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PubMed1997

Age-related change in the neuropeptide Y and NADPH-diaphorase-positive neurons in the cerebral cortex and striatum of aged rats.

Age-related changes of neuropeptide Y (NPY) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) were examined in the rat cerebral cortex and striatum by immunohistochemical and histochemical methods. Double labeling for NPY and NADPH-d showed that about 30-70% of NPY-immunoreactive (NPY-IR) neurons in the cerebral cortex of the control (4-month-old) rats contained NADPH-d and that 50-75% in the aged (24-month-old) rats. The aged rats showed a significant increase in percentage of colocalization of NPY and NADPH-d in comparison with the control rats in the temporal cortex, occipital cortex, cingulate cortex, insular cortex, retrosplenial cortex and caudatoputamen. However, colocalization percentage between control and aged rats in the frontal cortex, parietal cortex, perirhinal cortex, entorhinal cortex and nucleus accumbens were practically identical. In the aged group, the number of NPY-IR/NADPH-d-positive neurons was not significantly decreased in the cerebral cortex and striatum compared to the control group. However, the number of NPY-IR/NADPH-d-negative neurons was significantly decreased in all cerebral cortical areas and caudatoputamen in the aged group except in the nucleus accumbens. Major loss of NPY-IR/NADPH-d-negative neurons in the aged group were observed in the neurons of layer II/III and V/VI. These results demonstrate that the NADPH-d containing NPY-IR neurons are less influenced by aging than the control group in the cerebral cortex and striatum of rats.

Aging↗
PubMed1997

In vitro autoradiographic localization of 5-HT1A receptor-activated G-proteins in the rat brain.

Serotonin 5-HT1A receptors belong to the superfamily of G-protein-coupled receptors. Receptor activation of G-proteins can be determined by agonist-stimulated [35S]GTPgammaS binding in the presence of excess GDP, and in vitro autoradiographic adaptation of this technique allows visualization of receptor-activated G-proteins in tissue sections. The present study was performed to examine 5-HT1A receptor activation of G-proteins using 8-OH-DPAT-stimulated [35S]GTPgammaS binding in membranes and brain sections. In hippocampal membranes, 8-OH-DPAT stimulated [35S]GTPgammaS binding by twofold, with an ED50 value of 25 nM. 5-HT1 antagonists, but not 5-HT2 antagonists, increased the ED50 of 8-OH-DPAT in a manner consistent with competitive antagonists. Scatchard analysis of [35S]GTPgammaS binding showed that 8-OH-DPAT induced the formation of high affinity [35S]GTPgammaS binding sites with a KD for GTPgammaS of 3.2 nM. [35S]GTPgammaS autoradiography, performed in brain sections with the 5-HT1A agonist 8-OH-DPAT, revealed high levels of 5-HT1A-stimulated [35S]GTPgammaS binding in the hippocampus, lateral septum, prelimbic cortex, entorhinal cortex, and dorsal raphe nucleus. 5-HT1A-stimulated [35S]GTPgammaS binding in sections was blocked by the addition of the 5-HT1 antagonist methiothepin. These results show that the use of agonist-stimulated [35S]GTPgammaS autoradiography for the 5-HT1A receptor system should provide new information regarding signal transduction in specific brain regions.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

Effects of nicotine on ethanol dependence and brain damage.

