he died eight years after the disease onset. During the clinical course, there had been no episode of stroke. Postmortem examinations revealed the typical pathology of Parkinson's disease with frequent cortical Lewy bodies in the amygdala. The most striking pathological feature of this patient was widespread CAA where prominent beta-amyloid (A beta) deposition was observed in the capillaries of the neocortex, most pronouncedly in the occipital lobe, as well as leptomeningeal and cerebral medium-sized and small vessels. Further, perivascular plaques were found in half of the amyloid-laden capillaries. Tau-positive dystrophic neurites were only sparsely detectable within a few perivascular plaques. Despite the severe A beta pathology, there was no microaneurysmal dilatation, fibrinoid necrosis or vascular occlusion. There was only one small ischemic lesion in the brain. The cerebral white matter was unremarkable. Senile plaques of neuritic type and neurofibrillary tangles were mostly limited to the hippocampal regions and, to a lesser degree, in the amygdaloid nucleus, which did not meet the neuropathological criteria of Alzheimer's disease. On the gene analyses, his apolipoprotein E (ApoE) genotyping was verified to be heterozygous epsilon 3/epsilon 4, and no mutation was seen in exons 16 and 17 of the amyloid precursor protein gene. Severe A beta capillary angiopathy as seen in our patient is exceptional in sporadic CAA. Further, A beta angiopathy of this patient was notable in the absence of an associated cerebrovascular disease despite prominent A beta deposition in the vessel walls. Regarding the development of his severe dementia, the limbic pathology of Lewy body disease might be one of the potential causes, but A beta angiopathy appears more likely because of its severity. We speculate that widespread A beta deposition disregulates the blood-brain barrier of the capillaries leading to a disturbance of the microcirculation throughout the cerebral cortex without obvious ischemic disintegration of the neuropil. We should take into consideration that A beta angiopathy can present as progressive dementia without cerebrovascular disease.

Aged↗
PubMed1992

Glucose utilization and insulin binding in discrete brain areas of obese rats.

The present study was carried out to determine whether genetically obese Zucker rats present changes in brain glucose utilization and/or insulin binding when compared to their lean counterparts. Glucose utilization in the whole brain, determined by measurement of 2-deoxy(1-3H)glucose-6-phosphate, was significantly lower in obese than in lean Zucker rats. In order to precise the structure involved, we then used quantitative autoradiography methods after either (1-14C) 2-deoxyglucose injection or 125I-insulin incubation. In obese rats, local cerebral glucose utilization (LCGU) was significantly decreased in the external plexiform layer (-37%, p < 0.05), in the lateral hypothalamus (-23%, p < 0.05), and in the basolateral amygdaloid nucleus (-30%, p < 0.05). In contrast, no difference in specific insulin binding was found between the two genotypes in any of the areas studied. These results are consistent with some data showing a decrease of LCGU in hyperinsulinemic rats. All together, these data show perturbations of glucose utilization, particularly in structures linked to the regulation of body weight and food intake in obese Zucker rats.

Amygdala↗
PubMed2002

[Argyrophilic grain disease (AgD), a frequent and largely underestimated cause of dementia in old patients].

