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PubMed1989

Kindling of the visual cortex in cats: comparison with amygdaloid kindling.

Kindling of the primary visual cortex (VC) was compared with that of the amygdala in cats. VC kindling was basically similar to kindling of the amygdala in that daily electrical stimulation can lead to the development of a generalized convulsion in most subjects, a growth of afterdischarges in their configuration and duration, and a reduction of the afterdischarge threshold. The kindling response of the VC differed from that of the amygdala in a number of respects, i.e., a high afterdischarge threshold, a different pattern of behavioral seizure development, an abrupt growth of electroclinical seizures coincident with the onset of a generalized convulsion, an intersubject variability in seizure susceptibility, and a marked seizure instability. In VC kindling the afterdischarge propagation into the amygdala was not observed until the generalized convulsion developed, and the early involvement of afterdischarge was seen in the pulvinar, lateral geniculate body, and superior colliculus. These data suggest that a neural mechanism different from amygdaloid kindling may participate in VC kindling, and that the subcortical structures of the visual system are involved in the preferential pathway for a seizure generalization from the VC.

Amygdala↗
PubMed1994

Corticotropin releasing factor neurons are innervated by calcitonin gene-related peptide terminals in the rat central amygdaloid nucleus.

The central nucleus of the rat amygdala (CeA) contains many corticotropin releasing factor (CRF) immunoreactive neurons. Previous studies have demonstrated that these CRF neurons project to brain stem regions responsible for modulation of autonomic outflow. Calcitonin gene-related peptide (CGRP) terminals overlap the distribution of CRF cell bodies in the CeA. These CGRP terminals mainly originate from cell bodies that are located in the pontine parabrachial nucleus. The present study examined the possibility that CRF cell bodies are innervated by CGRP terminals. The results suggest that over 35% of the CRF neurons in the CeA are contacted by CGRP terminals as judged by the indiscernible distances between the terminals and cell bodies and or dendrites. In addition, a dual-labeled electron microscopic technique demonstrates that CGRP terminals form synaptic contacts with CRF cell bodies and dendrites. This suggests that CGRP neurons in the parabrachial nucleus can modulate the activity of CRF amygdaloid brain stem efferents. Previous studies have shown that CRF, when administered into the central nervous system, produces increases in heart rate, blood pressure, and plasma catecholamines. CGRP administration into the amygdala has been shown to have a similar effect on the autonomic nervous system. It is, therefore, possible that CGRP could exert these effects via an amygdaloid CRF pathway.

Amygdala↗
PubMed2003

Excessive weight gain in rats over extended kindling of the basolateral amygdala.

Previous lesion studies have indicated a role of the amygdala in the central regulation of food intake. In the present experiments, twice-daily electrical stimulation of the basolateral nucleus of the amygdala in female Wistar rats was found to be associated with a significant body weight gain compared to unstimulated controls. On average, significant increases in body weight were observed after 25 amygdala stimulations, using a kindling paradigm for stimulation. Compared to kindled rats, in which amygdala stimulations were terminated after about 20 stimulations, extended kindling of the amygdala with up to 280 stimulations led to progressive weight increases and compulsive hyperphagia. No gross neuronal damage was seen in thionin-stained sections of the amygdala after extended kindling, but degeneration of a specific type of neurons can not be excluded. The results substantiate that amygdaloid nuclei are an important extrahypothalamic site for the regulation of food intake and body weight. The extensive weight gain over extended amygdala kindling provides an interesting new model for experimentally induced obesity.

Amygdala↗
PubMedDate not supplied

[Generalization of an instrumental defensive conditioned reflex elaborated to electric stimulation of the hypothalamus in dogs].

Generalization of defensive conditioned reflexes elaborated to electrical stimulation of the lateral hypothalamus (LH) was studied in four dogs with electrodes implanted in various structures of the limbic system. Electrocutaneous stimulation was switched off when the dog lifted the foreleg to a definite level. Generalization of the conditioned reflex was manifested in different degrees when testing different formations of the limbic system, or testing one and the same structure, but at different stages of conditioning. Two types of generalization were found: the first one--a well pronounced motor reaction, by its latency, level and duration of lifting the foreleg similar to movements appearing in response to the conditioned stimulus; and the second one--low amplitude or short-term movements differing from conditioned ones. The first type of generalization was observed in response to stimulation of LH, contralateral to the point of signal stimulation, of the ventromedial hypothalamic nucleus, the mammillary bodies and the basal, lateral and to a lesser degree, the central nucleus of the amygdaloid complex; the second type--in response to stimulation of the ventral hippocampus, the medial and lateral septum nuclei.

