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stereology and epilepsy

David A Menassa, Carolyn Sloan, Steven A Chance
BACKGROUND: Autism Spectrum Disorder is characterized by sensory anomalies including impaired olfactory identification. 30% of individuals with autism have a clinical diagnosis of epilepsy. Primary olfactory cortex (piriform cortex) is central to olfactory identification and is an epileptogenic structure. Cytoarchitectural changes in olfactory cortex may underlie olfactory differences seen in autism. METHODS: Primary olfactory cortex was sampled from 17 post-mortem autism cases with and without epilepsy, 11 epilepsy cases without autism and 11 typically developed cases...
July 13, 2016: Brain Pathology
Victoria M Golub, Jonathan Brewer, Xin Wu, Ramkumar Kuruba, Jenessa Short, Maunica Manchi, Megan Swonke, Iyan Younus, Doodipala Samba Reddy
Neuronal injury and neurodegeneration are the hallmark pathologies in a variety of neurological conditions such as epilepsy, stroke, traumatic brain injury, Parkinson's disease and Alzheimer's disease. Quantification of absolute neuron and interneuron counts in various brain regions is essential to understand the impact of neurological insults or neurodegenerative disease progression in animal models. However, conventional qualitative scoring-based protocols are superficial and less reliable for use in studies of neuroprotection evaluations...
2015: Frontiers in Aging Neuroscience
Jerzy Wegiel, Michael Flory, N Carolyn Schanen, Edwin H Cook, Krzysztof Nowicki, Izabela Kuchna, Humi Imaki, Shuang Yong Ma, Jarek Wegiel, Eric London, Manuel F Casanova, Thomas Wisniewski, W Ted Brown
INTRODUCTION: Autism is diagnosed in numerous genetic and genomic developmental disorders associated with an overlap in high-risk genes and loci that underlie intellectual disability (ID) and epilepsy. The aim of this stereological study of neuronal soma volume in 25 brain structures and their subdivisions in eight individuals 9 to 26 years of age who were diagnosed with chromosome 15q11.2-13.1 duplication syndrome [dup(15)], autism, ID and epilepsy; eight age-matched subjects diagnosed with autism of unknown etiology (idiopathic autism) and seven control individuals was to establish whether defects of neuronal soma growth are a common denominator of developmental pathology in idiopathic and syndromic autism and how genetic modifications alter the trajectory of neuronal soma growth in dup(15) autism...
October 13, 2015: Acta Neuropathologica Communications
C Isgor, C Pare, B McDole, P Coombs, K Guthrie
Structural changes that alter hippocampal functional circuitry are implicated in learning impairments, mood disorders and epilepsy. Reorganization of mossy fiber (MF) axons from dentate granule cells is one such form of plasticity. Increased neurotrophin signaling is proposed to underlie MF plasticity, and there is evidence to support a mechanistic role for brain-derived neurotrophic factor (BDNF) in this process. Transgenic mice overexpressing BDNF in the forebrain under the α-calcium/calmodulin-dependent protein kinase II promoter (TgBDNF mice) exhibit spatial learning deficits at 2-3months of age, followed by the emergence of spontaneous seizures at ∼6months...
March 12, 2015: Neuroscience
Ruth Yamawaki, Khushdev Thind, Paul S Buckmaster
Inhibiting the mammalian target of rapamycin (mTOR) signaling pathway with rapamycin blocks granule cell axon (mossy fiber) sprouting after epileptogenic injuries, including pilocarpine-induced status epilepticus. However, it remains unclear whether axons from other types of neurons sprout into the inner molecular layer and synapse with granule cell dendrites despite rapamycin treatment. If so, other aberrant positive-feedback networks might develop. To test this possibility stereological electron microscopy was used to estimate the numbers of excitatory synapses in the inner molecular layer per hippocampus in pilocarpine-treated control mice, in mice 5 days after pilocarpine-induced status epilepticus, and after status epilepticus and daily treatment beginning 24 hours later with rapamycin or vehicle for 2 months...
February 1, 2015: Journal of Comparative Neurology
Lauren L Jantzie, Christopher J Corbett, Jacqueline Berglass, Daniel J Firl, Julian Flores, Rebekah Mannix, Shenandoah Robinson
BACKGROUND: Infants born preterm commonly suffer from a combination of hypoxia-ischemia (HI) and infectious perinatal inflammatory insults that lead to cerebral palsy, cognitive delay, behavioral issues and epilepsy. Using a novel rat model of combined late gestation HI and lipopolysaccharide (LPS)-induced inflammation, we tested our hypothesis that inflammation from HI and LPS differentially affects gliosis, white matter development and motor impairment during the first postnatal month...