Almost all alcoholics (80%-95%) smoke tobacco. When alcoholics binge, they achieve high, sustained blood alcohol levels, become physically dependent, and often suffer loss of cognition and other higher cortical functions. Nicotine could have a modulatory effect on ethanol drinking behavior and ethanol-induced brain damage through its cholinergic actions. To determine whether nicotine altered alcohol dependence, alcohol-induced brain damage, or both, a rat model of binge drinking was used to study the effects of nicotine on the alcohol withdrawal syndrome and its associated brain damage. After administration of the last dose of ethanol in a 4-day binge model, rats remained intoxicated for approximately 5 h, slowly returned to a neutral state, and entered a hyperexcited period, which peaked around 24 h and lasted a total of 60 h. Behavioral signs of withdrawal included splayed limbs, tremors, and seizures. Continuous transdermal nicotine did not alter the duration or severity of ethanol withdrawal. The 4-day binge ethanol treatment caused considerable brain damage in the perirhinal cortex, entorhinal cortex, ventral dentate gyrus, and olfactory bulb as visualized with amino cupric silver stain. Nicotine alone caused little or no brain damage and did not markedly alter binge ethanol-induced damage in cortical or hippocampal regions. In the olfactory bulb, nicotine reduced ethanol-induced brain damage. Although results of other studies seem to indicate that nicotine increases alcohol consumption, our findings indicate that nicotine does not markedly change the development of alcohol dependence or alcohol-induced cortical damage.

Alcoholic Intoxication↗
PubMed1999

Neuroprotective effect of remacemide hydrochloride in a perforant pathway stimulation model of status epilepticus in the rat.

Previous studies have demonstrated that remacemide and its desglycinyl metabolite, AR-R 2495AA, reduce neuronal damage in animal models of ischemia, subarachnoid hemorrhage, and traumatic brain injury. The aim of the present study was to investigate whether remacemide hydrochloride also alleviates seizure-induced neuronal damage in a model of status epilepticus induced by the stimulation of the perforant pathway (PP) in the rat. Chronic oral remacemide treatment (3 x 25 mg/kg/day) was started either 2 days before or 2 h after the beginning of PP stimulation (2 mA, 20 Hz, 0.1 ms pulse duration for 60 min). The effects of remacemide treatment on the severity of seizures, electroencephalogram (EEG) parameters, seizure-induced neuronal damage in the temporal lobe regions, and memory impairment were compared to unstimulated and stimulated vehicle-treated controls, and carbamazepine-pre-treated (3 x 40 mg/kg/day) rats. Both remacemide and carbamazepine pretreatments, but not remacemide posttreatment, decreased pyramidal cell damage in the CA3 and CA1 subregions of the hippocampus (P < 0.05). In addition, overall neuronal damage in the extrahippocampal temporal lobe regions (the piriform cortex, entorhinal cortex, and the amygdaloid complex) was milder in remacemide-pretreated rats compared to stimulated control rats (P < 0.01). The neuroprotective effect was most evident on the side contralateral to stimulation. Remacemide or carbamazepine pretreatment had no evident effect on the number or duration of behavioral seizures during PP stimulation. Neither drug altered the spectral parameters of the baseline EEG or prevented status epilepticus-induced EEG slowing observed 2 weeks after PP stimulation. Nor did remacemide or carbamazepine treatment alleviate spatial memory impairment determined in a Morris water-maze task 2 weeks after PP stimulation. Our data provide evidence that pretreatment with remacemide has a moderate neuroprotective effect against status epilepticus-induced neuronal damage.

Acetamides↗
PubMed2001

Animal cognition and the rat olfactory system.

Is smell a 'primitive' sense used primarily to guide biologically basic behaviors or might it be the sensory modality that allows some species to express complex learning and other forms of cognitive behavior? Historically, the olfactory system has been considered primitive and it is not surprising that, until recently, cognitive neuroscientists have ignored odor-guided behavior. However, we now know that the olfactory system has projections to the prefrontal cortex, entorhinal cortex and hippocampus, and that these connections support the acquisition of simple and higher-order instrumental tasks, as well as a robust memory for odors. It appears that animals with a well-developed sense of smell have the neural machinery to think with their noses.

Journal Article↗
PubMed1979

Specific distribution of metabolic alterations in cerebral cortex following apomorphine administration.

