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At least 199 records · Page 11Linked to original sources

Influence of passive avoidance learning by substance P in the basolateral amygdala.

Neuropeptide substance P (SP) has reinforcing and memory facilitating effects after its peripheral or central application. Rats self-inject SP into the ventromedial caudate-putamen and SP microinjections into the basal forebrain induce place preference with a simultaneous increase of dopamine level. In the amygdaloid body SP positive neurones and terminals have been identified. The aim of the present study was to examine the possible reinforcing effects of SP in the basolateral amygdala (ABL). CFY male rats were conditioned in two-compartment passive avoidance paradigm and place preference was examined in two-compartment-box and in circular open field. Animals were microinjected bilaterally with 10 ng SP, 100 ng SP or vehicle solution (0.4 microl/side) into the ABL. Results showed that post-shock infusion of 10 ng SP significantly enhanced passive avoidance learning while 100 ng SP was ineffective. In two-compartment-box and in circular open field place preference did not develop after SP treatments, however. Our data are the first to demonstrate that SP in the ABL is involved in learning and memory processes related to aversive situations. Results that SP microinjections were not followed by rewarding-reinforcing consequences in place preference paradigms indicate that the local SP network in the ABL is not involved in neuronal circuitry responsible for addictive behaviour.

Amygdala↗

Case study: topographical brain mapping in hostility following mild closed head injury.

Previous research suggests that right frontal and temporal lobe arousal may inhibit and elicit hostility, respectively. For example, emotional lability (including rage) has resulted from lesion of the bulbar motor nuclei, and neocortical upper motor neurons in particular (Lieberman & Benson, 1977). Ablation of hypothalamic sites has resulted in sham rage (Flynn, Cummings & Tomiyasu, 1988; Sachdev, Smith, Matheson & Last, 1992; Tonkonogy & Geller, 1992) suggesting that these frontal pathways may inhibit hostility. In the present study, a patient with hostility management problems secondary to closed head injury from a motor vehicle accident was evaluated using topographical brain mapping and quantitative electroencephalograph (QEEG) techniques. Comparisons of beta magnitude were performed between frontal and temporal sites at the right and left cerebrums. The results support the contention of an oppositional anterior to posterior mediation of hostility. The present electroencephalagraphic research supports the predominant neuropsychological theory that the right orbital-frontal region inhibits the right amygdaloid bodies, thereby decreasing hostility level (Kolb & Wishaw, 1990).

Adult↗

The piriform cortex and the endopiriform nucleus in the rat reveal generally similar pattern of connections.

The afferent and efferent connections of the piriform cortex and the endopiriform nucleus in the rat were studied by the method of axonal transport of two fluorescent tracers: Fluoro-Gold and Fluoro-Ruby. The results indicate that both structures possess not only the connections with the olfactory system, but also the reciprocal connections with the limbic system (entorhinal cortex, amygdaloid body), thalamus (mediodorsal and midline nuclei), extrapyramidal system (ventral part of the nucleus accumbens). The topographic differences in the organization of the association connections between the anterior and posterior parts of the piriform cortex are reported. Additionally, the reciprocal and relatively numerous connections between the endopiriform nucleus and the piriform cortex may result in their modulatory function, which in some pathological circumstances may have a critical significance in epileptogenesis.

Afferent Pathways↗

[An autopsy case of motoneuron disease with dementia of long duration].

An autopsy case of MND with dementia, 67 years old, man, was reported. The behavioral disturbance appeared at 61 years old, and was followed by the upper limb weakness and respiratory failure. He had remained on a respirator for 56 months. The total duration of the disease was 74 months, which was far longer than mean duration of the cases previously reported, 25-30 months. The pathological findings were about essentially identical to those mentioned before, such as cortical alterations in temporal and frontal lobes, neuronal loss with gliosis in amygdaloid body and substantia nigra, and loss of lower motoneurons in anterior horn of spinal cord and in the several motor cranial nerve nuclei. There were several Bunina bodies in the remnant lower motoneurons, but no changes in the pyramidal tracts or loss of Betz cells in the precentral gyrus. Intracytoplasmic ubiquitin-immunopositive inclusions in the granule cells of hippocampal dentate gyrus were also encountered, but the number of which did not increased, compared to the preceding data. There may be frequently little correlation between the disease duration and the number of such inclusions. The regional alteration in the intermediate zone between subiculum and entorhinal cortex was revealed also at the level of the splenium of corpus callosum. It has been reported that such parahippocampal lesion may initiate at the anterior part of temporal lobe and become undiscernible at more posterior level than the lateral geniculate body. The formation of such parahippocampal lesion may be concerning with the length of disease duration. In addition, there were numerous senile plaques, diffuse or neuritic type only in the parietal lobe cortex without any other changes.

