Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Olfactory Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1987

An increase in glial fibrillary acidic protein follows brain hyperthermia in rats.

Previously, we have demonstrated that an increase in the astrocyte-associated protein, glial fibrillary acidic protein (GFAP), accompanies brain injury induced by a variety of chemical insults. In the present study we examined the effects of microwave-induced hyperthermia of the CNS on the concentration of GFAP in several brain regions of the Long-Evans rat. Irradiation resulted in a time-related increase in GFAP in olfactory bulbs and cortex, areas of maximum heating. The increase in GFAP following a brain temperature increase suggests that heating of brain tissue may be sufficient to provoke an injury response comparable to that induced by chemical and physical insult.

Animals↗
PubMed2003

Characterisation of [125I]-Tyr0DTrp8-somatostatin binding in sst1- to sst4- and SRIF-gene-invalidated mouse brain.

Five somatostatin receptors (sst) have been cloned and mRNAs for the first four (sst1-4) are expressed in many brain regions. In the present work, we compared the distribution of the non-selective ligand [125I]-Tyr0-DTrp8-SRIF14 by autoradiography in 24 brain regions and pituitary in wild type, sst1- to sst4- or SRIF-gene invalidated (KO) mice. [125I]-Tyr0-DTrp8-SRIF14 binding was not significantly modified in sst1 KO mouse brain with the noticeable exception of the substantia nigra and only moderately decreased in pituitary. For sst2 KO mice, a general decrease (>75%) was observed in most regions, with the noticeable exception of the olfactory bulb and CA1 field of the hippocampus. SST3 KO brain displayed a decrease in binding in the external plexiform layer of the olfactory bulb only (-54%). For sst4 KO mice, [125I]-Tyr0-DTrp8-SRIF14 binding levels in the external plexiform (-35%) and glomerular (-39%) layers of the olfactory bulb as well as the hippocampus CA1 field (-68%) were significantly decreased. In SRIF KO mice, a significant increase in binding levels was observed in olfactory bulb, anterior olfactory nucleus, frontal cortex upper layers, lateral septum, CA1 field, zona incerta and lateral hypothalamus, substantia nigra, periaqueductal grey and parabrachial nucleus. Competition with selective ligands (CH275, octreotide or L-779,976, L-796,778, L-803,087, and octreotide or L-817,778, for sst1-5 receptors, respectively) was in accordance with these findings. Moreover, octreotide was still able to compete on residual [125I]-Tyr0-DTrp8-SRIF14 binding sites in sst2 KO pituitary. It is concluded that most [125I]-Tyr0-DTrp8-SRIF14 binding sites in mouse brain and pituitary belong to the sst2 subtype but for the olfactory bulb (sst3 and sst4 receptors), the CA1 of the hippocampus (sst4 receptors) and the pituitary (sst5 and sst1 receptors) in which other subtypes are also expressed. The overall increase in [125I]-Tyr0-DTrp8-SRIF14 binding in SRIF KO mice indicates that SRIF receptors, mostly from the sst2 subtype, are regulated by the endogenous ligand(s).

Animals↗
PubMed1988

Differential distribution of beta and theta EEG activity in the entorhinal cortex of the cat.

The basic characteristics of the electroencephalograms (EEGs) of the entorhinal cortex (EC) were compared to those of the olfactory bulb (OB) and prepiriform cortex (PPC) in the awake cat, using methods that take into account linear (coherence functions) and non-linear relationships (mutual information). The frequency spectra of EC signals differ from those of EEG signals recorded from OB or PPC, but in the beta frequency band (35-40 Hz) coherent activity between these latter two areas and the EC could be put in evidence. Taking the values of coherence as a measure of linear coupling between populations of neurons, this coupling is strong between PPC and the rostral part of the EC, and becomes weaker towards more lateral, caudal and medial areas. This decrease in coupling is confirmed by non-linear analysis methods. On the basis of intracortical depth profiles it was shown that the beta activity is locally generated in layer II of the EC. Another rhythmic activity was also recorded in EC in the theta frequency range. Theta rhythm is generated mainly in the caudal part of EC. This area has the strongest coupling with the hippocampal formation. These analyses lead to the conclusion that in the EC olfactory and limbic domains have different topographical distributions but with a certain degree of overlap.