Amygdala↗
PubMed1999

Effect of hypothermia on kainic acid-induced limbic seizures: an electroencephalographic and 14C-deoxyglucose autoradiographic study.

The effect of body temperature on kainic acid (KA)-induced limbic seizures was examined in Wistar rats. In rats undergoing limbic seizure induced by 1 microgram intra-amygdaloid injection of KA, the post-injection latency of initial ictal discharges in the left amygdala was significantly longer in rats whose body temperature was lowered to 30 degrees C (2.55+/-0.94 min at 37 degrees C, 13.19+/-5. 70 min at 30 degrees C; p=0.0017). The post-injection latency of initial ictal discharges in the left hippocampus was also significantly longer under the same conditions (23.68+/-9.96 min at 37 degrees C, 43.85+/-17.98 min at 30 degrees C; p=0.0253). The number of limbic seizures occurring in the first 2 h post-injection was significantly lower in hypothermic rats (30.0+/-10.7 at 37 degrees C, 8.71+/-2.69 at 30 degrees C; p=0.0017), as was the total duration of limbic seizures over the same period (23.61+/-8.45 min at 37 degrees C, 10.30+/-4.48 min at 30 degrees C; p=0.0060). Local cerebral glucose utilization (LCGU), measured 2 h post-injection, was significantly lower in hypothermic rats, mainly in the limbic structures. 14C-deoxyglucose autoradiograms showed decreased radiation density not only in the left amygdala and bilateral hippocampus, but also in the cerebral cortex of hypothermic rats. The results of the present experiment demonstrate that the use of hypothermia, which has been shown to be effective in the treatment of acute cerebral ischemia and brain injury, may also be effective in the treatment of status epileptics.

Amygdala↗
PubMed2000

Differential projection of the posterior paralaminar thalamic nuclei to the amygdaloid complex in the rat.

The thalamic paralaminar nuclei that border the medial and ventral edges of the medial geniculate body, viz. the suprageniculate nucleus (SG), the posterior intralaminar nucleus (PIN), the medial division of the medial geniculate nucleus (MGm), and the peripeduncular nucleus (PP), are regarded as important extralemniscal relay nuclei for sensory stimuli and as an important link for the direct transmission of sensory stimuli to the amygdala. Each of these thalamic nuclei receives a unique pattern of afferent input but an unresolved question is, how each of these thalamic nuclei project to the amygdala and whether there are zones of convergence and/or non-overlapping regions within amygdaloid target nuclei. Small injections of PHA-L or Miniruby, which were made into single thalamic nuclei at different rostrocaudal levels, revealed a non-uniform distribution of anterogradely labeled axons within the amygdaloid complex. Injections into the SG, MGm, and rostral PIN predominantly labeled axons in the laterodorsal and lateroventral portions of the lateral nucleus of the amygdala (LA). Axons from the MGm were located rather in the dorsal part of the LA, whereas SG-derived axons were concentrated in the ventrolateral part of the LA. Injections into the PP labeled axons predominantly in the medial part of the LA, whereas after injections into the caudal PIN axons were seen in the entire LA. In addition, the PIN projects heavily to the anterior basomedial nucleus and medial division of the central nucleus, whereas this projection is virtually absent from the other thalamic nuclei. The lateral part of the central nucleus and the basal nucleus of the amygdala are spared by axons from the thalamic paralaminar nuclei. The present results suggest that, despite a considerable degree of convergence of the thalamoamygdaloid projection in the lateral nucleus, each thalamic nucleus plays a unique role in the transmission of sensory stimuli to the amygdala and in the modulation of intraamygdaloid circuits.

Amygdala↗
PubMedDate not supplied

Discrete mapping of brain Mu and delta opioid receptors using selective peptides: quantitative autoradiography, species differences and comparison with kappa receptors.