Argyrophilic grain disease (AgD) is a late-onset dementia morphologically characterized by abundant neuropil grains (ArGs). ArGs are mainly found in the CA1 subfield of the cornu ammonis, entorhinal and transentorhinal cortices, the amygdala and the hypothalamic lateral tuberal nuclei. We have recently shown that abnormally phosphosphorylated tau protein is the main protein constituent of ArGs and that tau is hyperphosphorylated in up to 80p.100 of nerve cels in areas rich in ArGs. We could demonstrate that at least a subset of grains are formed within dendrites and dendritic side-branches of neurons containing hyperphosphylated tau. Morphology of dendrites containing grains suggests that a process of progressive dendritic shrinkage is taking place in neurons bearing ArGs. Furthermore it became apparent that the presence of ArGs is not necessarily associated with a cognitive decline. Our studies on AgD cases with and without dementia suggest that AgD is a progressive neurodegenerative disorder with early subclinical lesions in anterior part of the hippocampal formation. At later stages involvement of more caudal parts of the hippocampal formation generally results in a cognitive decline. Thus, one possible explanation for the dementia observed in some subjects with AgD is that there is a more widepread loss of postsynaptic structures, including synaptic contacts, throughout the hippocampus-entorhinal/parahippocampal complex and the amygdaloid nuclei. Most of the reported AgD cases are associated with neurofibrillary lesions (e.g. neurofibrillary tangles) which are also typical of Alzheimer's disease (AD). However, neurofibrillary changes do not exceed early (entorhinal and limbic) Braak stages which generally are not associated with a cognitive decline. Additional neuropathological features of AgD include oligodendroglial tau filamentous inclusions ( coiled bodies ), ballooned neurons and astrocytic tau pathology. The clinical features of AgD are poorly understood. However, preliminary data from retrospective studies suggest that in AgD behavioural disturbances will precede memory failure and memory decline. Furthermore, it has been shown that the ApoEe4 allele does not constitute a risk factor for the development of AgD. In conclusion it seems very likely that AgD is a distinct dementing disorder of old age that has to be distinguished from other tauopathies, e.g. AD, by both morphological and genetic criteria.

Age Factors↗
PubMed2001

Expression of calbindin D28K in the dopaminergic mesotelencephalic system in embryonic and fetal human brain.

A subset of tyrosine-hydroxylase (TH) neurons of the substantia nigra (A9) containing calbindin D28K (CaBP) appeared to be less vulnerable to cell death induced by Parkinson's disease than the subset containing dopamine (DA) alone. Because grafting procedures of fetal human neurons are increasingly used in the therapy of Parkinson's disease, it is important to study the development of DA neurons coexpressing CaBP. In humans, the genesis of TH immunoreactivity of A9, of the ventral tegmental area (A10), and of the retrorubral area (A8) occurred during a 2-week period from the 4. 5th gestational week (g.w.) in the ventricular zone of the floor plate and the contiguous basal plate of the mesencephalon and diencephalon, i.e., the prosomeres p1-p3. Double-immunolabeled TH-CaBP neurons were detected from 5.5 g.w. on, in the first wave of DA neuron's migration, and were observed in their final residence in the dorsal A9 by 10.5 g.w. Calretinin immunoreactivity was expressed in TH-immunoreactive (IR) neurons from 10.5 g.w. on. Ascending TH-CaBP-IR axons were observed toward the telencephalon from 6-7 g.w. , reaching the anlage of the nucleus accumbens and amygdaloid complex at 10.5 g.w., but were not detected in the ganglionic eminence at this latter stage. Dopaminergic patches were detected at 13 g.w. in the anlage of the putamen, but no TH-CaBP-IR fibers were observed in the matrix at this stage. In conclusion, even if CaBP immunoreactivity was detected in TH-IR cell bodies during the embryonic period, the TH-CaBP-IR axonal terminal was observed earlier in some limbic-related areas than in the matrix compartment of the basal ganglia in humans.

Axons↗
PubMed2005

Distribution of nitric oxide synthase immunoreactivity in the mouse brain.