Animals↗
PubMed1993

Area-dependent changes in GABAergic function after acute and chronic cold stress.

(1) The function of the gamma-aminobutyric acid (GABA)ergic system in certain areas of the rat brain was investigated after acute and chronic cold stress. (2) GABA concentration, [3H]GABA uptake and the activity of the synthesis enzyme glutamate decarboxylase (GAD) were measured. (3) Acute stress: (a) reduced GABA concentration in the corpus striatum (29%); (b) decreased GAD activity (under non-saturating substrate concentration) in the olfactory bulbs (24%); (c) diminished neuronal uptake of [3H]GABA in the frontal cerebral cortex (65%), hypothalamus (86%) and olfactory bulbs (82%). (4) Chronic stress: (a) reduced the endogenous levels of GABA in the frontal cerebral cortex (51%), hypothalamus (26%) and olfactory bulbs (15%); (b) decreased GAD activity in the corpus striatum (32%) and olfactory bulbs (34%); (c) decreased neuronal uptake of [3H]GABA in the hypothalamus (83%). (5) These findings suggest that compensatory changes may develop in the GABAergic system after chronic stress.

Acute Disease↗
PubMed1994

Ontogenesis of quisqualate-associated phosphoinositide metabolism in various regions of the rat nervous system.

The effect of postnatal age on phosphoinositide metabolism per se and on quisqualate-stimulated phosphoinositide metabolism was characterized in synaptoneurosomes prepared from nine different regions of the rat nervous system, namely the brainstem, cerebellum, cerebral cortex, colliculi, hippocampus, hypothalamus, olfactory bulb, spinal cord and striatum. In the hippocampus, striatum, cerebellum, cerebral cortex, brainstem, colliculus and spinal cord, the basal levels of inositol phosphate (inositol-1-phosphate+inositol-4,5-bisphosphate) formation were maximal two days after birth and declined steeply to steady-state levels from the age of 10 postnatal days. Similarly, in the olfactory bulb, basal inositol phosphate synthesis did not significantly change when measured during the period from postnatal day 10 to 42. The extent of [3H]-inositol labelling of phosphoinositides as a function of age presented similar profiles when measured in hippocampal, striatal, cerebellar and cerebral cortical synaptoneurosomes, i.e. maximal at perinatal ages and minimal at adult ages. In the hypothalamus, [3H]-inositol labelling of phosphoinositides showed an increase from postnatal day 12 to higher levels from postnatal days 14 to 18 subsequently followed by a dramatic increase from postnatal day 21 to 42. A similar developmental trend was also obtained for basal inositol phosphate synthesis. On the whole, four types of developmental profiles for quisqualate-stimulated inositol phosphate formation (expressed as the percentage of the basal level and as the difference between stimulated and basal levels of radioactive inositol phosphates) were obtained depending on the nervous system region studied. In the early, prenatally developed nervous system regions, namely the brainstem and the spinal cord, no postnatal stimulation peaks of quisqualate-induced inositol phosphate formation were recorded. This was also the case for the colliculi when the stimulation of IP formation was expressed as the difference in basal and stimulated levels of inositol phosphates. Secondly, in the olfactory bulb a region known to possess a continuous capacity for developmental plasticity both structurally and functionally during the first three weeks of postnatal development, a simultaneous sustained high level of quisqualate stimulation of phosphoinositide metabolism (fluctuating around 200% of the basal level) during the early postnatal period was evident. Thirdly, in regions of the central nervous system like the cerebellum, cerebral cortex, hippocampus and the striatum known to undergo intense developmental activity during the first two postnatal weeks, peaks of quisqualate-stimulated phosphoinositide metabolism were initially detected around the first week after birth in each of these brain areas.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Terminal field of cholecystokinin-8-like immunoreactive projection neurons of the rat main olfactory bulb.

