Loss Of Granule Cells Research Articles

Brain pathology in fatal serotonin syndrome: Presentation of two cases

Serotonin syndrome is a potentially life-threatening reaction that occurs in patients using drugs that elevate the serotonin level in the body. Excess serotonergic activity in the CNS and peripheral serotonin receptors results in neuromuscular hyperactivity, mental changes and autonomic symptoms. Hyperthermia is a characteristic feature of the syndrome. We describe neuropathological findings from two cases of lethal serotonin syndrome, both patients presenting with hyperthermia and neuromuscular symptoms. One of the patients had been taking amitriptylin and mirtazapin and the other had used amitriptylin and citalopram. They died, respectively, 10 days and 2½ months after the onset of serotonin syndrome symptoms. Post-mortem examination of the brains showed subtotal loss of cerebellar Purkinje cells in both cases. In the case with shorter survival time, areas with partial loss of cerebellar granule cells were observed, whereas in the case with longer survival time general and extensive loss of granule cells was found. Cells in other areas of the brain known to be sensitive to hypoxic injury were not affected. Selective loss of Purkinje cells has previously been described in neuroleptic malignant syndrome and heatstroke, conditions that are characterized by hyperthermia. This suggests that hyperthermia may be a causative factor of brain damage in serotonin syndrome. This is the first report describing neuropathological findings in serotonin syndrome.

Low proliferation and differentiation capacities of adult hippocampal stem cells correlate with memory dysfunction in humans

The hippocampal dentate gyrus maintains its capacity to generate new neurons throughout life. In animal models, hippocampal neurogenesis is increased by cognitive tasks, and experimental ablation of neurogenesis disrupts specific modalities of learning and memory. In humans, the impact of neurogenesis on cognition remains unclear. Here, we assessed the neurogenic potential in the human hippocampal dentate gyrus by isolating adult human neural stem cells from 23 surgical en bloc hippocampus resections. After proliferation of the progenitor cell pool in vitro we identified two distinct patterns. Adult human neural stem cells with a high proliferation capacity were obtained in 11 patients. Most of the cells in the high proliferation capacity cultures were capable of neuronal differentiation (53 ± 13% of in vitro cell population). A low proliferation capacity was observed in 12 specimens, and only few cells differentiated into neurons (4 ± 2%). This was reflected by reduced numbers of proliferating cells in vivo as well as granule cells immunoreactive for doublecortin, brain-derived neurotrophic factor and cyclin-dependent kinase 5 in the low proliferation capacity group. High and low proliferation capacity groups differed dramatically in declarative memory tasks. Patients with high proliferation capacity stem cells had a normal memory performance prior to epilepsy surgery, while patients with low proliferation capacity stem cells showed severe learning and memory impairment. Histopathological examination revealed a highly significant correlation between granule cell loss in the dentate gyrus and the same patient's regenerative capacity in vitro (r = 0.813; P < 0.001; linear regression: R²(adjusted) = 0.635), as well as the same patient's ability to store and recall new memories (r = 0.966; P = 0.001; linear regression: R²(adjusted) = 0.9). Our results suggest that encoding new memories is related to the regenerative capacity of the hippocampus in the human brain.

Chronic 835-MHz radiofrequency exposure to mice hippocampus alters the distribution of calbindin and GFAP immunoreactivity

Exponential interindividual handling in wireless communication system has raised possible doubts in the biological aspects of radiofrequency (RF) exposure on human brain owing to its close proximity to the mobile phone. In the nervous system, calcium (Ca 2+) plays a critical role in releasing neurotransmitters, generating action potential and membrane integrity. Alterations in intracellular Ca 2+ concentration trigger aberrant synaptic action or cause neuronal apoptosis, which may exert an influence on the cellular pathology for learning and memory in the hippocampus. Calcium binding proteins like calbindin D28-K (CB) is responsible for the maintaining and controlling Ca 2+ homeostasis. Therefore, in the present study, we investigated the effect of RF exposure on rat hippocampus at 835 MHz with low energy (specific absorption rate: SAR = 1.6 W/kg) for 3 months by using both CB and glial fibrillary acidic protein (GFAP) specific antibodies by immunohistochemical method. Decrease in CB immunoreactivity (IR) was noted in exposed (E1.6) group with loss of interneurons and pyramidal cells in CA1 area and loss of granule cells. Also, an overall increase in GFAP IR was observed in the hippocampus of E1.6. By TUNEL assay, apoptotic cells were detected in the CA1, CA3 areas and dentate gyrus of hippocampus, which reflects that chronic RF exposure may affect the cell viability. In addition, the increase of GFAP IR due to RF exposure could be well suited with the feature of reactive astrocytosis, which is an abnormal increase in the number of astrocytes due to the loss of nearby neurons. Chronic RF exposure to the rat brain suggested that the decrease of CB IR accompanying apoptosis and increase of GFAP IR might be morphological parameters in the hippocampus damages.