The opioid peptides, [3H]DAGO and [3H]DPDPE, bound to rat and guinea pig brain homogenates with a high, nanomolar affinity and to a high density of mu and delta receptors, respectively. [3H]DAGO binding to mu receptors was competitively inhibited by unlabelled opioids with the following rank order of potency: DAGO greater than morphine greater than DADLE greater than naloxone greater than etorphine much greater than U50488 much greater than DPDPE. In contrast, [3H]DPDPE binding to delta receptors was inhibited by compounds with the following rank order of potency: DPDPE greater than DADLE greater than etorphine greater than dynorphin(1-8) greater than naloxone much greater than U50488 much greater than DAGO. These profiles were consistent with specific labelling of the mu and delta opioid receptors, respectively. In vitro autoradiographic techniques coupled with computer-assisted image analyses revealed a discrete but differential anatomical localization of mu and delta receptors in the rat and guinea pig brain. In general, mu and delta receptor density in the rat exceeded that in the guinea pig brain and differed markedly from that of kappa receptors in these species. However, while mu receptors were distributed throughout the brain with "hotspots" in the fore-, mid- and hindbrain of the two rodents, the delta sites were relatively diffusely distributed, and were mainly concentrated in the forebrain with particularly high levels within the olfactory bulb (OB), n. accumbens and striatum. Notable regions of high density of mu receptors in the rat and guinea pig brain were the accessory olfactory bulb, striatal "patches" and "streaks," amygdaloid nuclei, ventral hippocampal subiculum and dentate gyrus, numerous thalamic nuclei, geniculate bodies, central grey, superior and inferior colliculi, solitary and pontine nuclei and s. nigra. Tissues of high delta receptor concentration included, OB (external plexiform layer), striatum, n. accumbens, amygdala and cortex (layers I-II and V-VI). Delta receptors in the guinea pig were, in general, similarly distributed to the rat, but in contrast to the latter, the hindbrain regions such as the thalamus, geniculate bodies, central grey and superior and inferior colliculi of the guinea pig were apparently more enriched than the rat. These patterns of mu and delta site distribution differed dramatically from that of the kappa opioid sites in these species studied with the peptide [125I]dynorphin(1-8).

Animals↗
PubMed1980

The role of epileptic activity in hippocampal and "remote" cerebral lesions induced by kainic acid.

Kainic acid (KA) was injected systemically, intracerebroventricularly (i.c.v.) and focally in the amygdala and other deep brain structures in the rat. EEG and behavioral changes were studied in relation to the neuropathology which developed subsequently. Following intra-amygdaloid KA injection, diazepam blocked the epileptic events induced by the toxin, and abolished the neuronal loss usually seen in the lateral septum, claustrum, and contralateral cortex and hippocampus. The lesions in medial thalamic structures and ipsilateral hippocampus were also reduced by diazepam. Prior transection of the perforant path ipsilateral to the KA injection also decreased the severity of the electrographic and motor effects of the toxin and similarly reduced the extent of distant ("remote") pathological brain damage. Neither diazepam nor perforant path transection reduced the damage at the site of KA injection. Kainic acid (0.4-2 microgram) injected into the bed nucleus of the stria terminalis (BST) or the medial septum produced seizures with a longer latency and little brain damage outside the injection site. In contrast, intrastriatal KA injections were followed by ipsilateral hippocampal lesions. i.c.v. Injection of KA (0.4-1.6 microgram) produced a complex syndrome which included bilateral exophthalmos, mydriasis, foaming, tremor of the vibrissae, and paw and body tremor. The pattern of brain damage resembled that seen following intra-amygdaloid administration of the toxin. In addition, however, there was a bilateral necrosis of the pyriform and prepyriform cortices up to the rhinal fissure. Systemic administration of diazepam (i.p.) reduced the extent of the damage and in particular completely prevented the cortical damage. Systemic administration of KA (9-15 mg/kg i.p.) readily produced motor and EEG seizures similar to those seen after intra-amygdaloid injection of the toxin. The pattern of brain damage was however more symmetrical than that which followed focal i.c.v. injection of the toxin and included necrosis of the pyriform cortex. It is concluded that spread of seizure activity from the injection site plays a crucial role in the induction of "remote" brain damage after focal intracerebral injections.

Afferent Pathways↗
PubMed1991

Comparative distribution of immunoreactive pituitary adenylate cyclase activating polypeptide and vasoactive intestinal polypeptide in rat forebrain.

Pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) are structurally similar, share the same high affinity site in same peripheral tissues and increase the intracellular content of adenylate cyclase. To establish which neural circuits are signaling with each of these two peptides, we systematically compared the immunohistochemical distribution of PACAP and VIP in selected rat forebrain regions using previously characterized antiserum. The PACAP antiserum recognized both PACAP27 and PACAP38, and PACAP immunoreactivity was unaffected by preincubation with various other peptides. PACAP-immunoreactive perikarya and fibers were observed in both hypothalamic and extrahypothalamic regions. In the hypothalamus PACAP perikarya were located in the supraoptic, paraventricular, anterior commissural, periventricular, and perifornical nuclei. In intact rats PACAP immunolabeled fibers were present in the internal zone of the median eminence and posterior pituitary. One week after hypophysectomy the intensity of staining in the internal zone was enhanced and immunoreactive fibers appeared in the external zone of the median eminence. Two or 3 weeks later a dense fiber network was observed around the portal capillaries in the external zone, and immunoreactive material further accumulated in the fibers of the internal zone. PACAP-immunoreactive perikarya and fibers were also observed in several extrahypothalamic regions including central thalamic nuclei, amygdaloid complex, bed nucleus of stria terminalis, septum, hippocampus and cingulate, and entorhinal cortices. In the lateral septum and entorhinal cortex PACAP fibers surrounded unstained neuronal cell bodies and small blood vessels. In intact rats, VIP-immunoreactive perikarya were present in all regions of the cerebral cortex, hippocampus, amygdaloid complexus and in the suprachiasmatic nucleus, but not in the paraventricular and supraoptic nuclei. In colchicine-treated rats the VIP perikarya appeared in the preoptic area and paraventricular nucleus. The fibers were organized in two main pathways: the stria terminalis and an ascending pathway from the suprachiasmatic nucleus to the paraventricular area. Hypophysectomy induced the appearance of VIP-immunoreactive fibers in the internal zone of the median eminence and perikarya in the supraoptic and paraventricular nuclei in addition to the suprachiasmatic nucleus. The dissimilar distributions of PACAP and VIP suggest that PACAP neural circuits are independent of that of VIP in the rat forebrain. These findings support possible multifunctional roles for PACAP as a posterior pituitary hormone, a hypophysiotrophic factor, and a neurotransmitter/neuromodulator.

Amygdala↗
PubMed1992

Distribution of neurons expressing neurokinin B in the rat brain: immunohistochemistry and in situ hybridization.

Neurokinin B (NKB) belongs to the family of neuropeptides named tachykinins. Members of this family such as substance P or neurokinin A have been proposed to function as neurotransmitters or neuromodulators. Searching for possible sites of action of NKB in the central nervous system, we have now investigated its distribution within the rat brain by immunohistochemical techniques and in situ hybridization. For immunohistology two different antisera directed against amino acid sequences within preprotachykinin B were used. One antiserum had been raised against a synthetic derivative of NKB; the other one was directed towards the amino acids 50-79 of preprotachykinin B, which are referred to as peptide 2. Essentially the same distribution of immunoreactive perikarya was obtained with both antisera and it closely corresponded to the cellular localization of preprotachykinin B mRNA. Neurons containing NKB immunoreactivity and mRNA were present in many areas including cerebral cortex, hippocampal formation, amygdaloid complex, bed nucleus of the stria terminalis, ventral pallidum, habenula, medial preoptic area, arcuate nucleus, and lateral mammillary bodies. Dense immunoreactive fibers were observed in various parts of the brain and were most prominent in the olfactory bulb and tubercle, the lateral olfactory tract, medial hypothalamus, around blood vessels of the median eminence and interpeduncular nucleus, amygdaloid nuclei, stria terminalis, subbrachial nucleus, and medial geniculate nucleus. Fibers of less intense staining were seen among other brain areas in the substantia nigra, the reticular formation, and the area of the nucleus of the solitary tract. Surgical lesion of the fasciculus retroflexus revealed that the dense fiber network observed in the interpeduncular nucleus originates from the ventral and dorsal parts of the medial habenula. Our data suggest a widespread and distinct distribution of neurons expressing NKB within the central nervous system, suggesting possible neuromodulatory roles of this neuropeptide for various brain functions.

Amino Acid Sequence↗
PubMed1986

Distribution of galaninlike immunoreactivity in the rat central nervous system.