The terminal field of cholecystokinin-8 (CCK)-like immunoreactive (CCK-IR) tufted cells in the rat main olfactory bulb was examined by means of immunohistochemistry combined with either an anterograde tracer or a degeneration method. CCK immunostaining was carried out in animals in which Phaseolus vulgaris agglutinin (PHA) had been injected into the main olfactory bulb. Pairs of adjacent sections were processed for CCK and PHA immunostaining, respectively. Dense CCK-IR terminallike staining was noted in layer Ia of the anterior olfactory nucleus and lateral part of the olfactory tubercle; weaker staining was also observed in the transitional area between the anterior olfactory nucleus and the piriform cortex, in the medial part of the olfactory tubercle, and in the cortical amygdaloid nucleus. The CCK-IR staining was limited to the area containing PHA-labeled terminals and was diminished in these sites after unilateral olfactory bulbectomy. Immuno-electron microscopic analysis showed that CCK-IR profiles in such regions made asymmetric synaptic contacts, mainly with dendritic spines. These results suggest that CCK-IR tufted cells project mainly to the anterior olfactory nucleus and lateral part of the olfactory tubercle, and act mainly via axospinous synapses.

Animals↗
PubMed1994

Localization of corticotropin-releasing hormone (CRH) receptor mRNA in adult rat brain by in situ hybridization histochemistry.

Even though functional CRH receptors have been identified in several brain regions by ligand binding, the identity of brain areas expressing the CRH receptor gene has not been described. The recent cloning of the rat CRH receptor gene has permitted us to conduct an in situ hybridization histochemistry study to localize CRH receptor mRNA in brain, using an antisense 35S-labeled riboprobe and autoradiography. In virus- and pathogen-free, unstressed, adult male Sprague-Dawley rats we observed CRH receptor gene expression in several brain regions, most of which had been previously shown to bind radiolabeled CRH. Those regions include the pituitary, olfactory bulb, hippocampal formation, cerebral and cerebellar cortexes, hypothalamus, median eminence, amygdala, olfactory tubercle, choroid plexus, thalamus, and inferior colliculus. Further studies are needed to determine the cell types expressing both CRH receptor mRNA and the CRH receptor peptide in nervous system as well as in peripheral tissues.

Animals↗
PubMed2003

Coxsackievirus B3 and the neonatal CNS: the roles of stem cells, developing neurons, and apoptosis in infection, viral dissemination, and disease.

Neonates are particularly susceptible to coxsackievirus infections of the central nervous system (CNS), which can cause meningitis, encephalitis, and long-term neurological deficits. However, viral tropism and mechanism of spread in the CNS have not been examined. Here we investigate coxsackievirus B3 (CVB3) tropism and pathology in the CNS of neonatal mice, using a recombinant virus expressing the enhanced green fluorescent protein (eGFP). Newborn pups were extremely vulnerable to coxsackievirus CNS infection, and this susceptibility decreased dramatically by 7 days of age. Twenty-four hours after intracranial infection of newborn mice, viral genomic RNA and viral protein expression were detected in the choroid plexus, the olfactory bulb, and in cells bordering the cerebral ventricles. Many of the infected cells bore the anatomical characteristics of type B stem cells, which can give rise to neurons and astrocytes, and expressed the intermediate filament protein nestin, a marker for progenitor cells. As the infection progressed, viral protein was identified in the brain parenchyma, first in cells expressing neuron-specific class III beta-tubulin, an early marker of neuronal differentiation, and subsequently in cells expressing NeuN, a marker of mature neurons. At later time points, viral protein expression was restricted to neurons in specific regions of the brain, including the hippocampus, the entorhinal and temporal cortex, and the olfactory bulb. Extensive neuronal death was visible, and appeared to result from virus-induced apoptosis. We propose that the increased susceptibility of the neonatal CNS to CVB infection may be explained by the virus' targeting neonatal stem cells; and that CVB is carried into the brain parenchyma by developing neurons, which continue to migrate and differentiate despite the infection. On full maturation, some or all of the infected neurons undergo apoptosis, and the resulting neuronal loss can explain the longer-term clinical picture.

Aging↗
PubMed1983

Immunohistochemical evidence for a new group of catecholamine-containing neurons in the basal forebrain of the monkey.