2014: Journal of Neuroinflammation
José Eduardo Marques-Carneiro, Jean-Baptiste Faure, Brigitte Cosquer, Estelle Koning, Arielle Ferrandon, Anne Pereira de Vasconcelos, Jean-Christophe Cassel, Astrid Nehlig
OBJECTIVE: The Genetic Absence Epilepsy Rats from Strasbourg (GAERS) is a genetic model, derived from Wistar rats by selective breeding. In all previous studies, GAERS were compared to their paired selected strain not expressing spike-and-wave discharges (SWDs), namely nonepileptic controls (NECs). Because the occurrence/absence of SWDs is of polygenic origin, some other traits could have been selected along with occurrence/absence of SWDs. Therefore, we explored the importance of using a second control group consisting in Wistar rats, the strain of origin of GAERS, in addition to NECs, on locomotion and anxiety in GAERS...
September 2014: Epilepsia
Paul S Buckmaster
Many patients with temporal lobe epilepsy display structural changes in the seizure initiating zone, which includes the hippocampus. Structural changes in the hippocampus include granule cell axon (mossy fiber) sprouting. The role of mossy fiber sprouting in epileptogenesis is controversial. A popular view of temporal lobe epileptogenesis contends that precipitating brain insults trigger transient cascades of molecular and cellular events that permanently enhance excitability of neuronal networks through mechanisms including mossy fiber sprouting...
2014: Advances in Experimental Medicine and Biology
Fernando V Lobo Ladd, Aliny A B Lobo Ladd, Andrea A P da Silva, A Augusto Coppi
The superior cervical ganglion (SCG) plays an important role in neuropathies including Horner's syndrome, stroke, and epilepsy. While mammalian SCGs seem to share certain organizational features, they display natural differences related to the animal size and side and the complexity and synaptic coverage of their dendritic arborizations. However, apart from the rat SCG, there is little information concerning the number of SCG neurons and synapses, and the nature of relationships between body weight and the numbers and sizes of neurons and synapses remain uncertain...
2014: International Review of Cell and Molecular Biology
Joan Y W Liu, Matthew Ellis, Hannah Brooke-Ball, Jane de Tisi, Sofia H Eriksson, Sebastian Brandner, Sanjay M Sisodiya, Maria Thom
INTRODUCTION: In epilepsy, the diagnosis of mild Malformation of Cortical Development type II (mMCD II) predominantly relies on the histopathological assessment of heterotopic neurons in the white matter. The exact diagnostic criteria for mMCD II are still ill-defined, mainly because findings from previous studies were contradictory due to small sample size, and the use of different stains and quantitative systems. Advance in technology leading to the development of whole slide imaging with high-throughput, automated quantitative analysis (WSA) may overcome these differences, and may provide objective, rapid, and reliable quantitation of white matter neurons in epilepsy...
2014: Acta Neuropathologica Communications
Ismini E Papageorgiou, Andriani F Fetani, Andrea Lewen, Uwe Heinemann, Oliver Kann
Activation of microglial cells (brain macrophages) soon after status epilepticus has been suggested to be critical for the pathogenesis of mesial temporal lobe epilepsy (MTLE). However, microglial activation in the chronic phase of experimental MTLE has been scarcely addressed. In this study, we questioned whether microglial activation persists in the hippocampus of pilocarpine-treated, epileptic Wistar rats and to which extent it is associated with segmental neurodegeneration. Microglial cells were immunostained for the universal microglial marker, ionized calcium-binding adapter molecule-1 and the activation marker, CD11b (also known as OX42, Mac-1)...
July 2015: Brain Structure & Function
Ismail Yilmaz, Ilgaz Akdogan, Ertugrul Kaya, Goksin Nilufer Yonguc
AIM: Epileptic seizures lead to neuronal loss in the hippocampus. Experimental epilepsy can be induced by direct application of various chemicals to cerebral cortex. Nifedipine is an L-type voltage-dependent calcium channel blocker. In spite of several studies that show the seizure-suppressing effects of nifedipine, it has been shown that nifedipine does not suppress but conversely increases epileptic seizures. Similarly, contradictory effects of nifedipine have been reported, such as neuroprotection, failed neuroprotection and neurotoxicity...
2014: Turkish Neurosurgery
Paul S Buckmaster, Xiling Wen, Izumi Toyoda, Frances M D Gulland, William Van Bonn
California sea lions (Zalophus californianus) are abundant human-sized carnivores with large gyrencephalic brains. They develop epilepsy after experiencing status epilepticus when naturally exposed to domoic acid. We tested whether sea lions previously exposed to DA (chronic DA sea lions) display hippocampal neuropathology similar to that of human patients with temporal lobe epilepsy. Hippocampi were obtained from control and chronic DA sea lions. Stereology was used to estimate numbers of Nissl-stained neurons per hippocampus in the granule cell layer, hilus, and pyramidal cell layer of CA3, CA2, and CA1 subfields...
May 1, 2014: Journal of Comparative Neurology
N Huusko, A Pitkänen
Traumatic brain injury (TBI) causes 10-20% of acquired epilepsy in humans, resulting in an ictogenic region that is often located in the cerebral cortex. The thalamus provides heavy projections to the cortex and the activity of thalamocortical pathways is controlled by GABAergic afferents from the reticular nucleus of the thalamus (RT). As rats with TBI induced by lateral fluid-percussion injury (FPI) undergo epileptogenesis, we hypothesized that damage to the parvalbumin (PARV)-immunoreactive (ir) neurons in the RT is associated with seizure susceptibility after lateral FPI...