The localization of galanin (GAL) immunoreactive (IR) neuronal structures in the rat central nervous system has been investigated by using the indirect immunofluorescence technique. GAL-IR structures were seen in high concentrations in the hypothalamus, medulla oblongata, and spinal cord. Less extensive systems were detected in the telencephalon, thalamus, mesencephalon, and pons, while virtually no GAL-positive structures were seen in the olfactory bulb and cerebellum. Major populations of cell bodies staining for GAL-like material were seen in many areas. In the telencephalon somata were revealed in the bed nucleus of stria terminalis, in the nucleus of the diagonal band, medial septum, and in the medial aspects of the central amygdaloid nucleus, and in small numbers in cortical areas. The anterodorsal and periventricular nuclei of the thalamus contained positive cell bodies. In the hypothalamus GAL-IR somata were seen in the medial and lateral preoptic nuclei, arcuate nucleus, periventricular nucleus, in the dorsomedial nucleus, in the medial forebrain bundle area, in the tubular, caudal, accessory, supraoptic, and paraventricular magnocellular nuclei and lateral to the mammillary recess. The dorsal raphe nucleus hosted a large number of GAL-positive somata. Locus coeruleus of the pons contained a large number of GAL-IR perikarya. In the medulla oblongata positive somata were found in the caudal spinal trigeminal nucleus, the nucleus of the solitary tract, and in the ventral lateral area just rostral to area postrema. Small cell bodies were detected in the superficial layers of the dorsal horn of the spinal cord at all levels and in lamina X at lumbar levels. Analysis of GAL-positive fibers in the telencephalon revealed highly or medium-dense networks in the lateral septal nucleus, in the bed nucleus of stria terminalis, and in the central and medial amygdaloid nuclei. Positive fibers were found in the thalamus in and around the periventricular nucleus as well as in the lateral habenular nucleus and extending in a lateral, caudal direction from the third ventricle and fasciculus retroflexus to the lateral tip of the medial lemniscus. In the hypothalamus the external layer of the median eminence contained a very dense fiber network. Dense or medium-dense GAL-IR networks were detected in the periventricular nucleus, throughout the medial and lateral preoptic areas, in the medial forebrain bundle area, in the dorsomedial nucleus, and lateral to the mammillary recess. In the pons GAL-IR fibers were seen in the parabrachial nuclei, dorsal to the superior olive, and in the periaqueductal central gray.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

[Memory: clinico-pathologic data].

Synaptic modifications are probably the basis of the memory processes that take place in the central nervous system. They have been studied in Aplysia or in hippocampal slices. How these minute alterations of the synaptic strength are integrated in larger neural systems is still poorly understood. In man, hippocampal lesions, when bilateral, cause a deficit in anterograde episodic memory. The loss of previously acquired memories (retrograde amnesia) is limited. Procedural memory is spared. Young patients with hippocampal lesions remain able to learn how to read or to write (abilities that belong to semantic memories). Recordings obtained with intracerebral electrodes have shown that some neurons of the hippocampus act as "place cells". They fire when the animal is in a specific place of the experimental maze, an observation that suggests that the hippocampus acts as a map that may also be viewed as a context indicator (a "cognitive map"). Computer models have been devised to test the hypothesis that the hippocampus recorded the map of the activated synapses at a particular moment in time. This pattern of activity could secondarily be transferred to the isocortex during a process known as consolidation. The frontal lobe plays a role in attention, which greatly influences the memory process. It also plays a role in the various strategies that are used to recall a memory and in the analysis of the quality of the recall (metamemory). An asymmetry has been shown by the PET-scan: the left frontal lobe is activated during acquisition, and the right one during recall. The ability to integrate one's own memories in one's own history and consciousness (self-awareness or "autonoesis") also depends on the activity of the prefrontal region. The loss of acquired memories (retrograde amnesia) is most often observed in cases of large lesions of the anterior part of the temporal lobe. Partial amnesias are difficult to separate from possibly localized deficits of a cognitive function (some types of aphasia may be considered as an amnesia of words). Subcortical amnesias are caused by diencephalic lesions; the topography of the critical structures is still discussed: mamillary bodies and mamillo-thalamic tract or dorsomedial nucleus of the thalamus. The amygdaloid nucleus, the frontal lobe and the dorsomedial nucleus of the thalamus belong to a network of connections that could be involved in emotions. It could be responsible for the emotional flavor of a memory. Basal ganglia could play a role in procedural memory, but experimental or clinicopathological confirmations are still scarce. Finally, the involvement of the cholinergic innervation in the memory processes has been discussed: it could be direct, or according to more recent data, related to its role in attention.