Object/context-specific memory deficits associated with loss of hippocampal granule cells after adrenalectomy in rats

Chronic adrenalectomy (ADX) causes a gradual and selective loss of granule cells in the dentate gyrus (DG) of the rat. Here, we administered replacement corticosterone to rats beginning 10 wk after ADX. We then tested them in three discrimination tasks based on object novelty, location, or object/context association. Only during testing of the object/context association did ADX rats demonstrate deficits. These findings add to a body of evidence that the hippocampus is necessary when contextual information is important. We also confirm that memory deficits after chronic adrenalectomy are not a result of loss of corticosterone per se.

Exercise Neuroprotection in a Rat Model of Binge Alcohol Consumption

Excessive alcohol intake produces structural and functional deficits in corticolimbic pathways that are thought to underlie cognitive deficits in the alcohol use disorders (AUDs). Animal models of binge alcohol administration support the direct link of high levels of alcohol consumption and neurotoxicity in the hippocampus and surrounding cortex. In contrast, voluntary wheel running enhances hippocampal neurogenesis and generally promotes the health of neurons. We investigated whether voluntary exercise prior to binge alcohol exposure could protect against alcohol-induced cell loss. Female Long-Evans rats exercised voluntarily for 14 days before undergoing 4 days of binge alcohol consumption. Brains were harvested immediately after the last dose of alcohol and examined for various histological markers of neurodegeneration, including both cell death (FluoroJade B) and cell birth (Ki67) markers. Rats that exercised prior to binge exposure were significantly less behaviorally intoxicated, which was not a result of enhanced hepatic metabolism. Rats that exercised prior to binge alcohol consumption had reduced loss of dentate gyrus granule cells and fewer FluoroJade B positive cells in the dentate gyrus and associated entorhinal-perirhinal cortex compared to nonexercisers. However, exercise did not protect against cell death in the piriform cortex nor protect against alcohol-induced decreases in cell proliferation, evidenced by a similar alcohol-induced reduction in Ki67 labeled cells between exercise and sedentary rats. We conclude that exercise can reduce behavioral sensitivity to ethanol intoxication and protect vulnerable brain areas from alcohol-induced cell death. Exercise neuroprotection of alcohol-induced brain damage has important implications in understanding the neurobiology of the AUDs as well as in developing novel treatment strategies.

Comparative Study of Cerebellar Degeneration in Canine Neuroaxonal Dystrophy, Cerebellar Cortical Abiotrophy, and Neuronal Ceroid-Lipofuscinosis

The cerebellar lesions of three dogs with canine neuroaxonal dystrophy (NAD), one dog with cerebellar cortical abiotrophy (CCA), and 4 dogs with neuronal ceroid-lipofuscinosis (NCL) were examined to understand their pathogeneses. Purkinje cell loss was most severe in the vermis of a dog with CCA, and granule cell loss was most prominent in the cerebellar hemisphere of dogs with NCL. Immunohistochemically, CD3-and HLA-DR-positive cells were most frequent in the dogs with NCL, and moderate in dogs with NAD, but not in a dog with CCA. The number of cleaved caspase 3-positive cells was prominent in a dog with CCA, but no significant in the dogs with NAD. The results indicate different pathway of neuronal loss of these canine neuronal disorders.

