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PubMed1995

Four-day hyperinsulinemia in euglycemic conditions alters local cerebral glucose utilization in specific brain nuclei of freely moving rats.

Although insulin is a well known regulator of peripheral tissue glucose metabolism, there is little agreement over its effects on brain glucose metabolism. Several investigators report that peripheral insulin may enter the brain via several routes. The presence of insulin receptors specific to brain, coupled to diverse reports of the effect of acute insulin administration on brain glucose use, led us to carry out a 4-day hyperinsulinemic euglycemic clamp in freely moving rats with subsequent labelled 2-deoxyglucose metabolic mapping studies. It was found that after 4 days of peripheral insulin infusion, several brain regions (Anterior Hypothalamic area, Suprachiasmatic nucleus, Basolateral Amygdaloid nucleus, Supramammillary bodies, Medial Geniculate nucleus and Locus Coeruleus) had an altered local cerebral glucose utilization. Upon subsequent analysis of their anatomical and functional connections it is proposed that insulin may regulate an integrated circuit of pathways within the central nervous system.

Animals↗
PubMed2005

The nigro-striatal and nigro-amygdaloid pathways undergo different degeneration processes in brains of dementia with Lewy bodies.

We immunohistochemically investigated the degeneration processes of the nigro-striatal and nigro-amygdaloid pathways and the relationship between the loss of dopaminergic neurons and Lewy bodies (LB) formation in the substantia nigra using 15 autopsied cases of dementia with Lewy bodies (DLB). The number of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra and TH-positive axonal terminals in the putamen decreased with a specific pattern. The substantia nigra possessed alpha-synuclein-positive LB-bearing neurons that were almost evenly distributed, while the putamen exhibited diffuse or granular alpha-synuclein-immunostaining. Most of the granular stains were positive for anti-phosphorylated alpha-synuclein antibody, whereas the diffuse stains were negative. These findings suggest that the axonal terminals in the putamen undergo abnormal alpha-synuclein accumulation, but may not always originate from LB-bearing neurons in the substantia nigra. The central amygdaloid nucleus contained anti-alpha-synuclein- and -phosphorylated alpha-synuclein-positive dystrophic axonal terminals, the degree of which was greater for cases with granular staining in the putamen, and which was proportional to the number of alpha-synuclein-positive neurons in the substantia nigra. Thus, the axonal terminals in the central amygdaloid nucleus may have originated from LB-bearing neurons in the substantia nigra. The results of the present study indicate that the nigro-striatal and nigro-amygdaloid pathways undergo different degeneration processes in DLB, and suggest that the degeneration of the nigro-amygdaloid pathway more strongly reflects LB formation in dopaminergic neurons of the substantia nigra than that of the nigro-striatal pathway. In addition, they indicate that there is no direct relationship between the loss of dopaminergic neurons and LB formation in the substantia nigra.

Aged↗
PubMed1995

Distribution of parvalbumin-immunoreactive cells and fibers in the human amygdaloid complex.

The calcium-binding protein, parvalbumin, was localized immunohistochemically in the human amygdaloid complex. Neuronal cell bodies and fibers that are immunoreactive to parvalbumin were observed in most of the amygdaloid nuclei and cortical areas. Three types of immunoreactive aspiny neurons, ranging from small spherical cells (type 1) to large multipolar cells (type 2) and fusiform cells (type 3), were observed. The densities of the types of neurons that were parvalbumin-immunoreactive varied in the different regions of the amygdala. The highest densities of parvalbumin-immunoreactive neurons were observed in the lateral nucleus, in the magnocellular and intermediate divisions of the basal nucleus, in the magnocellular division of the accessory basal nucleus and in the amygdalohippocampal area. The regions containing the lowest density of parvalbumin-immunoreactive cells were the paralaminar nucleus, the parvicellular division of the basal nucleus, the central nucleus, the medial nucleus and the anterior cortical nucleus. In general, the distribution of immunoreactive fibers and terminals paralleled that of immunoreactive cells. Parvalbumin-immunoreactive varicose fibers formed basket-like plexi and cartridges around the unstained neurons, which suggests that parvalbumin is located in GABAergic basket cells and chandelier cells, respectively. The distribution of parvalbumin-immunoreactive profiles in the human amygdaloid complex was similar to, rather than different from that previously reported in the monkey amygdala (Pitkänen and Amaral [1993] J. Comp. Neurol. 331:14-36). This study provides baseline information about the organization of GABAergic inhibitory circuitries in the human amygdaloid complex.

Adult↗
PubMed1986

Intrinsic neurons in the amygdaloid field projected to by the medial geniculate body mediate emotional responses conditioned to acoustic stimuli.