Amnesia↗
PubMed1986

[An autopsy case of amyotrophic lateral sclerosis with dementia and neck extension].

A 58-year-old man recognized hoarseness and dysarthria followed by weakness of the left upper extremity. Examination five months later disclosed dementia which was manifested dominantly by changes in personality and behavior, but also by symptoms of amyotrophic lateral sclerosis. He became progressively weak, and his neck became rigid and extended for two months. He expired due to respiratory failure at the age of 60. At autopsy, the brain weighed 1120 g with atrophy of the temporal lobes. Microscopic examination revealed marked diminution of Betz cells with astrocytic proliferation in the motor cortex. There was a mild, localized spongy state in the upper layer in the frontal and temporal cortices. There were very few neurofibrillary changes and senile plaques, and no Pick's argentophilic bodies. Fibrillary gliosis was found in the white matter of the temporal lobes, external segment of the globus pallidus and the amygdaloid nucleus. The substantia nigra showed depletion of pigmented cells, free melanin pigment and reactive astrocytosis. A diminished number of motor neurons in the brain stem and spinal cord accompanied astrocytic gliosis, while the remaining cell contained many Bunina bodies. The pyramidal tracts showed mild degeneration bilaterally below the pyramis in the medulla. There are a number of cases in the literature whose pictures consist of amyotrophic lateral sclerosis, dementia and/or extrapyramidal symptoms. This case is identical to those cases. But in this case, the clinical and pathological features of amyotrophic lateral sclerosis are more dominant than in other cases.

Amyotrophic Lateral Sclerosis↗
PubMed2003

[Brain central amygdaloid nucleus: cytoarchitechtonics, neuronal organization, connections].

This review describes different aspects of structural and functional organization of amygdaloid central nucleus (CN) in association with the findings indicating its involvement in the development of stress reactions and adaptive behavior in animals. The data on the distribution of neuropeptides, neurotransmitters and neuromodulators in CN are discussed. It is emphasized that CN appears at the earliest stages of amygdaloid formation, undergoes remodeling together with it and reflects the evolution of the whole amygdaloid. The detailed data are presented on the cytoarchitectonic of amygdaloid CN, its heteromorphism and subdivision into zones (subnuclei), based on the different methods of investigation and evaluation criteria. The neuronal organization of CN and its subnuclei is discussed, and the detailed description of neurons of different types is given according to their topography, cell body dimensions and shape, dendrite orientation and branching pattern, organization of spine apparatus and axon structure. The developmental features of amygdaloid CN in mammalian animal and human ontogenesis are considered. The analysis covering the literature data and the results of authors' own investigations indicates that CN functions not only as intraamigdaloid integrative center, but also as one of the major channels providing both afferent and efferent connections of amygdaloid with other brain structures.

Amygdala↗
PubMed2005

Immunohistological characterization of striatal and amygdalar structures in the telencephalon of the fire-bellied toad Bombina orientalis.

The subpallium of the fire-bellied toad Bombina orientalis was studied by means of enzyme-histological detection of NADPH-diaphorase and immunohistological demonstration of aspartate, GABA, calretinin, choline-acetyl transferase, Leu-and Met-enkephalin, neuropeptide Y, 5-hydroxy-tryptamine (serotonin), somatostatin, substance P and tyrosine-hydroxylase. As in other vertebrates, the striato-pallidum is characterized by GABA-, substance P- and enkephalin-immunoreactivity. Neurons and fibers differing in immunoreactivity are arranged in layers. Choline-acetyl transferase-immunoreactive neurons were found in a position corresponding to the mammalian cholinergic cell-group (Ch4-group), which therefore may be homologous to the nucleus basalis of Meynert. Within the amygdaloid complex, the cortical and lateral (vomeronasal) nuclei are similar in calretinin-, GABA-, NADPH-diaphorase-, enkephalin, substance P- and neuropeptide Y-(immuno)histology. The medial and central amygdaloid nuclei reveal a dense peptidergic innervation, and the medial amygdala additionally exhibits serotonergic fibers and cell bodies staining for neuropeptides and tyrosine-hydroxylase. Differences between Bombina and other anuran species exist, such as the absence of cholinergic neurons in the striatum. Our findings corroborate the view based on recent studies on the hodology and cytoarchitecture of the anuran telencephalon that the anuran ventral telencephalon contains most of the structures found in the mammalian brain. This concerns a septal region, a dorsal and ventral striato-pallidum including a nucleus accumbens and an amygdaloid complex consisting of a central, cortical and vomeronasal amygdala. The only major difference appears to concern the lack of a basolateral amygdala.