Aged↗

[The effect of adren- and serotoninergic substances on the behavior of amygdalectomized rats and on the aggressiveness evoked by intra-amygdaloid administration of acetylcholine].

The effect of serotoninergic (serotonin, 1-trytophane, imipramime, methysergide), catecholaminergic (noradrenaline, amphetamine, dopamine, 1-DOPA, iproniazid) and cholinergic drugs (physostigmine, atropine, benactyzine) on emotional reactions and orienting-motor activity, as well as the effect of these drugs on shock-elicited aggressiveness enhanced by intraamygdaloid microinjection of acetylcholine was investigated in experiments on amygdalectomized male albino rats. In amygdalectomized animals, as compared to control false-operated rats, the stimulating effect of amphetamine, imipramine, tryptophane and m-cholinoblockators was enhanced and their inhibitory effect was weakened. Bilateral microinjection of cholinergic drugs (acetylcholine, physostigmine and carbacholine) and noradrenaline into the amygdaloid body intensified emotional reactivity and aggressiveness. Microinjection of serotonin and dopamine inhibited aggressiveness and caused facilitaion of orienting-motor activity. It is suggested that the adrenergic system intensifies and serotoninergic system depresses the m-cholinergic trigger mechanism of aggressive behavior in limbico-diencephalic structures.

Acetylcholine↗

[Analysis of the morphological substrate of information processing in the dog brain pallidal complex based on organizational characteristics of its afferent projections].

Projections from functionally diverse cortical and subcortical structures (cortex, amygdaloid body, substantia nigra, ventral tegmental area, and thalamus) to the pallidum (globus pallidus, entopeduncular nucleus and ventral pallidum) were studied in dogs using the method of axonal transport of the retrograde markers. Anatomical aspects of both the functional heterogeneity of the pallidal structures and integrative processing of information which underlie the mechanisms of adaptive behavior, were analyzed on the basis of the results obtained.

Afferent Pathways↗

Effect of estradiol implanted in the corticomedial amygdala on the sexual behavior of castrated male rats.

1. The purpose of the present investigation was to study the effect of beta-estradiol crystals implanted in the corticomedial area of the amygdaloid body on the sexual behavior of castrated male rats. 2. The animals were divided into the following groups: group I (N = 9), castrated rats; group II (N = 4), rats which had been castrated and stereotaxically implanted with cholesterol, both groups being used as controls; group III (N = 6), castrated rats with estradiol implants. Latency to the first anogenital exploration, latency to the first mount and mount frequency were determined during the pre-castration and post-castration phases and after the material had been implanted in groups II and III in 10-min observation sessions. 3. There was diminished sexual behavior of the animals in group I without spontaneous recurrence within the period observed. Group II animals, who had undergone implantation of cholesterol, an inert substance, maintained low levels of sexual behavior (post-castration 0.8 +/- 0.7 vs 0.0 +/- 0.0 and 0.5 +/- 0.5 on the 6th and 9th day after implantation, respectively). Group III animals presented a gradual increase in the number of mounts (from post-castration 1.2 +/- 0.5 to 6.5 +/- 2.7 and 4.1 +/- 1.0 on the 6th and 9th day after implantation, respectively) and a decrease of mount latency (from post-castration 431.2 +/- 55.9 to 226.1 +/- 119.6 and 51.0 +/- 28.9 on the 6th and 9th day after implantation, respectively) reaching pre-castration levels on the 6th and 9th day after beta-estradiol implantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗

Antidepressant binding sites in brain: autoradiographic comparison of [3H]paroxetine and [3H]imipramine localization and relationship to serotonin transporter.