Characterization of cells newly generated after granule cell loss in the hippocampal dentate gyrus of mice

Characterization of cells newly generated after granule cell loss in the hippocampal dentate gyrus of mice

Laser Capture Microdissection Reveals Specific Genes Related to Purkinje Cell Death in the Leaner Mice

The leaner mouse carries a mutation in the gene encoding the α1A subunit of P/Q-type calcium channels. Leaner mice exhibit extensive cerebellar granule and Purkinje cell loss that results in cerebellar dysfunction. A previous study suggested that a small population of leaner Purkinje cells undergo apoptosis, however the cell death mode of the rest of degenerating Purkinje cells has not been identified. In order to investigate the mechanisms underlying leaner Purkinje cell death, gene arrays that contain 243 cell death related genes were carried out. To increase the chance of detecting Purkinje cell specific genes, laser capture microdissection was employed to obtain Purkinje cell enriched samples. The gene array analysis revealed several potential genes that are involved in autophagic cell death pathway including cathepsin D, a key lysosomal protease that triggers autophagic degradation. Further analysis on LC3, which is a hallmark for autophagic cell death showed that leaner Purkinje cells are degenerating via autophagic process. The present study provides evidence that calcium channel defects trigger different modes of neurodegeneration in the cerebellum.

Variant Creutzfeldt–Jakob disease: the first confirmed case from Portugal shows early onset, long duration and unusual pathology

We present clinical and autopsy findings in the first case of variant Creutzfeldt–Jakob disease diagnosed and confirmed in Portugal. Onset was at 11 years, the earliest onset reported, and the...

Survival of mossy cells of the hippocampal dentate gyrus in humans with mesial temporal lobe epilepsy

Hippocampal sclerosis can be identified in most patients with mesial temporal lobe epilepsy (TLE). Surgical removal of the sclerotic hippocampus is widely performed to treat patients with drug-resistant mesial TLE. In general, both epilepsy-prone and epilepsy-resistant neurons are believed to be in the hippocampal formation. The hilar mossy cells of the hippocampal dentate gyrus are usually considered one of the most vulnerable types of neurons. The aim of this study was to clarify the fate of mossy cells in the hippocampus in epileptic humans. Of the 19 patients included in this study, 15 underwent temporal lobe resection because of drug-resistant TLE. Four patients were used as controls because they harbored tumors that had not invaded the hippocampus and they had experienced no seizures. Histological evaluation of resected hippocampal tissues was performed using immunohistochemistry. Mossy cells were identified in the control as well as the epileptic hippocampi by using cocaine- and amphetamine-regulated transcript peptide immunohistochemistry. In most cases the number of mossy cells was reduced and thorny excrescences were smaller in the epileptic hippocampi than in controls; however, there was a significant loss of pyramidal cells and a partial loss of granule cells in the same epileptic hippocampi in which mossy cell loss was apparent. The loss of mossy cells could be correlated with the extent of hippocampal sclerosis, patient age at seizure onset, duration of epilepsy, and frequency of seizures. In many cases large numbers of mossy cells were present in the hilus of the dentate gyrus when most pyramidal neurons of the CA1 and CA3 areas of the Ammon's horn were lost, suggesting that mossy cells may not be more vulnerable to epileptic seizures than the hippocampal pyramidal neurons.

Borna disease virus infection alters synaptic input of neurons in rat dentate gyrus

Granule cells are major targets of entorhinal afferents terminating in a laminar fashion in the outer molecular layer of the dentate gyrus. Since Borna disease virus (BDV) infection of newborn rats causes a progressive loss of granule cells in the dentate gyrus, entorhinal fibres become disjoined from their main targets. We have investigated the extent to which entorhinal axons react to this loss of granule cells. Unexpectedly, anterograde DiI tracing has shown a prominent layered termination of the entorhinal projection, despite an almost complete loss of granule cells at 9 weeks after infection. Combined light- and electron-microscopic analysis of dendrites at the outer molecular layer of the dentate gyrus at 6 and 9 weeks post-infection has revealed a transient increase in the synaptic density of calbindin-positive granule cells and parvalbuminergic neurons after 6 weeks. In contrast, synaptic density reaches values similar to those of uninfected controls 9 weeks post-infection. These findings indicate that, after BDV infection, synaptic reorganization processes occur at peripheral dendrites of the remaining granule cells and parvalbuminergic neurons, including the unexpected persistence of entorhinal axons in the absence of their main targets.