Using a specific antibody to the catecholamine (CA) synthesizing enzyme, tyrosine hydroxylase (TH), in combination with the avidin-biotin-peroxidase complex method, we have found evidence for the existence of a new CA-containing cell group extending from the orbitofrontal cortex through the olfactory and pyriform cortices in the brain of two species of monkey. The TH-positive perikarya, which are 4000-5000 in number, are situated within the outer layers of these cortices and also within the olfactory tubercle and horizontal limbs of the diagonal band of Broca. They have small (10-20 microns) somata of round or oval shape. A majority are bipolar with long, slender dendrites but some are small, multipolar with widely branching dendrites. The shape and laminar distribution of these TH-positive neurons suggest that they may serve functions as cortical interneurons.

Animals↗
PubMed1988

Localization of the GABAA receptor in the rat brain with a monoclonal antibody to the 57,000 Mr peptide of the GABAA receptor/benzodiazepine receptor/Cl- channel complex.

The mAb 62-3G1 to the GABAA receptor/benzodiazepine receptor/Cl- channel complex was used with light-microscopy immunocytochemistry for studying the localization of the GABAA receptors (GABAR) in the rat brain. The results have shown a receptor distribution identical to the one obtained by others using 3H-muscimol binding in combination with autoradiographic techniques. The external plexiform layer of the olfactory bulb, cerebral cortex, granule cell layer of the cerebellum, hippocampus, dentate gyrus, substantia nigra, dorsolateral and medium geniculate nuclei, and the lateral posterior thalamic nucleus, among other areas, were rich in GABAA receptor immunoreactivity. In the cerebellum the granule cell layer had more immunoreactivity than did the molecular layer. In the hippocampus the receptor was most abundant in the stratum oriens and in the molecular layer of the dentate gyrus. The immunocytochemical techniques have also allowed us to study the distribution of the GABAA receptor with high-resolution light microscopy. These studies have shown that the GABAA receptors are localized in neuronal membranes and concentrated in structures rich in GABAergic synapses, such as the cerebellar and olfactory glomeruli and the external plexiform layer of the olfactory bulb, the deep cerebellar nuclei, and the substantia nigra. The mAb 62-3G1 was generated by immunizing mice with the affinity-purified GABAA receptor/benzodiazepine receptor (BZDR) complex. This mAb bound to the 57,000 Mr peptide but not to the benzodiazepine binding 51,000 Mr peptide. The distribution of the GABAR immunoreactivity in the rat brain colocalized better with 3H-muscimol than with 3H-benzodiazepine binding. Therefore, it is suggested that (1) the 57,000 Mr peptide that is recognized by the mAb 62-3G1 is the muscimol (GABAA receptor agonist) binding subunit of the receptor complex, (2) there is an important population of brain GABAA receptors that is not functionally coupled to the benzodiazepine receptors, and (3) both the BZDR-coupled and uncoupled forms of the GABAA receptor are immunologically similar, if not identical.

Animals↗
PubMed2001

Oxytocin in the medial amygdala is essential for social recognition in the mouse.

Oxytocin (OT) knock-out mice fail to recognize familiar conspecifics after repeated social exposures, despite normal olfactory and spatial learning abilities. OT treatment fully restores social recognition. Here we demonstrate that OT acts in the medial amygdala during the initial exposure to facilitate social recognition. OT given before, but not after, the initial encounter restores social recognition in OT knock-out mice. Using c-Fos immunoreactivity (Fos-IR) as a marker of neuronal activation in this initial encounter, we found similar neuronal activation in the wild-type (WT) and OT knock-out mouse in olfactory bulbs, piriform cortex, cortical amygdala, and the lateral septum. Wild-type, but not OT knock-out mice exhibited an induction of Fos-IR in the medial amygdala. Projections sites of the medial amygdala also failed to show a Fos-IR induction in the OT knock-out mice. OT knock-out, but not WT, mice showed dramatic increases in Fos-IR in the somatosensory cortex and the hippocampus, suggesting alternative processing of social cues in these animals. With site-specific injections of OT and an OT antagonist, we demonstrate that OT receptor activation in the medial amygdala is both necessary and sufficient for social recognition in the mouse.

Amygdala↗
PubMed1975

Subcellular and regional distribution of 125I-labeled alpha-bungarotoxin binding in rat brain and its relationship to acetylcholinesterase and choline acetyltransferase.