In previous experiments we implicated projections from the medial geniculate body (MG) to a subcortical field, involving portions of the posterior caudate-putamen and amygdala, in the classical conditioning of emotional responses to acoustic stimuli in the rat. In the present series of experiments we examined whether intrinsic neurons in the subcortical field mediate emotional conditioning and, if so, whether the critical neurons are contained within the amygdala or the caudate-putamen. Rats were prepared with a unilateral electrolytic lesion of the MG. Contralaterally, intrinsic neurons were destroyed in the subcortical field by microinjection of ibotenic acid. This lesion combination leaves one MG and one subcortical field intact but disconnected. Controls received unilateral injection of phosphate buffer vehicle into the subcortical field contralateral to the MG lesion or were unoperated. After two weeks the animals were instrumented for continuous, computer-assisted recording of arterial pressure and heart rate and subjected to classical conditioning trials involving the presentation of a pure tone in association with foot-shock. The occurrence of the shock with respect to the tone was random for a pseudoconditioned control group. Conditioned changes in mean arterial pressure, heart rate and emotional behavior ('freezing') elicited by the tone were assessed during extinction trials. Following completion of the experiments, the rats were sacrificed and their brains were removed and sectioned using standard procedures. Lesion location and size was evaluated with the assistance of a computer-based image processing system. In unoperated conditioned rats the acoustic stimulus elicited increases in arterial pressure and heart rate, and induced freezing. The arterial pressure and freezing responses differed in conditioned and pseudoconditioned rats, but the heart rate response did not. Therefore, only the arterial pressure and freezing responses reflect the formation of an association between the tone and shock. Destruction of intrinsic neurons in the subcortical field contralateral to a unilateral MG lesion disrupted the associative conditioning of the arterial pressure and freezing responses. These were reduced in magnitude to the level observed in pseudoconditioned rats. The non-associative heart rate change was not affected by the lesions. That ibotenic acid destroyed intrinsic neurons and spared fibers in the subcortical field was demonstrated anatomically and biochemically.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed1999

[An 80-year-old woman with parkinsonism and progressive dementia].

We report an 80-year-old Japanese woman who presented levodopa-responsible parkinsonism followed by progressive dementia. She was well until her 61 years of age (in 1978) when she noted onset of resting tremor in her right hand followed by tremor in her right leg. She was treated with levodopa and trihexyphenidyl with good response, however, later on, she suffered from gait disturbance. In 1985, she had an episode of cardio-pulmonary arrest from which she was resuscitated, however, she started to show hypermetamorphosis, memory defect, and aggressive behaviors. She also developed motor fluctuations and dyskinesias from levodopa. She was admitted to our service in 1986; she showed rather typical parkinsonism and mild dementia. She received left Vim thalamotomy in the same year. Her dyskinesias improved, however, her gait disturbance became progressively worse. In 1995, she was admitted to our service again; she showed marked dementia and advanced parkinsonism; she was unable to walk unsupported. She became bedridden in 1996 and gastrostomy was placed. She was transferred to Zushi Aoki Hospital. Her dementia became progressively worse, and she was in the akinetic and mute state. She expired on April 22, 1998. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that the patient had Parkinson's disease with complication by Alzheimer's disease in her later clinical course. The diagnoses of participants were divided among Parkinson's disease with dementia, Parkinson's disease and Alzheimer's disease, and diffuse Lewy body disease. Postmortem examination revealed marked neuronal loss in the substantia nigra and the locus coeruleus. Lewy bodies were found in the substantia nigra. In addition, rather many Lewy bodies of cortical type were seen in the cingulate gylus, inferior temporal gylus, and in the amygdaloid nucleus. These Lewy bodies were positive for alpha-synuclein. Also, tau-positive intra-neuronal tangles were seen in the hippocampus and in the substantia nigra. The Meynert nucleus showed marked neuronal loss. Pathologic findings were consistent with the diagnosis of diffuse Lewy body disease.

Aged↗
PubMed1977

Nigro-amygdaloid fiber connections in the cat.

Relatively discrete unilateral lesions were made in the lateral portion of the substantia nigra of eight cats and in the medial substantia nigra of two. After a 10-day survival period the animals were killed, brains were stored in buffered 10% formalin, and frozen sections were stained for degenerating axons and terminals, or by Weil and cresyl violet methods. Electordes passed through the midial suprasylvian gyrus, pulvinar and/or posterolateral thalamic nucleus and the medial geniculate body. The stria terminalis and hippocampus were undamaged. Degeneration from the lesion followed two paths. One projected through the reticular nucleus into the internal capsule and then ventrolaterally below the putamen to enter the lateral and central amygdaloid nuclei, with degenerated terminals. The second path ran dorsolaterally in the internal capsule to enter the external capsule where some of the fibers spread into the lateral amygdaloid nucleus. It appears that some of the terminals in the lateral amygdaloid nucleus are from the external capsule. Perhaps these connections link the extrapyramidal system to the amygdaloid body.