May 16, 2014: Neuroscience
Noora Huusko, Christine Römer, Xavier Ekolle Ndode-Ekane, Katarzyna Lukasiuk, Asla Pitkänen
Reduced hippocampal GABAergic inhibition is acknowledged to be associated with epilepsy. However, there are no studies that had quantitatively compared the loss of various interneuron populations in different models of epilepsy. We tested a hypothesis that the more severe the loss of hippocampal interneurons, the more severe was the epilepsy. Epileptogenesis was triggered in adult rats by status epilepticus (SE) (56 SE, 24 controls) or by traumatic brain injury (TBI) (45 TBI, 23 controls). The total number of hippocampal parvalbumin (PARV), cholecystokinin (CCK), calretinin (CR), somatostatin (SOM), or neuropeptide Y (NPY) positive neurons was estimated using unbiased stereology at 1 or 6 months post-insult...
January 2015: Brain Structure & Function
Adele Finardi, Francesca Colciaghi, Laura Castana, Denise Locatelli, Carlo Efisio Marras, Paola Nobili, Maddalena Fratelli, Manuela Adele Bramerio, Giorgio Lorusso, Giorgio Stefano Battaglia
To investigate hypothesized effects of severe epilepsy on malformed cortex, we analyzed surgical samples from eight patients with type IIB focal cortical dysplasia (FCD) in comparison with samples from nine non-dysplastic controls. We investigated, using stereological quantification methods, where appropriate, dysplastic neurons, neuronal density, balloon cells, glia, glutamatergic synaptic input, and the expression of N-methyl-D-aspartate (NMDA) receptor subunits and associated membrane-associated guanylate kinase (MAGUK)...
August 2013: Acta Neuropathologica
Yuanzhen Ye, Jiajia Xiong, Jun Hu, Min Kong, Li Cheng, Hengsheng Chen, Tingsong Li, Li Jiang
The damage of white matter, primarily myelinated fibers, in the central nervous system (CNS) of temporal lobe epilepsy (TLE) patients has been recently reported. However, limited data exist addressing the types of changes that occur to myelinated fibers inside the hippocampus as a result of TLE. The current study was designed to examine this issue in a lithium-pilocarpine rat model. Investigated by electroencephalography (EEG), Gallyas silver staining, immunohistochemistry, western blotting, transmission electron microscopy, and stereological methods, the results showed that hippocampal myelinated fibers of the epilepsy group were degenerated with significantly less myelin basic protein (MBP) expression relative to those of control group rats...
July 19, 2013: Brain Research
Kay L Richards, Nyoman D Kurniawan, Zhengyi Yang, Tae Hwan Kim, Marianne D Keller, Jun Low, Jeremy F P Ullmann, Stacey Cole, Samuel Foong, Graham J Galloway, Christopher A Reid, George Paxinos, David C Reutens, Steven Petrou
OBJECTIVE: The human γ-aminobutyric acid type A (GABAA)γ2R43Q (R43Q) mutation is associated with genetic epilepsy with febrile seizures. R43Q mice in the C57Bl/6J background do not display spontaneous seizures, but are significantly more susceptible to hyperthermic seizures, providing a model with enhanced seizure susceptibility without the confounding influence of ongoing epileptic activity. Because of GABA's role in brain development, we sought to determine whether the R43Q mutation alters brain structure before the appearance of seizures...
March 26, 2013: Neurology
H Kubová, P Mareš
The present study examined whether status epilepticus (SE) induced by LiCl-pilocarpine in immature rats (postnatal day [P]12) interferes with normal development; leads to progressive epileptogenesis, or cognitive decline and to pathology similar to that seen in human temporal lobe epilepsy. We correlated the extent of pathologic changes with the severity of functional alterations or epilepsy. SE-induced changes were compared with those of rats with SE induced at P25. Animals of both ages were exposed to a battery of behavioral tests for up to 3months after SE...
April 3, 2013: Neuroscience
John F Kerrigan, Angela Parsons, Stephen G Rice, Kristina Simeone, Andrew G Shetter, Adib A Abla, Erin Prenger, Stephen W Coons
BACKGROUND: The neuropathological consequences of Gamma Knife radiosurgery (GK) on hypothalamic hamartoma (HH) are unknown. OBJECTIVE: In a cohort of patients undergoing surgery for treatment-resistant epilepsy, we compared surgically resected HH tissue from patients without (group I; n = 19) and with (group II; n = 10) a history of GK (median dose 16 Gy to the 50% isodose margin). METHODS: Techniques included thick-section stereology for total nucleated and total neuron cell counts, and thin-section immunohistochemistry...
2013: Stereotactic and Functional Neurosurgery
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