1. The subcellular distribution of binding sites for 125I-labeled alpha-bungarotoxin was studied in rat cerebral cortex. Primary fractions showing higher specific activity than homogenate were P2 (crude mitochondria and nerve endings) and P3-P2 was subfractionated on a Ficoll gradient with the P2B (nerve ending) subfraction exhibiting the greatest recovery (65%) and enrichment of toxin binding. Toxin binding showed a distribution similar to that of acetylcholinesterase, choline acetyltransferase, and sodium and potassium ion-activated ATPase. 2. P2B and P3 were subfractionated on five-step discontinuous sucrose gradients. The highest specific activity of toxin binding and acetylcholinesterase was associated with fractions of relatively low buoyant density, while choline acetyltransferase activity was associated with fractions of higher density. 3. Toxin binding, acetylcholinesterase, and choline acetyltransferase activities were relatively high in olfactory lobes, cerebral cortex, thalamic region, caudate nucleus, and brain stem; intermediate in hippocampus; low in cerebellum. 4. The relationship of toxin binding to the putative acetylcholine receptor in brain is discussed.

Acetylcholinesterase↗
PubMed1993

Effects of chronic stress on anterior pituitary and brain corticotropin-releasing factor receptors.

[125I]Corticotropin-releasing factor binding was measured in membrane homogenates prepared from the anterior pituitary, frontal cortex, motor cortex, somatosensory cortex, mesolimbic area (olfactory tubercle and nucleus accumbens), caudate putamen, hypothalamus, midbrain, and cerebellum from control and chronically stressed rats. The stressor consisted of 3 or 14 days of around-the-clock intermittent foot-shock (approximately one trial per 5-min frequency) that could be avoided or escaped on 90% of the trials presented by pulling a ceiling chain. Plasma corticosterone levels were almost doubled in stressed rats following 3 days of chronic stress and remained significantly elevated in rats stressed for 14 days as compared to controls. Plasma corticotropin levels were similar in controls and stressed animals in both the 3- and 14-day experiments. [125I]Corticotropin-releasing factor binding was decreased in anterior pituitary and frontal cortex following 3 days of chronic stress; binding affinity of anterior pituitary membranes was not different between control and stressed animals. [125I]Corticotropin-releasing factor binding was similar in control and 3-day-stressed animals in the other brain areas examined. After 14 days of chronic stress, hypothalamic [125I]corticotropin-releasing factor binding was decreased in stressed rats as compared to control animals but no other differences were seen. The decrease in the apparent number of anterior pituitary corticotropin-releasing factor receptors following 3 days of stress may be due, in part, to increased plasma corticosterone levels and/or increased corticotropin-releasing factor secretion during that time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed2002

Autoradiographic analysis of 5-hydroxytryptamine 5-HT2A binding sites in the rat brain after chronic intragastric ethanol treatments.

Several evidences indicate altered regulation of brain serotonergic mechanisms in alcohol abuse; changes in 5-HT2A receptor density and functioning have been observed in several lines of alcohol-preferring rats. Using quantitative autoradiography, the present study investigated the influence of chronic intragastric ethanol treatment on forebrain 5-HT2A binding sites in rats. Administration for 7 days of high doses of ethanol, which induced physical dependence, lowered the levels of 5-HT2A binding sites in the cingulate cortex, the frontal cortex and in the agranular insular cortex. The effect was observed immediately after the last ethanol administration, was statistically significant 14 h later, when marked withdrawal signs were observed, and remained significant after 8 days of detoxification, when withdrawal signs were no longer evident. No significant differences were detected in the claustrum, parietal cortex, piriform cortex, caudate putamen, olfactory tubercle, nucleus accumbens, shell and core. Chronic treatment with 6 g/kg of ethanol, which did not induce dependence, did not modify 5-HT2A binding sites. These long-lasting changes in brain 5-HT2A binding sites observed in the present study might contribute to specific aspects of ethanol dependence, such as development of depression and alcohol craving.

Animals↗
PubMed1991

Localization of type I insulin-like growth factor receptor messenger RNA in the adult rat brain by in situ hybridization.