Binding of two different antidepressant drugs, [3H]paroxetine and [3H]imipramine in 30 rat brain regions was visualized, compared and quantified by means of autoradiography and densitometry. Specific binding of [3H]paroxetine to coronal sections of diencephalon represented 85% of total binding and was saturable and of high affinity (KD, 0.36 +/- 0.07 nM) with a maximum number of binding sites of 276 +/- 41 fmol/mg protein. The autoradiograms showed a heterogenous distribution of [3H]paroxetine in brain with selective accumulation of label in brain regions known to contain serotonergic terminals, axons and cell bodies (amygdaloid and raphe nuclei, superior colliculus, substantia nigra and medial forebrain bundle). Binding was displaced selectively with other serotonin uptake inhibitors (clomipramine and fluoxetine) and almost abolished by lesioning the serotonergic neurons with p-chloroamphetamine. The desipramine-sensitive [3H]imipramine binding was more diffuse with relatively high density in cerebral cortex and hippocampus and was only decreased partially in animals treated with p-chloroamphetamine. The results indicate that [3H]paroxetine, but not [3H]imipramine, is a ligand of choice to selectively label serotonergic structures in brain.

Animals↗

[Effect of hypokinesia on the ultrastructure of emotion-controlling structures in the rat brain].

Hypokinesia lasting 40 and 90 days causes a number of ultramicroscopic reorganizations in neurons, synapses and glial elements of the singular cortex and the central amygdaloid nucleus. The longer the time of hypokinesia, the more numerous and variable the reorganizations become. For the amygdaloid body presence of neurons with various degree of chromatolysis, reactive and destructive changes of organells, agglutination and reduction in number of the synaptic vesicles, increasing number of synapses, possessing certain features of low functional activity are most specific. For the singular cortes are peculiar convolution of nuclear and cellular membranes, synaptic contact, increasing intercellular spaces, as well as changes in the structure of some axo-spine synapses, the spine apparatus including.

Amygdala↗

Brain evolution and Alzheimer's disease.

It is argued that rapid evolution of the hominid brain was accomplished by the molecular mechanisms of "regulatory evolution" and "gene duplication". These genomic processes may have made newly elaborated brain regions--including the association neocortices and parts of the hippocampal formation, nucleus basalis of Meynert and amygdaloid body--vulnerable to Alzheimer's disease, by increasing the value of a disease-specific genomic character function. Trisomy 21, it is proposed, further increases this value.

Alzheimer Disease↗

Thalamoamygdaloid connections studied by the method of retrograde transport.

On the basis of retrograde horseradish peroxidase transport from nuclei ot the amygdaloid body of the rat to the thalamus, it was found that several groups of thalamic nuclei send fibers to the amygdala. These are: (i) nuclei of posterior region of thalamus and neighboring area of the tegmentum - peripeduncular nucleus, suprageniculate-limitans nucleus, (ii) midline nuclei - paraventricular nucleus, parataenial nucleus, nucleus reuniens, (ii) intralaminar nuclei - central medial nucleus, parafascicular nucleus, (iv) medidorsal nucleus. There are two main systems of thalamoamygdaloid connections. One of them arising in the posterior region of the thalamus terminates in the lateral nucleus of the amygdala and the lateral part of its central nucleus. The other system begins in the intralaminar and midline nuclei and in the mediodorsal nucleus of the thalamus. It reaches the remaining nuclei of the amygdala. Amygdalopetal connections of the interlaminar and middline nuclei of the thalamus, especially those arising in the paraventricular and parataenial nucleus, are mostly bilateral.

Amygdala↗

The organization of intraamygdaloid connections; an HRP study.

The localization of neurons from which the projections to other amygdaloid nuclei arise was studied using the retrograde transport of horseradish peroxidase. It was found that the basal nuclei (dorsal and ventral) appear to be the main source of intraamygdaloid connections; they project to the central, medial and lateral nucleus of the amygdala. The medial and the central nucleus receive the most intraamygdaloid connections: the medial--from the basal dorsal, basal ventral, posterior part of the cortical nucleus and from the nucleus of the lateral olfactory tract; the central nucleus--from the basal (dorsal and ventral) nuclei and from the nucleus of the lateral olfactory tract. The afferent intraamygdaloid connections of the cortical and lateral nucleus were also found. These results are discussed with reference to the physiological differentiation and hypothalamic afferents of the amygdaloid body.