Amygdala↗
PubMed1999

[The inhibitory effect of amygdaloid stimulation on the "on-off" response of medial geniculate body neurons in rabbits].

Experiments were performed on 23 New Zealand rabbits immobilized with Flaxedil. The characteristics of on-off responses of medial geniculate body (MGB) neurons to tone bursts of varying frequency, intensity and duration were affected by lateral amygdaloid nucleus (LAm) stimulation, which was in form of altering the pattern of discharge or complete suppression. The effect also varied with the changes of the interval between amygdaloid stimulation and the tone bursts. The results of the present work show that LAm could modulate temporal processing of auditory information.

Acoustic Stimulation↗
PubMed1987

Limbic and brainstem afferents to thalamic mediodorsal nucleus: a horseradish peroxidase study.

Subcortical ipsilateral afferents to mediodorsal (MD) thalamic nucleus were investigated by retrograde transport of horseradish peroxidase (HRP). HRP was injected into the rostral and caudal part of MD following both a vertical and an oblique stereotaxic approach. We have identified MD afferents from the following structures: area septalis, amygdaloid complex, hypothalamus, mamillary bodies, tuberculum olfactorium, claustrum, ventral tegmental area, zona incerta, substantia nigra, griseum centralis, formatio reticularis mesencephali and pontis oralis. The projections from hypothalamus, amygdaloid nuclei and area septalis and reticular formation are in agreement with the integrative function of sensory afferents of this thalamic nucleus.

Animals↗
PubMed1975

Sensorimotor responsiveness in rats with unilateral superior collicular and amygdaloid lesions.

Large unilateral lesions of superior colliculus, but not amygdala, result in strong ipsiversive progression tendencies and permanent neglects of visual, auditory, and whisker-touch stimuli presented on the contralateral side of the body. Combined collicular-amygdaloid lesions also yield circling behaviors and multimodal neglects that are completely independent of the order or laterality of the amygdaloid lesion. Rats with colliculectomy either neglect or else turn away from pinches of the contralateral ear and forepaw. Subjects with combined lesions display more crossed orientations, and this tendency is greatly potentiated by ipsilateral lesion placement. The nature and time course of the crossed response in rats with sensory neglects is reminiscent of the clinical syndrome described as alloaesthesia or as contralateral sensory displacement.

Amygdala↗
PubMedDate not supplied

Contextual and auditory fear conditioning are mediated by the lateral, basal, and central amygdaloid nuclei in rats.

A large body of literature implicates the amygdala in Pavlovian fear conditioning. In this study, we examined the contribution of individual amygdaloid nuclei to contextual and auditory fear conditioning in rats. Prior to fear conditioning, rats received a large electrolytic lesion of the amygdala in one hemisphere, and a nucleus-specific neurotoxic lesion in the contralateral hemisphere. Neurotoxic lesions targeted either the lateral nucleus (LA), basolateral and basomedial nuclei (basal nuclei), or central nucleus (CE) of the amygdala. LA and CE lesions attenuated freezing to both contextual and auditory conditional stimuli (CSs). Lesions of the basal nuclei produced deficits in contextual and auditory fear conditioning only when the damage extended into the anterior divisions of the basal nuclei; damage limited to the posterior divisions of the basal nuclei did not significantly impair conditioning to either auditory or contextual CS. These effects were typically not lateralized, although neurotoxic lesions of the posterior divisions of the basal nuclei had greater effects on contextual fear conditioning when the contralateral electrolytic lesion was placed in the right hemisphere. These results indicate that there is significant overlap within the amygdala in the neural pathways mediating fear conditioning to contextual and acoustic CS, and that these forms of learning are not anatomically dissociable at the level of amygdaloid nuclei.

Acoustic Stimulation↗
PubMed1993

Distribution of parvalbumin-immunoreactive cells and fibers in the monkey temporal lobe: the amygdaloid complex.