The topographic distribution of dopaminergic receptors in the cerebral cortex closely parallels that of the dopaminergic innervation. In the rat, dopaminergic axons which originate in the mesencephalon are confined to a few discrete regions of the neocortex--anterior cingulate cortex, entorhinal cortex, frontal cortex (particularly anteromedial and supragenual areas) and the transitional zone between the neocortex and the pyriform cortex. Moreover, biochemical examinations of processes generally considered to be indicative of dopaminergic neuro-transmission--neuronal uptake of labelled dopamine or dopamine-activation of adenylate cyclase activity--have confirmed a highly restricted locus of action of dopaminergic systems in the cerebral cortex. We describe here data obtained using the 2-deoxyglucose technique in conjunction with conventional neuropharmacological techniques, suggesting that the influence of dopaminergic systems on cortical function extends beyond the known confines of the mesocortical dopaminergic system.

Animals↗
PubMed1990

Interactions of phencyclidine receptor agonist MK-801 with dopaminergic system: regional studies in the rat.

Interactions of the potent phencyclidine receptor agonist MK-801 with the dopaminergic system were examined in various brain regions in the rat. MK-801 increased dopamine (DA) metabolism in the pyriform cortex, entorhinal cortex, prefrontal cortex, striatum, olfactory tubercle, amygdala, and septum without affecting DA metabolism in the cingulate cortex and nucleus accumbens. In pyriform cortex and amygdala, MK-801 was more potent than phencyclidine at increasing DA metabolism. Local injections of MK-801 into ventral tegmental area and into the amygdala/pyriform cortex interface indicated that MK-801 may act at the cell body as well as the nerve terminal level to increase DA metabolism and that ongoing dopaminergic neuronal activity is a prerequisite for full drug action.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Intrinsic and efferent connections of the endopiriform nucleus in rat.

The endopiriform nucleus is a large group of multipolar cells located deep to the piriform cortex. The function of this nucleus is unknown, but studies with animal models suggest that it plays an important role in temporal lobe epileptogenesis. To address questions concerning mechanisms of epileptogenesis and to gain insights into its normal function, efferent axons from the endopiriform nucleus were labeled by anterograde transport from small extracellular injections of Phaseolus vulgaris leucoagglutinin. Several principles of organization were derived: (1) heavy local and long intrinsic connections are present throughout the endopiriform nucleus; (2) endopiriform efferents target cortical rather than nuclear structures; (3) extensive projections from the endopiriform nucleus extend to most basal forebrain areas including the piriform cortex, entorhinal cortex, insular cortex, orbital cortex, and all cortical amygdaloid areas. The perirhinal cortex, olfactory tubercle, and most subdivisions of the hippocampal formation receive light projections; (4) projections are highly distributed spatially within all target areas; (5) efferent axons from the endopiriform nucleus are unmyelinated and give rise to boutons along their entire course rather than arborizing locally; and (6) the endopiriform nucleus and piriform cortex share target areas, but efferents from the endopiriform nucleus lack the precise laminar order of those from the piriform cortex, and provide a heavy caudal to rostral pathway that is lacking in the cortex. The significance of these findings for the triggering of generalized seizures from the deep piriform region are discussed. An hypothesis for a role of the endopiriform nucleus in memory storage is presented.

Amygdala↗
PubMedDate not supplied

Age-dependent effects of 5,7-dihydroxytryptamine on serotonin transporter in different brain areas in the rat.

In the present study, we investigated the [(3)H]citalopram binding using a quantitative autoradiography following intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) in neonatal and adult male Wistar rats. One group of animals was injected with 5,7-DHT at 3 days after birth while the second group received the neurotoxin at 3 months after birth. Control group was injected with saline. Afterwards, all rats were examined at 4(th) months after birth to determine the serotonin (5-HT) and catecholamines concentrations using the liquid chromatography with electrochemical detection HPLC system and distribution and density of [(3)H]citalopram binding sites in the brain using the quantitative autoradiography. A marked depletion of brain 5-HT was observed in rats lesioned either in postnatal or adult period of life. Rats lesioned in their adult period of life showed dramatic reduction of 5-HT transporter in all investigated brain areas (i.e.the frontal cortex, entorhinal cortex, hippocampus, caudate-putamen, nucleus accumbens and ventral tegmental area). On the other hand, administration of 5,7-DHT to newborn rats failed to reduce 5-HT transporter sites in the ventral tegmental area, and produced only slight or moderate reduction in the nucleus accumbens. Thus, it appears that the mesolimbic ventral tegmental area-nucleus accumbens systems are relatively more resistant to 5,7-DHT neurotoxicity in the early postnatal period.