Afferent Pathways↗

[Non-herpetic acute limbic encephalitis].

We reported four cases of acute encephalitis, in which MRI abnormalities localized in the limbic system. In the four cases, fever and consciousness disturbance were commonly found and convulsive seizures appeared in three. Within 10 days, their consciousness level became clear, but severe amnestic syndrome remained as sequela. Cerebrospinal fluid (CSF) at the acute stage revealed mild lymphocytic pleocytosis and elevated protein. MRI revealed abnormal signal intensities in both hippocampi and amygdaloid bodies, although CT scans were normal. Herpes simplex encephalitis selectively affects one or both temporal lobes and the limbic system, But our cases spared the temporal lobes. Additionally, serum and CSF antibody titers by CF and ELISA for herpes simplex virus (HSV) were within normal range from the acute to convalescent stages. Neither HSV type 1 and 2 DNA genomes by sensitive PCR-hybridization method were detected in CSF taken from the acute stage of all four cases. On the other hand, paraneoplastic limbic encephalitis is known as a subacute encephalitis predominantly involving the limbic system. MRI shows high signal intensities on T2-weighted in both medial temporal lobes. In our cases, this type of limbic encephalitis was excluded because of the acute onset and lack of malignancy. Accordingly, our four cases are regarded as non-herpetic acute limbic encephalitis. Several Japanese similar cases have been reported. Further etiological studies should be performed.

Acute Disease↗

Distinct mRNA expression of the highly homologous convertases PC5 and PACE4 in the rat brain and pituitary.

Posttranslational endoproteolysis is essential for the production of biologically active peptides from inactive precursors. Six kexin/substilisin-like endoproteases have been characterized in mammalian species. To understand the complex physiological functions of each convertase within a cellular context it is necessary to comprehensively define its tissue distribution and cohabitation with other members of the family. Previous studies demonstrated the distinct distribution of PC1, PC2, and furin mRNAs in the pituitary and brain, suggesting a unique function for each enzyme. In the present study, the mRNA tissue distributions of the two most recent and homologous members, PC5 and PACE4, were analyzed in rat pituitary and brain using in situ hybridization histochemistry. In the pituitary, the anterior lobe exhibited moderate levels of PC5 and high levels of PACE4 mRNAs. The intermediate lobe showed low levels of PC5 expression, while PACE4 mRNA levels were undetectable. PACE4 transcripts were detected throughout cells of the neural lobe suggesting expression in pituicytes. In the brain, PC5 expression was more restricted than PACE4. PC5 mRNA was detected only in neuronal cells, whereas PACE4 mRNA was expressed in both neuronal and glial cells. In areas that are rich in neuropeptides such as cortex, hippocampus, and hypothalamus, mRNA levels of PC5 were high but PACE4 were low or undetectable. In regions, such as the amygdaloid body and thalamus, distinct but complementary distributions of PC5 and PACE4 mRNAs were observed. The medial habenular and cerebellar Purkinje cells expressed very high levels of PACE4 mRNA. The present data strongly suggest unique tissue-specific functions of PC5 and PACE4.

Animals↗

[Age-related alterations on GTP binding proteins in postmortem human brain].

It is important that natural aging-related alterations are characterized to understand disabilities associated with aging. In this study, age-related alterations of GTP binding (G) proteins were examined in membrane preparations from several regions (frontal cortex, temporal cortex, parietal cortex, occipital cortex, caudate nucleus, amygdaloid body) in postmortem human brain. Subjects were free from neurologic or psychiatric disease. The quantity of G proteins (Gs alpha, Gi alpha, Go alpha, Gq alpha, G beta subunit) was determined by immunoblotting with polyclonal antibody (RM/1, AS/7, GC/2, QL, SW/1, respectively). The function of G proteins was examined by photoaffinity GTP analog [azidoanilido GTP (AAGTP)] binding. The immunoreactivities of Gi alpha and Gq alpha subunits were correlated inversely with age in many areas. In caudate nucleus, the GsL alpha (45 kDa) and Go alpha subunit immunoreactivities were decreased with age. And the G beta subunit immunoreactivities showed a negative correlation with age in temporal and occipital cortex areas. However, AAGTP labeling to Gs alpha and Gi/o alpha and the ratio of Gs alpha to Gi/o alpha AAGTP binding showed no age-dependent changes. Our findings suggest that the functional modulation may compensate for quantitative alterations of G proteins with human senescence.