The calcium-binding protein parvalbumin was immunohistochemically localized in the monkey amygdaloid complex. Parvalbumin-immunoreactive neuronal cell bodies, fibers, and terminals were observed in several amygdaloid nuclei and cortical areas. Three types of aspiny neurons, ranging from small spherical cells (Type 1) to large multipolar cells (Type 2) and fusiform cells (Type 3) were observed in most amygdaloid regions, though the proportions of the cell types were different in each region. The density of parvalbumin-immunoreactive fibers and terminals tended to parallel the density of labeled cell bodies. The highest densities of parvalbumin profiles were observed in the nucleus of the lateral olfactory tract, the periamygdaloid cortex (PAC2), the magnocellular division of the basal nucleus, the ventrolateral portion of the lateral nucleus, and the accessory basal nucleus. The regions containing the lowest densities of parvalbumin-positive profiles were the medial nucleus, anterior cortical nucleus, central nucleus, and the paralaminar nucleus. In regions with fiber and terminal labeling, pericellular networks of fibers, reminiscent of basket cell terminations, were commonly observed to surround unstained neuronal cell bodies and proximal dendrites. In the magnocellular division of the basal nucleus, and to a lesser extent in the lateral nucleus, parvalbumin-labeled "cartridges" of axo-axonic terminals were observed on the initial segments of unlabeled cells. Parvalbumin-positive varicosities were also commonly observed in close apposition to the soma and dendrites of parvalbumin-immunoreactive cells. Given the close correspondence between the distribution of parvalbumin-positive neurons and a subset of GABAergic neurons in many brain regions, these data provide a first indication of the organization of the inhibitory circuitry of the primate amygdaloid complex.

Amygdala↗
PubMed1991

Calcitonin gene-related peptide (hCGRP alpha) binding sites in the nucleus accumbens. Atypical structural requirements and marked phylogenic differences.

The distribution of [125I]hCGRP alpha binding sites was studied in tissue sections from rat brain and, at the level of the nucleus accumbens in the brains of 6 other species. In the rat, very high levels of binding were found in the nucleus accumbens, the amygdaloid complex and mammillary body while high amounts were localized to the superficial layers of the superior colliculus, temporal cortex, cerebellum (molecular layer), frontal cortex and inferior olive. Moderate densities of [125I]hCGRP alpha binding were observed in the medial geniculate nucleus, inferior colliculus and substantia nigra. Regional competition studies in rat brain showed that salmon calcitonin was almost as effective as hCGRP alpha in competing for [125I]hCGRP alpha binding sites in the nucleus accumbens but was mostly inactive in other regions such as the mesolimbic cortex and the striatum. On the basis of their atypical sensitivity to salmon calcitonin, [125I]hCGRP alpha binding sites in the rat nucleus accumbens, which appear between postnatal days 4 and 7, do not seem to correspond to either the CGRP1 or CGRP2 receptor subtypes. Marked species differences were observed in the distribution of [125I]hCGRP alpha binding sites, especially in the nucleus accumbens. In the mouse, low densities of hCGRP alpha sites were observed in striatum and fronto-parietal cortex while low to moderate levels were found in the medial and posterior aspects of the nucleus accumbens. A similar distribution was seen in the guinea pig brain albeit of generally higher density. In the rat, very high amounts of [125I]hCGRP alpha binding were seen in the nucleus accumbens while lower levels were found in the striatum and certain cortical areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Effects of methylenedioxymethamphetamine on local cerebral glucose utilization in the rat.

The effects of (+-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") (5, 10, 15 or 30 mg/kg, i.p.) on local cerebral utilization of glucose were studied by the quantitative autoradiographic 2-deoxy-D-[1-14C]glucose method in awake adult male Fischer-344 rats. Statistically significant effects on local utilization of glucose, 5 min after the administration of MDMA were observed in 20 of 60 areas of brain sampled. Marked stimulation was seen in components of the extrapyramidal motor system (substantia nigra, globus pallidus, entopenduncular nucleus, subthalamic nucleus, cerebellar vermis). The limbic system showed decrements in the medial cortex and hippocampal dentate gyrus (outer blade) and the lateral habenula, while there was stimulation in the mammillary body and the basolateral amygdaloid nucleus. Glucose utilization in MDMA-treated rats was reduced in the superior colliculus and medial terminal nucleus of the accessory optic system, but was unchanged in the visual cortex and components of the auditory system. Some of the effects of MDMA on cerebral utilization of glucose resembled those previously reported with l-cocaine, d-amphetamine, and phencyclidine, implicating some common mechanisms in the actions of these drugs.

3,4-Methylenedioxyamphetamine↗
PubMed1986

Distribution of corticotropin-releasing factor receptors in primate brain.