Amygdala↗
PubMed1990

[Infarction in the territory of the anterior choroidal artery due to embolic occlusion of the internal carotid artery--report of two cases].

A case with infarction in the territory of the anterior choroidal artery (AChA) due to embolic occlusion of the internal carotid artery (ICA) is rare. We described two cases and investigated the mechanism of the territory of the AChA. Case 1 was a 69-year-old man. Case 2 was a 71-year-old woman. The neurological examination in both cases showed left homonymous hemianopsia, left facial palsy, left hemiparesis and left hemisensory disturbance. CT scan in these cases showed infarctions of the right uncus, amygdaloid nucleus, genu and posterior limb of the internal capsule, globus pallidus, lateral geniculate body and tail of the caudate nucleus. The right common carotid angiogram showed a complete occlusion of the ICA at its cervical segment in case 1 and at its carotid siphon in case 2. In both cases, the left carotid injection visualized the right anterior cerebral artery and right middle cerebral artery via the anterior communicating artery well, but the right AChA was not visualized. In case 1, the collateral pathways from the right external carotid artery (ECA) and the right posterior communicating artery (PCoA) to the right ICA were not supplied and the precommunicating segment of the right posterior cerebral artery was hypoplastic. In case 2, the collateral pathway from the right ECA to the right ICA was not supplied.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Development of a dopamine- and cyclic adenosine 3':5'-monophosphate-regulated phosphoprotein (DARPP-32) in the prenatal rat central nervous system, and its relationship to the arrival of presumptive dopaminergic innervation.

The development of a dopamine- and adenosine 3':5'-monophosphate-regulated phosphoprotein with an apparent Mr of 32,000 (DARPP-32) has been investigated in the central nervous system of the prenatal and newborn rat by immunocytochemical methods. DARPP-32 first appears in the rat brain at day 14 of gestation, in the anlage of the primary olfactory cortex and the caudate nucleus. Over the next few days, the number of immunoreactive cell bodies in these 2 areas, and in the olfactory tubercle and frontal cortex, increases rapidly. By the day of birth, most of the brain regions that will ultimately contain DARPP-32-positive somata already display a disposition toward DARPP-32-like immunoreactivity similar to that observed in the adult animal. In addition to the nuclei mentioned above, DARPP-32-containing cell bodies also appear over the intervening period in the olfactory nucleus, nucleus accumbens, central amygdaloid nucleus, lateral funiculus, and the choroid plexus and ependymal layers of the third, fourth, and lateral ventricles and the Sylvian aqueduct. Many of these immunoreactive cells disappear during subsequent postnatal maturation. DARPP-32-immunoreactive fibers were also observed in the prenatal and newborn rat CNS. As in the adult, the processes were observed in known target areas of the DARPP-32-containing neurons, namely, the globus pallidus, ventral pallidum, internal capsule, and substantia nigra. The ontogeny of tyrosine hydroxylase (TH)-like immunoreactivity was analyzed simultaneously. Of particular interest was the observation that the arrival within a given brain region of the presumed dopaminergic, TH-containing innervation, part of whose postsynaptic function is putatively mediated by DARPP-32, was preceded by at least 2 d by the appearance of the DARPP-32-containing cells. Moreover, the subsequent reorganization of the DARPP-32-positive somata within the caudate nucleus into distinct clumps also predated by 1 or 2 d the aggregation of the TH fibers into the same microzones. The development of DARPP-32-like immunoreactivity is mostly complete by the day of birth, and is consistent with its playing a role in mediating some of the postsynaptic actions of dopamine pathways. The appearance of this protein does not seem to be dependent on the presence of a dopaminergic innervation.

Animals↗