Using multiple 35S-labeled oligonucleotide probes concurrently, the type I insulin-like growth factor receptor (IGF-I-R) mRNA was demonstrated by Northern blot hybridization in newborn and adult rat brain as a single species of approximately 11 kilobases. The probes were used to localize IGF-I-R mRNA by in situ hybridization in slices of adult rat brain. The highest levels of IGF-I-R mRNA expression were found in the glomerular and mitral cell body layers of the olfactory bulb, the granule cell body layers of the dentate gyrus and cerebellum, the pyramidal cell body layers of the piriform cortex and Ammon's horn, and the choroid plexus. The lowest levels of IGF-I-R mRNA expression were found in white matter. At the cellular level, IGF-I-R mRNA was expressed by a variety of neurons, by epithelial cells of the choroid plexus, and by ependymal cells of the third ventricle. Of the neuron types studied, the highest levels of IGF-I-R mRNA were consistently found in perikarya of mitral and tufted cells in the olfactory bulb, in pyramidal cells of the piriform cortex and Ammon's horn, and in granule cells of the dentate gyrus. There was a close congruency between the distribution of IGF-I binding and IGF-I-R mRNA at the regional level. Neuropil layers in the cerebral cortex, olfactory bulb, hippocampus, and cerebellum contained a high level of IGF-I binding, whereas the adjacent cell body layers contained a high level of the IGF-I-R mRNA. We conclude that in these regions, IGF-I-R mRNA is synthesized in neuronal cell bodies, and the receptors are transported to axons and dendrites in adjacent synapse-rich layers, where appropriate IGF effects are achieved.

Animals↗
PubMed2003

Preserved sigma1 (sigma1) receptor expression and behavioral efficacy in the aged C57BL/6 mouse.

The sigma(1) (sigma(1)) receptor represents a unique intracellular neuronal protein modulating several neurotransmitter responses with relevant effects on cognitive functions. We examined here its expression and behavioral efficacy during aging. The sigma(1) receptor expression was examined in young (2 months old) and aged (24 months old) C57BL/6 mouse brain using comparative RT-PCR and immunohistochemistry. The promnesic effect of PRE-084, a selective sigma(1) agonist, was assessed using a water-maze procedure. The sigma(1) mRNA expression was not affected during aging in the olfactory bulb, hippocampus, hypothalamus, cortex or cerebellum. The sigma(1) immunolabeling was intense in the olfactory bulb, hippocampus, hypothalamus and midbrain of the young mouse and the distribution appeared unchanged in the aged. The subcellular localization was similar in aged and younger animals, the protein being present on nuclear, mitochondrial, endoplasmic reticular and plasmic membranes. At the behavioral level, aged C57BL/6 mice showed deficits in the invisible platform learning, but not when the platform was visible. Animals subjected to a transfer test under repeated treatment with saline or PRE-084 significantly learned the new platform location. This study shows that sigma(1) receptor expression is preserved in aged animals and demonstrates the efficacy of a selective sigma(1) agonist against age-related memory deficits. Targeting this unique receptor may offer an original drug strategy during aging.

Aging↗
PubMed1985

Thiamine deficiency depletes cortical norepinephrine and impairs learning processes in the rat.

Several lines of evidence indicate that thiamine deficiency causes the Wernicke-Korsakoff syndrome, a human memory disorder. The present study examined behavioral deficits in rats after recovery from a bout of thiamine deficiency. Following behavioral testing, the brains were dissected into regions and assayed biochemically for levels of dopamine, norepinephrine, serotonin and the primary metabolites of these monoamines. Based on previous findings in this laboratory, we predicted that thiamine deficiency not only produces behavioral deficits but loss in catecholamines as well. Impairments were observed for a spatial delayed alternation task that had been learned prior to experimental treatment. In addition, experimental animals were impaired in their ability to acquire two novel tasks, active and passive shock avoidance, after recovery from the acute effects of thiamine deficiency. Comparable deficits were not observed for a number of reflex responses that were measured to assess the general neurological state of the animals. Biochemical analyses revealed that the concentration of norepinephrine was reduced significantly in cortex-hippocampus and olfactory bulb but not in other regions, while dopamine and serotonin levels were not altered in any brain region examined. These data demonstrate that a bout of thiamine deficiency can produce persistent deficits in brain norepinephrine and concomitant decrements in behavioral measures of learning and memory. These results are consistent with our hypothesis and evidence that noradrenergic deficits contribute to the amnesic symptoms of Korsakoff's psychosis.

Alcohol Amnestic Disorder↗