Interleukin-1 Mediates Long-Term Hippocampal Dentate Granule Cell Loss Following Postnatal Viral Infection

Viral infections of the developing CNS can cause long-term neuropathological sequela through undefined mechanisms. Proinflammatory cytokines such as IL-1beta have gained attention in mediating neurodegeneration in corticohippocampal structures due to a variety of insults in adults, though there is less information on the developing brain. Little is known concerning the spatial-temporal pattern of IL-1beta induction in the developing hippocampus following live virus infection, and there are few studies addressing the long-term consequences of this cytokine induction. We report that infection of rats with lymphocytic choriomeningitis virus on postnatal day 4 induces IL-1beta protein in select regions of the hippocampus on 6, 15, 21, and 45 days after infection. This infection resulted in a 71% reduction of dentate granule cell neurons by the time the rats reached mid-adulthood. We further investigated the causative role of IL-1 in this dentate granule cell loss by blocking IL-1 activity using an IL-1ra-expressing adenoviral vector administered at the time of infection. Blockade of IL-1 abrogated the infection-associated neuron loss in this vivo model. Considering that IL-1 can be triggered by multiple perinatal insults, our findings suggest that early therapy with anti-inflammatory agents that block IL-1 may be effective for reducing adulthood neuropathology.

Late onset cerebellar cortical degeneration in a koala

A 10-year-old male koala started to fall from the tree while sleeping. Subsequently, the koala often fell down while walking and showed a gait abnormality, abnormal nystagmus and hypersalivation. At 12 years of age, the koala became ataxic and seemed blind. At 13 years of age, the koala exhibited signs of dysstasia and was euthanased. Necropsy revealed marked symmetrical atrophy of the cerebellum. Histopathologically, a severe loss of Purkinje and granule cells was evident in the cerebellum, while the molecular layer was more cellular than normal with cells resembling small neurons, which were positively stained with parvalbumin immunohistochemistry. Reactive Bergmann glial cells (astrocytes) were present adjacent to the depleted Purkinje cell zone. The very late onset and slow progression of the cerebellar cortical degeneration in this case is particularly interesting and appears to be the first report in the koala.

Co-occurrence of X-Linked Congenital Adrenal Hypoplasia and Autistic Disorder

Back to table of contents Previous article Next article LETTERFull AccessCo-occurrence of X-Linked Congenital Adrenal Hypoplasia and Autistic DisorderKarl G. Sieg M.D.,Karl G. Sieg M.D.Search for more papers by this author,Published Online:1 Apr 2009AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: One form of congenital adrenal hypoplasia is associated with the Xp21 chromosomal region. These patients have clinical abnormalities including mental retardation, hearing loss, hypogonadism, glycerol kinase deficiency, ornithine transcarbamoylase deficiency, and Duchenne muscular dystrophy. This letter presents a case of a patient with X-linked congenital adrenal hypoplasia whose mental status as a preadolescent male was also consistent with the diagnosis of autistic disorder. Case ReportA 12-year-old Caucasian boy presented with features of autistic disorder including marked lack of awareness of the feelings of others; no seeking of comfort in times of distress; gross impairment in ability to make peer friendships; abnormal nonverbal communication; abnormalities in speech production including perseveration and echolalia; stereotyped body movements including flapping, clapping, and rocking; and persistent preoccupation with parts of objects reflecting a restricted range of interests. His Autism Behavior Checklist total score was 126 with the following subscale profile results: sensory 15, relating 33, body and object use 31, language 25, social and self-help 22. Speech and language testing indicated an age equivalency of 2.8 to 3.0 years old with severe delays of receptive and expressive language as well as speech articulation. MRI brain scan was unremarkable. Chromosomal analysis had confirmed a deletion at the Xp21 region. His family pedigree noted several female congenital adrenal hypoplasia carriers including his mother as well as male infants who had died from congenital adrenal hypoplasia with no family history of autism, nor other developmental, neurologic, or psychiatric conditions. The patient had been prenatally diagnosed with congenital adrenal hypoplasia and survived with in utero replacement therapy initiated at 40 weeks gestation with 100 mg of dehydroepiandrosterone sulfate infused into the amniotic space. Subsequent assessments revealed normalizing maternal estriol excretion. After birth at 43.5 weeks gestation, mineralocorticoid replacement therapy was administered during infancy. Later evaluations revealed steroid deficiencies as well as chronic failure to thrive. Progressive motor, language, and socialization delays followed as described.Comment Despite receiving replacement treatment, it is conceivable that congenital adrenal hypoplasia-related neurophysiologic abnormalities may have already been staged. Adrenal hormone imbalances have been linked to disturbances of development, language, memory, and mood. 1 Congenital adrenal hypoplasia can impact the function of the mineralocorticoid and glucocorticoid receptor systems for cortisol binding in the limbic system. The mineralocorticoid receptors, located in the lateral septum and hippocampus, affect tonic influences on brain function. 2 They demonstrate a 10-fold higher binding affinity for cortisol over glucocorticoid receptors. 1 Glucocorticoid receptors are more widely distributed in the lateral septum, central amygdala, locus coeruleus, and dentate nucleus having involvement with feedback action on stress-activated brain mechanisms. 2 Other studies demonstrated the selective loss of hippocampal granule cells after adrenalectomy suggesting adrenal hormones are a requirement for limbic structural integrity. 3 Adrenal deficiency causes hippocampal serotonin receptor density to selectively increase along with development of subsensitivity at presynaptic receptors. 4 Such impacts on serotonin receptors are particularly significant as alterations of serotonergic neurotransmission have been implicated in both autistic disorder and mental retardation. 5La Amistad Behavioral Health Services, Maitland, Florida