5,7-Dihydroxytryptamine↗
PubMed1991

Immunohistochemical localization of an inositol 1,4,5-trisphosphate receptor, P400, in neural tissue: studies in developing and adult mouse brain.

The immunohistochemical localization of P400/inositol 1,4,5-trisphosphate (InsP3) receptor protein was studied in developing and adult mouse brain by using monoclonal antibodies. The developmental expression pattern of P400/InsP3 receptor protein differed among different classes of neurons. It was first detected in the somata of immature Purkinje cells at embryonic day 17, in the ventrolateral region of the posterior vermis in the cerebellum. Axonal immunoreactivity within the cerebellar nuclei was first present at postnatal day 3. Neurons in the retrosplenial cortex, the anterior olfactory nucleus, and the CA1 region of the hippocampus expressed immunoreactivity earlier than other regions of the brain. In the adult brain, not only the Purkinje cell but also many other types of cells in many areas of the brain expressed P400/InsP3 receptor, though to a lesser extent. These included the neurons in the striatum, globus pallidus, nucleus accumbens septi, anterior olfactory nucleus, olfactory tubercle, precommissural hippocampus, hippocampus, substantia nigra, cerebral cortex, pons, and certain hypothalamic nuclei. Forebrain cortical regions that receive afferents from the olfactory bulb, such as the anterior olfactory nucleus, olfactory tubercle, prepiriform cortex, entorhinal cortex, and amygdala, exhibited distinct immunoreactivity, while olfactory bulb was almost devoid of staining. Immunoreactivity in the axonal pathways was also found in the limbic-hypothalamic pathways, strionigral projection, and part of the corpus callosum. Results of Western blot analysis and 3H-InsP3 binding assay were consistent with the qualitative regional differences of immunoreactivity demonstrated by immunohistochemical study. The location of InsP3 receptor in the brain correlates well with the InsP3 binding sites demonstrated by an autoradiographic study.

Animals↗
PubMed1989

Neuropeptide Y receptor binding sites in rat brain: differential autoradiographic localizations with 125I-peptide YY and 125I-neuropeptide Y imply receptor heterogeneity.

Neuropeptide Y (NPY) receptor binding sites have been localized in the rat brain by in vitro autoradiography using picomolar concentrations of both 125I-NPY and 125I-peptide YY (PYY) and new evidence provided for differentially localized receptor subtypes. Equilibrium binding studies using membranes indicate that rat brain contains a small population of high-affinity binding sites and a large population of moderate-affinity binding sites. 125I-PYY (10 pM) is selective for high-affinity binding sites (KD = 23 pM), whereas 10 pM 125I-NPY labels both high- and moderate-affinity sites (KD = 54 pM and 920 pM). The peptide specificity and affinity of these ligands in autoradiographic experiments match those seen in homogenates. Binding sites for 125I-PYY are most concentrated in the lateral septum, stratum oriens, and radiatum of the hippocampus, amygdala, piriform cortex, entorhinal cortex, several thalamic nuclei, including the reuniens and lateral posterior nuclei, and substantia nigra, pars compacta, and pars lateralis. In the brain stem, 125I-PYY sites are densest in a variety of nuclei on the floor of the fourth ventricle, including the pontine central grey, the supragenual nucleus, and the area postrema. 125I-NPY binding sites are found in similar areas, but relative levels of NPY binding and PYY binding differ regionally, suggesting differences in sites labeled by the two ligands. These receptor localizations resemble the distribution of endogenous NPY in some areas, but others, such as the hypothalamus, contain NPY immunoreactivity but few binding sites.