The distribution and properties of receptors for corticotropin-releasing factor (CRF) were analyzed in the brain of cynomolgus monkeys. Binding of [125I]tyrosine-labeled ovine CRF to frontal cortex and amygdala membrane-rich fractions was saturable, specific, and time- and temperature-dependent, reaching equilibrium in 30 min at 23 degrees C. Scatchard analysis of the binding data indicated one class of high-affinity sites with a Kd of 1 nM and a concentration of 125 fmol/mg (approximately equal to 30% of the receptor number in monkey anterior pituitary membranes). As in the rat pituitary and brain, CRF receptors in monkey cerebral cortex and amygdala were coupled to adenylate cyclase. Autoradiographic analysis of specific CRF binding in brain sections revealed that the receptors were widely distributed in the cerebral cortex and limbic system. Receptor density was highest in the pars tuberalis of the pituitary and throughout the cerebral cortex, specifically in the prefrontal, frontal, orbital, cingulate, insular, and temporal areas, and in the cerebellar cortex. A very high binding density was also present in the hippocampus, mainly in the dentate gyrus, and in the arcuate nucleus and nucleus tuberis lateralis. A high binding density was present in the amygdaloid complex and mamillary bodies, olfactory tubercle, and medial portion of the dorsomedial nucleus of the thalamus. A moderate binding density was found in the nucleus accumbens, claustrum, caudate-putamen, paraventricular and posterior lateral nuclei of the thalamus, inferior colliculus, and dorsal parabrachial nucleus. A low binding density was present in the superior colliculus, locus coeruleus, substantia gelatinosa, preoptic area, septal area, and bed nucleus of the stria terminalis. These data demonstrate that receptors for CRF are present within the primate brain at areas related to the central control of visceral function and behavior, suggesting that brain CRF may serve as a neurotransmitter in the coordination of endocrine and neural mechanisms involved in the response to stress.

Adenylyl Cyclases↗
PubMed1999

Ontogeny of angiotensin II type 2 receptor mRNA expression in fetal and neonatal rat brain.

Recent studies have provided evidence for a specific role of the angiotensin II type 2 receptor (AT2) in in vitro neuron differentiation, and in AT2 knock-out mice that display central neurological anomalies. The role of AT2 in brain development is currently unknown. By using radiolabeled cRNA probes for in situ hybridization histochemistry, we determined the ontogenic development of AT2 mRNA in fetal and neonatal rat brain, from 11 days of gestation (E11) to 28 days postnatal (P28). Brain AT2 mRNA is first detected in the lateral hypothalamic neuroepithelium at E13. AT2 mRNA is detected beginning at E15 in the subthalamic and hypoglossus nuclei; at E17 in the pedunculopontine nucleus, cerebellum, motor facial nucleus, and the inferior olivary complex; at E19 in the thalamus, bed nucleus of the supraoptic decussation, interstitial nucleus of Cajal, nuclei of the lateral lemniscus, locus coeruleus, and supragenual nucleus; and at E21 in the lateral septal and medial amygdaloid nuclei, medial geniculate body, and the superior colliculus. The substantia nigra and many telencephalic and medullary nuclei express AT2 mRNA only after birth. Certain structures express AT2 mRNA strongly but transiently during embryonic life, such as the differentiating lateral hypothalamic area at E13, the superior olivary complex at E19 and E21, and the red nucleus at E15 and E17. In conclusion, during brain development, expression of AT2 mRNA appears early at E13, is strongly but transiently expressed in certain structures, and is high and persists until brain maturity in nuclei involved in motor functions and sensory integration. Our results support a dual role of AT2 during brain development in early maturation and differentiation, but also in modulation of established functions during perinatal and adult life.

Aging↗
PubMed1989

The release of endogenous histamine in distinct brain areas is modified by electrical stimulation.

In anaesthetized cats, mamillary bodies, hypothalamic areas and medial amygdaloid nuclei were bilaterally superfused through push-pull cannulae and the effects of the electrical stimulation on the release of endogenous histamine were investigated. Electrical stimulation of the mamillary body increased the release of histamine in the stimulated area, as well as in the contralateral mamillary body. Electrical stimulation of the lateral hypothalamic area enhanced the histamine release in the contralateral hypothalamic area. Stimulation of the posterior hypothalamic area led to a delayed increase in the histamine release in the stimulated area. Stimulation of the medial amygdaloid nucleus reduced the release if histamine in the ipsilateral posterior hypothalamic area, while the histamine release in the contralateral lateral hypothalamic area was enhanced. The results demonstrate that electrical stimulation of distinct brain areas rich in histaminergic neurons may either increase, or decrease the release rate of histamine in the stimulated area and/or in remote brain areas.

Amygdala↗