Aging↗

Autoradiographic distribution and receptor binding profile of [125I]Bolton Hunter-rat amylin binding sites in the rat brain.

Amylin is a recently isolated peptide from amyloid plaques in noninsulin-dependent diabetic patients and showed high sequence homology with calcitonin gene-related peptide. We investigated the distribution and the binding profile of [125I]Bolton Hunter-rat amylin ([125I]BH-rat amylin) binding sites in the rat brain, as well as the affinity of rat amylin for [125I]hCGRP alpha binding sites in the brain, atrium (CGRP1 receptor-enriched tissue) and vas deferens (CGRP2 receptor-enriched tissue). High amounts of high affinity [125I]BH-rat amylin binding sites were observed in the nucleus accumbens, various hypothalamic nuclei, amygdaloid body, dorsal raphe, tegmental and parabrachial nuclei and the locus ceruleus. Interestingly, both rat amylin and salmon calcitonin revealed low nanomolar affinities (2-19 nM) for [125I] BH-rat amylin binding sites in the various brain areas, whereas human calcitonin gene-related peptide-alpha (hCGRP alpha) showed lower affinities ranging between 13 to 150 nM. Moreover, the affinity of rat amylin was much lower than that of hCGRP alpha for [125I]hCGRP alpha binding in the brain, atrium and vas deferens, except for very few areas such as the nucleus accumbens and ventral striatum. Similarly, rat amylin was much weaker (100- to 400-fold) than hCGRP alpha to induce a biological effect in the atrium and vas deferens. These results thus suggest the existence of unique [125I]BH-rat amylin binding sites in the rat brain as well as limited cross-reactivity between rat amylin and [125I]hCGRP alpha receptors present in the brain, atrium and vas deferens.

Amyloid↗

Binding profile of a selective calcitonin gene-related peptide (CGRP) receptor antagonist ligand, [125I-Tyr]hCGRP8-37, in rat brain and peripheral tissues.

The calcitonin gene-related peptide (CGRP) C-terminal fragment human CGRP8-37 acts as a potent antagonist of various in vitro and in vivo effects of CGRP. Its iodinated counterpart, [125I-Tyr] hCGRP8-37, binds with high affinity (KD values between 7.5 x 10(-11)-2.1 x 10(-10) M) to what is apparently a single class of CGRP receptors in brain, atrium and vas deferens membrane preparations. The relative potencies of various CGRP-related fragments and analogs in competing for [125I-Tyr]hCGRP8-37 binding sites were similar in these three preparations, with hCGRP alpha being the most potent competitor, followed by unlabeled hCGRP8-37, the linear agonist [acetamidomethyl-cysteine2,7] hCGRP alpha, and finally by rat amylin-amide and salmon calcitonin. Competition profiles suggested the existence of a single affinity site (except in the case of hCGRP alpha, for which competition binding data were best fitted to two apparent affinity constants in all three tissues), whereas rat amylin-amide revealed two affinity constants in the rat brain. Guanylylimidodiphosphate (100 microM) failed to alter specific [125I-Tyr]hCGRP8-37 binding in the various tissues studied here. Quantitative receptor autoradiography in the rat brain revealed [125I-Tyr]hCGRP8-37 binding sites mostly concentrated in the nucleus accumbens (shell), caudate putamen (tail), amygdaloid body, pontine nuclei, cerebellum and inferior olive, whereas lower quantities of sites were present in the olfactory tubercle, nucleus accumbens (core), medial geniculate, superior colliculus, temporal cortex, inferior colliculus, lateral lemniscus, vestibular nuclei and principal sensory trigeminal nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[The amygdala-caudate system and behavior].

Discussion of the cortical-subcortical interactions in organization of the behavioral reaction of various biological significance. Analysis of vast original experimental data on the morphology of the amygdala-caudate relations, on the neuron reconstructions in the cortical-subcortical systems under the positive and inhibitory conditioned reflexes, on the role of individual nuclei of the amygdaloid body in the trophic and defensive reactions, in organization of internal inhibition.

Afferent Pathways↗