Nitric oxide (NO) is a gaseous intercellular messenger with a wide range of neural functions. NO is synthesized by activation of different isoforms of nitric oxide synthases (NOS). At present NOS immunoreactivity has been described in mouse brain in restricted and definite areas and no detailed mapping studies have yet been reported for NOS immunoreactivity. We have studied the distribution of neuronal NOS-containing neurons in the brain of three months male mice, using a specific commercial polyclonal antibody against the neuronal isoform of nitric oxide synthase (nNOS). Neuronal cell bodies exhibiting nNOS immunoreactivity were found in several distinct nuclei throughout the brain. The neurons that were positively stained exhibited different intensities of reaction. In some brain areas (i.e., cortex, striatum, tegmental nuclei) neurons were intensely stained in a Golgi-like fashion. In other regions, immunoreactive cells are moderately stained (i.e., magnocellular nucleus of the posterior commissure, amygdaloid nucleus, interpeduncular nucleus, lateral periaqueductal gray) or weakly stained (i.e., vascular organ of the lamina terminalis, hippocampus, inferior colliculus, reticular nucleus). In the mouse, the NO-producing system appears well developed and widely diffused. In particular, nNOS immunoreactive neurons seem chiefly present in several sensory pathways like all the nuclei of the olfactory system, as well as in many regions of the lymbic system. These data suggest a widespread role for the NO system in the mouse nervous system.

Animals↗
PubMedDate not supplied

Neuropathology of mouse hippocampus in acute trimethyltin intoxication.

BALB/c mice were injected IP with a single dose of trimethyltin chloride (3.0 mg TMT/kg body weight). Severe body tremor was observed within 12 hours post-injection. All animals were sacrificed 48 hours post-injection by means of intracardial perfusion with 2.5% buffered glutaraldehyde. Light microscopic examination revealed extensive neuronal necrosis in the granule cells of the fascia dentata of the hippocampus. Scattered neuronal loss was also observed in the pyriform cortex, the neocortex, amygdaloid nucleus, and the brainstem. Electron microscopic examination of the hippocampus revealed lysosomal accumulation in both the granule cells and pyramidal neurons. While extensive cellular necrosis was observed in the granule cells, the pyramidal neurons only displayed some dilatation and vacuolation of their endoplasmic reticulum. This report represents the first in depth pathological study in the mouse hippocampus following an acute exposure to TMT.

Animals↗
PubMed1986

Preliminary brain autopsy findings in progredient Rett syndrome.

Postmortem human brain analyses have been performed to further evaluate pathogenetic aspects of the Rett syndrome. While there are no significant abnormalities with respect to amino acid concentrations in putamen, caudate nucleus, red nucleus and thalamus, the concentration of kynurenine is increased in putamen, caudate nucleus, gl. pallidus, raphe and amygdaloid n. In contrast, serotonin and its metabolite 5-hydroxyindole acetic acid are below normal levels. D2-receptor number is decreased and there is a significant drop in the concentration of the iron-binding protein ferritin. It can be concluded, that reduction of D2-receptors is due to loss of cholinergic and GABA-ergic cell bodies in the striatum or may be a response to iron deficiency. Low serotonergic and high kynurenergic activity may be of pathogenetic importance in the frequently observed cerebral seizures in Rett syndrome.

Amino Acids↗
PubMedDate not supplied

Distribution of neuropeptide K-immunoreactivity in the rat central nervous system.

The distribution of neuropeptide K (NPK), a 36-residue amidated peptide originally isolated from porcine brain, is described in the rat CNS by immunohistochemical methods. Antibodies were generated in rabbits to N-terminus and C-terminus regions of the peptide and the distribution of immunoreactive cell bodies and fibers was mapped in colchicine-treated and normal rat brains. Major areas of cell body staining included the medial habenular nucleus, the ventromedial nucleus of the hypothalamus, the interpeduncular nucleus, the lateral dorsal tegmental nucleus, the nucleus raphe pallidus, and the nucleus of the solitary tract. Some of the areas of dense NPK-fiber immunoreactivity included the ventral pallidum, the caudate-putamen, certain areas of the hypothalamus, the central and medial amygdaloid nuclei, the entopeduncular nucleus, the habenular nuclei, the substantia nigra pars reticulata, the caudal part of the spinal nucleus of the trigeminal nerve, the nucleus of the solitary tract and the dorsal horn of the spinal cord. A striking similarity exists between this pattern of immunoreactive staining and that described for substance P, suggesting that the tachykinin systems do not exist independently in the brain. The possible roles for multiple tachykinins in the brain are discussed.

Animals↗