Animals↗
PubMed1995

Afferent projections to the cingulate cortex in albino rats: a study with a retrograde labeling method using fluoro-gold.

We studied the neuronal populations that project their axons to the cingulate cortex in albino rats using the retrograde fluorescent dye of 4% Fluoro-Gold injected into the anterior, middle and posterior portions of the cingulate cortex. The result showed that the following ipsilateral structures are sending fibers to these three portions: the prefrontal cortex, frontoparietal motor cortex, indusium griseum, dorsal endopiriform nucleus, lateral part of medial mammillary nucleus, nuclei of diagonal band of Broca, anterior pretectum, anterior part of caudate-putamen, hippocampal formation, anteroventral, anteromedial, lateroposterior, ventroposterior and dorsomedial thalamic nuclei. The anterior portion of the cingulate cortex receives inputs from the following ipsi- and contralateral structures: the accessory olfactory bulbs, anterior olfactory nuclei, middle and posterior portions of the cingulate cortex. The middle cingulate cortex receives fibers only from the ipsilateral dorsal part of the lateral septal nucleus in addition from the ipsi- and contralateral anterior and posterior portions of the cingulate cortex. While the posterior portion of the cingulate cortex receives separate inputs from the following ipsilateral structures: anterodorsal thalamic nucleus, temporal cortex, entorhinal cortex, areas 17 and 18, as well as from the ipsi- and contralateral anterior and middle portions of the cingulate cortex. The present study shows that the cingulate cortex receives various kinds of inputs from the other parts of the brain which are involved in emotion, memory, vision and motion, and also suggests that there are differences in afferent projections among the anterior, middle and posterior portions of the cingulate cortex.

Afferent Pathways↗
PubMed1995

Comparative localization of serotonin1A, 1C, and 2 receptor subtype mRNAs in rat brain.

Serotonin (5-HT) mediates its effects on neurons in the central nervous system through a number of different receptor types. To gain better insight as to the localization of 5-HT responsive cells, the distribution of cells expressing mRNAs encoding the three 5-HT receptor subtypes 1A, 1C, and 2 was examined in rat brain with in situ hybridization using cRNA probes. 5-HT1A receptor mRNA labeling was most pronounced in the olfactory bulb, anterior hippocampal rudiment, septum, hippocampus (dentate gyrus and layers CA1-3), entorhinal cortex, interpeduncular nucleus, and medullary raphe nuclei. 5-HT1C receptor mRNA labeling was the most abundant and widespread of the three 5-HT receptor subtypes examined. Hybridization signal was densest in the choroid plexus, anterior olfactory nucleus, olfactory tubercle, piriform cortex, septum, subiculum, entorhinal cortex, claustrum, accumbens nucleus, striatum, lateral amygdala, paratenial and paracentral thalamic nuclei, subthalamic nucleus, substantia nigra, and reticular cell groups. 5-HT2 receptor mRNA was localized to the olfactory bulb, anterior hippocampal rudiment, frontal cortex, piriform cortex, entorhinal cortex, claustrum, pontine nuclei, and cranial nerve motor nuclei including the oculomotor, trigeminal motor, facial, dorsal motor nucleus of the vagus, and hypoglossal nuclei. The distributions of mRNAs for the three different 5-HT receptor subtypes overlap with regions that bind various 5-HT receptor-selective ligands and are present in nearly all areas known to receive serotonergic innervation. The results of this study demonstrate that neurons which express these 5-HT receptor subtypes are very widespread in the central nervous system, yet possess unique distributions within the rat brain. Moreover, previously unreported regions of 5-HT receptor subtype expression were observed, particularly with the 5-HT2 receptor riboprobe in the brainstem. Finally, several brain areas contain multiple 5-HT receptor subtype mRNAs, which leads to the possibility that individual cells may express more than one 5-HT receptor subtype.

Animals↗
PubMed2004

Laser microdissection of immunolabeled astrocytes allows quantification of astrocytic gene expression.