Dentate gyrus and spatial behaviour

This article reviews evidence from studies employing colchicine-induced granule cell loss in the adult rat brain, and irradiation-induced hypoplasia of the neonatal dentate gyrus, on the performance of spatial and non-spatial behavioral tasks. The general picture emerging from this analysis reveals that the dentate gyrus granule cells are critically involved in spatial behavior, particularly when this requires the adoption of place strategies. This notion also provides an explanation for the behavioral effects of dentate gyrus granule cell loss seen in apparently non-spatial tasks.

Towards a clinico-pathological classification of granule cell dispersion in human mesial temporal lobe epilepsies

The dentate gyrus (DG) plays a pivotal role in the functional and anatomical organization of the hippocampus and is involved in learning and memory formation. However, the impact of structural DG abnormalities, i.e., granule cell dispersion (GCD), for hippocampal seizure susceptibility and its association with distinct lesion patterns in epileptic disorders, such as mesial temporal sclerosis (MTS) remains enigmatic and a large spectrum of pathological changes has been recognized. Here, we propose a clinico-pathological classification of DG pathology based on the examination of 96 surgically resected hippocampal specimens obtained from patients with chronic temporal lobe epilepsy (TLE). We observed three different histological patterns. (1) A normal granule cell layer was identified in 11 patients (no-GCP; 18.7%). (2) Substantial granule cell loss was evident in 36 patients (referred to as granule cell pathology (GCP) Type 1; 37.5%). (3) Architectural abnormalities were observed in 49 specimens, including one or more of the following features: granule cell dispersion, ectopic neurons or clusters of neurons in the molecular layer, or bi-lamination (GCP Type 2; 51%). Cell loss was always encountered in this latter cohort. Seventy-eight patients of our present series suffered from MTS (81.3%). Intriguingly, all MTS patients displayed a compromised DG, 31 (40%) with significant cell loss (Type 1) and 47 (60%) with GCD (Type 2). In 18 patients without MTS (18.7%), seven displayed focally restricted DG abnormalities, either cell loss (n = 5) or GCD (n = 2). Clinical histories revealed a significant association between DG pathology patterns and higher age at epilepsy surgery (p = 0.008), longer epilepsy duration (p = 0.004), but also with learning dysfunction (p < 0.05). There was no correlation with the extent of pyramidal cell loss in adjacent hippocampal segments nor with postsurgical seizure relief. The association with long-term seizure histories and cognitive dysfunction is remarkable and may point to a compromised regenerative capacity of the DG in this cohort of TLE patients.