Astrocytes represent the major glial cell population within the central nervous system. In order to elucidate the function of astrocytes under physiological conditions and during the course of neurological disease, astrocytic gene expression profiling is necessary. However, since astrocytes form an intimately connected network with neurons and other cell types in the brain, gene expression analysis of astrocytes with a sufficient degree of cellular specificity is difficult. Here we are presenting a rapid and, thus, RNA preserving immunostaining protocol for the detection of astrocytes in rodent brain. This protocol can readily be combined with laser microdissection (Leica AS LMD platform) and quantitative RT-PCR (qPCR). Employing this method, we studied changes in glial fibrillary acidic protein (GFAP) expression in astrocytes of mouse entorhinal cortex following entorhinal cortex lesion. Using laser microdissection, astrocytes (n = 60) were collected in the tissue surrounding the lesion, the entorhinal cortex contralateral to the lesion, and in unlesioned control animals. Changes in GFAP mRNA were quantified using qPCR. GFAP mRNA levels were 82-fold higher in astrocytes of lesioned animals at the site of the lesion compared to GFAP mRNA levels in entorhinal cortex astrocytes of control mice. GFAP mRNA levels were only slightly elevated at the contralateral side (lesioned animals). This optimized protocol for immunolabeling and laser microdissection of astrocytes followed by qPCR allows quantification of astrocytic gene expression levels with a high degree of cellular specificity. It may similarly be employed in different settings where other cell types need to be identified and microdissected for gene expression profiling.

Animals↗
PubMed1999

p75 neurotrophin receptor expression is induced in apoptotic neurons after seizure.

Seizure causes neuronal cell loss in both animal models and human epilepsy. To determine the contribution of apoptotic mechanisms to seizure-induced neuronal cell death, rat brains were examined for the occurrence of terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL)-positive nuclei after pilocarpine-induced seizure. Numerous TUNEL-positive cells were observed throughout the postseizure hippocampus, piriform cortex, and entorhinal cortex. Combined TUNEL/NeuN immunocytochemistry demonstrated that the vast majority of TUNEL-positive cells were neurons. To identify components of the signal transduction cascade promoting postseizure apoptosis, the expression of the p75 neurotrophin receptor (p75NTR) was examined. Seizure-induced increases in p75NTR protein and mRNA were detected in hippocampus, piriform cortex, and entorhinal cortex. Immunohistochemical double labeling revealed almost complete correspondence between TUNEL-positive and p75NTR-expressing cells, suggesting that seizure-induced neuronal loss within the CNS occurs through apoptotic signaling cascades involving p75NTR.

Animals↗
PubMed1978

Association and commissural fiber systems of the olfactory cortex of the rat.

The association and commissural fiber systems arising in the olfactory cortical areas caudal to the olfactory peduncle (the piriform cortex, nucleus of the lateral olfactory tract, anterior cortical nucleus of the amygdala, periamygdaloid cortex and entorhinal cortex) have been studied utilizing horseradish peroxidase as both an anterograde and a retrograde axonal tracer. In the piriform cortex two sublaminae within layer II (IIa and IIb) layer III have been found to give rise to distinctly different projections. Retrograde cell labeling experiments indicate that the association fiber projection from layer IIb is predominatnly caudally directed, while the projection from layer III is predominantly rostrally directed. Cells in layer IIa project heavily to areas both caudal and rostral to the piriform cortex. The commissural fibers from the piriform cortex are largely restricted in their origin to layer IIb of the anterior part of the piriform cortex and in their termination on the contralteral side to the posterior part of the piriform cortex and adjacent olfactory cortical areas. A projection to the olfactory bulb has also been found to arise from cells in layers IIb and III of the ipsilateral piriform cortex, but not in layer IIa. In addition to those from the piriform cortex, association projections have also been found from other olfactory cortical areas. The nucleus of the lateral olfactory tract has a heavy bilateral projection to the medial part of the anterior piriform cortex and the lateral part of the olfactory tubercle (as well as a lighter projection to the olfactory bulb); both the anterior cortical nucleus of the amygdala and the periamygdaloid cortex project ipsilaterally to several olfactory cortical areas. The entorhinal cortex has been found to project to the medial parts of the olfactory tubercle and the olfactory peduncle. The olfactory tubercle is the only olfactory cortical area from which no association fiber systems (instrinsic or extrinsic) have been found to originate. A broad topographic organization exists in the distribution of the fibers from several of the olfactory areas. This is most obvious in the anterior part of the olfactory cortex, in which fibers from the more rostral areas (the anterior olfactory nucleus and the anterior piriform cortex) terminate in regions near the lateral olfactory tract, while those from more caudal areas (the posterior piriform cortex and the entorhinal cortex) terminate in areas further removed, both laterally and medially, from the tract. Projection to olfactory areas from the hypothalamus, thalamus, diagonal band, and biogenic amine cell groups have been briefly described.

Animals↗
PubMed1997

Infusion of D-cycloserine into temporal-hippocampal areas and restoration of mnemonic function in rats with disrupted glutamatergic temporal systems.

Partial transections of the fiber connections between the temporal cortex and the lateral entorhinal cortex at a site of the white matter corresponding to the perirhinal cortex result in impaired visual memory accompanied by reduced concentrations of glutamate in both the temporal cortex and lateral entorhinal cortex. Intraperitoneal administration of the glycinergic receptor agonist D-cycloserine produces complete restoration of memory function, as measured by a brightness discrimination task in rats with temporal cortex/lateral entorhinal cortex transections. The purpose of the present study was to identify in which brain structures the compensatory activity might take place. The results show that infusion of cycloserine into either the temporal cortex or lateral entorhinal cortex fully ameliorated the impairment of temporal cortex/lateral entorhinal cortex lesions, whereas infusion into the hippocampal region caused only a mild improvement of the retention performance. Infusion of cycloserine into the frontal cortex or saline into the temporal cortex or lateral entorhinal cortex had no ameliorating effects on the memory dysfunction of rats bearing temporal cortex/lateral entorhinal cortex transections. It is concluded that the temporal cortex, lateral entorhinal cortex and perirhinal cortex are highly critical in forming visual memory.

Analysis of Variance↗
PubMed2005

Reduced parahippocampal connectivity produces schizophrenia-like memory deficits in simulated neural circuits with reduced parahippocampal connectivity.

CONTEXT: Episodic memory impairments are well characterized in schizophrenia, but their neural origin is unclear. OBJECTIVE: To determine whether the episodic memory impairments in schizophrenia may originate from reduced parahippocampal connectivity. DESIGN: Experimental in silico model. SETTING: Department of Psychology, University of Amsterdam, Amsterdam, the Netherlands. INTERVENTIONS: A new, in silico medial temporal lobe model that simulates normal performance on a variety of episodic memory tasks was devised. The effects of reducing parahippocampal connectivity in the model (from perirhinal and parahippocampal cortex to entorhinal cortex and from entorhinal cortex to hippocampus) were evaluated and compared with findings in schizophrenic patients. Alternative in silico neuropathologies, increased noise and loss of hippocampal neurons, were also evaluated. RESULTS: In the model, parahippocampal processing subserves integration of different cortical inputs to the hippocampus and feature extraction during recall. Reduced connectivity in this area resulted in a pattern of deficits that closely mimicked the impairments in schizophrenia, including a mild recognition impairment and a more severe impairment in free recall. Furthermore, the schizophrenic model was not differentially sensitive to interference, also consistent with behavioral data. Notably, neither increased noise levels nor a reduction of hippocampal nodes in the model reproduced this characteristic memory profile. CONCLUSIONS: Taken together, these findings highlight the importance of parahippocampal neuropathology in schizophrenia, demonstrating that reduced connectivity in this region may underlie episodic memory problems associated with the disorder.

Entorhinal Cortex↗