Close homologue of adhesion molecule L1 promotes survival of Purkinje and granule cells and granule cell migration during murine cerebellar development

Several L1-related adhesion molecules, expressed in a well-coordinated temporospatial pattern during development, are important for fine tuning of specific cerebellar circuitries. We tested the hypothesis that CHL1, the close homologue of L1, abundantly expressed in the developing and adult cerebellum, is also required for normal cerebellar histogenesis. We found that constitutive ablation of CHL1 in mice caused significant loss (20-23%) of Purkinje and granule cells in the mature 2-month-old cerebellum. The ratio of stellate/basket interneurons to Purkinje cells was abnormally high (+38%) in CHL1-deficient (CHL1-/-) mice compared with wild-type (CHL1+/+) littermates, but the gamma-aminobutyric acid (GABA)ergic synaptic inputs to Purkinje cell bodies and dendrites were normal, as were numbers of Golgi interneurons, microglia, astrocytes, and Bergmann glia. Purkinje cell loss occurred before the first postnatal week and was associated with enhanced apoptosis, presumably as a consequence of CHL1 deficiency in afferent axons. In contrast, generation of granule cells, as indicated by in vivo analyses of cell proliferation and death, was unaffected in 1-week-old CHL1-/- mice, but numbers of migrating granule cells in the molecular layer were increased. This increase was likely related to retarded cell migration because CHL1-/- granule cells migrated more slowly than CHL1+/+ cells in vitro, and Bergmann glial processes guiding migration in vivo expressed CHL1 in wild-type mice. Granule cell deficiency in adult CHL1-/- mice appeared to result from decreased precursor cell proliferation after the first postnatal week. Our results indicate that CHL1 promotes Purkinje and granule cell survival and granule cell migration during cerebellar development.

Cerebellar pathology and motor deficits in the palmitoyl protein thioesterase 1-deficient mouse

Infantile neuronal ceroid lipofuscinosis (INCL, Infantile Batten Disease) is an inherited, neurodegenerative lysosomal storage disorder. INCL is the result of a CLN1 gene mutation leading to a deficiency in palmitoyl protein thioesterase 1 (PPT1) activity. Studies in the forebrain demonstrate the PPT1-deficient mouse (PPT1−/−) mimics the clinical symptoms and underlying pathology of INCL; however, little is known about changes in cerebellar function or pathology. In this study, we demonstrate Purkinje cell loss beginning at 3 months, which correlates with changes in rotarod performance. Concurrently, we observed an early stage reactive gliosis and a primary pathology in astrocytes, including changes in S100β and GLAST expression. Conversely, there was a late stage granule cell loss, microglial activation, and demyelination. This study suggests that neuronal–glial interactions are the core pathology in the PPT1−/− cerebellum. In addition, these data identify potential endpoints for use in future efficacy studies for the treatment of INCL.

Mossy cells of the hippocampal dentate gyrus are not selectively vulnerable in human mesial temporal lobe epilepsy

Event Abstract Back to Event Mossy cells of the hippocampal dentate gyrus are not selectively vulnerable in human mesial temporal lobe epilepsy Hajnalka Ábrahám1*, Laszlo Seress1, Zsolt Horvath1, Tamas Doczi1, Jozsef Janszky2, Joyce Klemm3, Richard Byrne3 and Roy A. Bakay3 1 Department of Neurosurgery, University of Pécs, Hungary 2 Department of Neurology , University of Pécs, Hungary 3 Deparment of Neurosurgery, Rush Presbyterian-St. Luke’s Medical Center, United States Hippocampal sclerosis is a common pathology in temporal lobe epilepsy. It is generally believed that there are epilepsy-prone and epilepsy-resistant neurons in the hippocampal formation. Mossy cells of the hippocampal dentate gyrus are considered to be one of the most vulnerable neurons. Since selective histological marker for mossy cells was not available, it was previously difficult to assess whether mossy cells are among the remaining hilar neurons in the epileptic hippocampus. It has recently been described that the cocaine- and amphetamine-regulated transcript peptide (CART) is a reliable marker for human mossy cells. Therefore, we performed histological evaluation of resected epileptic hippocampi using CART immunocytochemistry to identify mossy cells. Cytoarchitecture and neuronal loss was determined with NeuN immunohistochemistry and Nissl staining. In most cases, the number of mossy cells was reduced and the thorny excrescences were smaller in epileptic hippocampi than in controls. Significant loss of pyramidal cells and partial loss of granule cells were accompanied by mossy cell loss. However, in many cases large numbers of mossy cells were still present in the dentate gyrus when most pyramidal neurons of Ammon’s horn were lost suggesting that mossy cells may not be more sensitive for epileptic seizures than the hippocampal pyramidal neurons. Thus, mossy cells are vulnerable to seizures, but a group of them appears to survive even decades of epilepsy. Supported by ETT grant 219/2006 (J. Janszky.) and OTKA grants F 68720 (J. Janszky), PD 73384 (H. Ábrahám) and by Bolyai Scholarship (H. Ábrahám). Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Pathophysiology and neurology - degenerative disorders Citation: Ábrahám H, Seress L, Horvath Z, Doczi T, Janszky J, Klemm J, Byrne R and Bakay RA (2009). Mossy cells of the hippocampal dentate gyrus are not selectively vulnerable in human mesial temporal lobe epilepsy. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.135 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Mar 2009; Published Online: 04 Mar 2009. * Correspondence: Hajnalka Ábrahám, Department of Neurosurgery, University of Pécs, Pecs, Hungary, hajnalka.abraham@aok.pte.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Hajnalka Ábrahám Laszlo Seress Zsolt Horvath Tamas Doczi Jozsef Janszky Joyce Klemm Richard Byrne Roy A Bakay Google Hajnalka Ábrahám Laszlo Seress Zsolt Horvath Tamas Doczi Jozsef Janszky Joyce Klemm Richard Byrne Roy A Bakay Google Scholar Hajnalka Ábrahám Laszlo Seress Zsolt Horvath Tamas Doczi Jozsef Janszky Joyce Klemm Richard Byrne Roy A Bakay PubMed Hajnalka Ábrahám Laszlo Seress Zsolt Horvath Tamas Doczi Jozsef Janszky Joyce Klemm Richard Byrne Roy A Bakay Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Normal memory recovery by activation of 5-HT4 receptors in hippocampal lesioned and normal aged rats

Event Abstract Back to Event Normal memory recovery by activation of 5-HT4 receptors in hippocampal lesioned and normal aged rats Evelyne Marchetti1*, Marlyse Jacquet1, Helene Jeltsh2, Martine Migliorati1, Emmanuel Nivet1, Jean-Christophe Cassel2 and Francois S. Roman1 1 Universite de Provence, Laboratoire de Neurobiologie des Processus Mnesiques, France 2 Universite Louis Pasteur, Laboratoire d-Imagerie et de Neurosciences Cognitives, France Colchicine lesions induced a substantial loss of granule cells and damage to the overlying pyramidal cell layer in region CA1 in adult male Long-Evans rats. All rats with such lesions showed a significant associative learning deficit in an olfactory discrimination task, while being unimpaired in the procedural component of this task. Injection of a partial selective 5-HT4 agonist (SL65.0155 ; 0.01 mg/kg, i.p.,vs.saline) before the third of six training sessions enabled complete recovery of associative learning performance in the lesioned rats. In the same way this specific agonist improved memory performance in the same task in aged rats. Activation of 5-HT4 receptors by a selective agonist such as SL65.0155 might therefore provide an opportunity to reduce learning and memory deficits associated with temporal lobe damage, and could be useful for the symptomatic treatment of memory dysfunctions related to normal an pathological aging such as Alzheimer's disease. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Poster Presentation Topic: Poster presentations Citation: Marchetti E, Jacquet M, Jeltsh H, Migliorati M, Nivet E, Cassel J and Roman FS (2009). Normal memory recovery by activation of 5-HT4 receptors in hippocampal lesioned and normal aged rats. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.223 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Jun 2009; Published Online: 11 Jun 2009. * Correspondence: Evelyne Marchetti, Universite de Provence, Laboratoire de Neurobiologie des Processus Mnesiques, 13331 Marseille, France, evelyne.marchetti-gauthier@univ-provence.fr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Evelyne Marchetti Marlyse Jacquet Helene Jeltsh Martine Migliorati Emmanuel Nivet Jean-Christophe Cassel Francois S Roman Google Evelyne Marchetti Marlyse Jacquet Helene Jeltsh Martine Migliorati Emmanuel Nivet Jean-Christophe Cassel Francois S Roman Google Scholar Evelyne Marchetti Marlyse Jacquet Helene Jeltsh Martine Migliorati Emmanuel Nivet Jean-Christophe Cassel Francois S Roman PubMed Evelyne Marchetti Marlyse Jacquet Helene Jeltsh Martine Migliorati Emmanuel Nivet Jean-Christophe Cassel Francois S Roman Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.