scholarly journals Effects of Swimming Exercise on Limbic and Motor Cortex Neurogenesis in the Kainate-Lesion Model of Temporal Lobe Epilepsy

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Vasavi R. Gorantla ◽  
Amulya Sirigiri ◽  
Yulia A. Volkova ◽  
Richard M. Millis

Temporal lobe epilepsy (TLE) is a common neurological disease and antiseizure medication is often inadequate for preventing apoptotic cell death. Aerobic swimming exercise (EX) augments neurogenesis in rats when initiated immediately in the postictal period. This study tests the hypothesis that aerobic exercise also augments neurogenesis over the long term. Male Wistar rats (age of 4 months) were subjected to chemical lesioning using KA and to an EX intervention consisting of a 30 d period of daily swimming for 15 min, in one experiment immediately after KA lesioning (immediate exposure) and in a second experiment after a 60 d period of normal activity (delayed exposure). Morphometric counting of neuron numbers (NN) and dendritic branch points and intersections (DDBPI) was performed in the CA1, CA3, and dentate regions of hippocampus, in basolateral nucleus of amygdala, and in several areas of motor cortex. EX increased NN and DDBPI in the normal control and the KA-lesioned rats in all four limbic and motor cortex areas studied, after both immediate and 60 d delayed exposures to exercise. These findings suggest that, after temporal lobe epileptic seizures in rats, swimming exercise may improve neural plasticity in areas of the brain involved with emotional regulation and motor coordination, even if the exercise treatment is delayed.

2001 ◽  
Vol 16 (5) ◽  
pp. 649 ◽  
Author(s):  
Min Cheol Lee ◽  
Jin Lee Rho ◽  
Myung Kyu Kim ◽  
Young Jong Woo ◽  
Jae Hyoo Kim ◽  
...  

2019 ◽  
Vol 20 (22) ◽  
pp. 5688
Author(s):  
Ítalo Rosal Lustosa ◽  
Joana I. Soares ◽  
Giuseppe Biagini ◽  
Nikolai V. Lukoyanov

The amygdala is a cerebral region whose function is compromised in temporal lobe epilepsy (TLE). Patients with TLE present cognitive and emotional dysfunctions, of which impairments in recognizing facial expressions have been clearly attributed to amygdala damage. However, damage to the amygdala has been scarcely addressed, with the majority of studies focusing on the hippocampus. The aim of this study was to evaluate epilepsy-related plasticity of cholinergic projections to the basolateral nucleus (BL) of the amygdala. Adult rats received kainic acid (KA) injections and developed status epilepticus. Weeks later, they showed spontaneous recurrent seizures documented by behavioral observations. Changes in cholinergic innervation of the BL were investigated by using an antibody against the vesicular acetylcholine transporter (VAChT). In KA-treated rats, it was found that (i) the BL shrunk to 25% of its original size (p < 0.01 vs. controls, Student’s t-test), (ii) the density of vesicular acetylcholine transporter-immunoreactive (VAChT-IR) varicosities was unchanged, (iii) the volumes of VAChT-IR cell bodies projecting to the BL from the horizontal limb of the diagonal band of Broca, ventral pallidum, and subcommissural part of the substantia innominata were significantly increased (p < 0.05, Bonferroni correction). These results illustrate significant changes in the basal forebrain cholinergic cells projecting to the BL in the presence of spontaneous recurrent seizures.


Neurocase ◽  
2004 ◽  
Vol 10 (4) ◽  
pp. 326-329 ◽  
Author(s):  
Pavel Chlebus ◽  
Milan Brázdil ◽  
Petr Hluštík ◽  
Michal Mikl ◽  
Marta Pažourková ◽  
...  

Toxins ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 486 ◽  
Author(s):  
José Liberato ◽  
Lívea Godoy ◽  
Alexandra Cunha ◽  
Marcia Mortari ◽  
Rene de Oliveira Beleboni ◽  
...  

Epilepsy is considered as one of the major disabling neuropathologies. Almost one third of adult patients with temporal lobe epilepsy (TLE) do not respond to current antiepileptic drugs (AEDs). Additionally, most AEDs do not have neuroprotective effects against the inherent neurodegenerative process underlying the hippocampal sclerosis on TLE. Dysfunctions in the GABAergic neurotransmission may contribute not only to the onset of epileptic activity but also constitute an important system for therapeutic approaches. Therefore, molecules that enhance GABA inhibitory effects could open novel avenues for the understanding of epileptic plasticity and for drug development. Parawixin2, a compound isolated from Parawixia bistriata spider venom, inhibits both GABA and glycine uptake and has an anticonvulsant effect against a wide range of chemoconvulsants. The neuroprotective potential of Parawixin2 was analyzed in a model of TLE induced by a long-lasting Status Epilepticus (SE), and its efficiency was compared to well-known neuroprotective drugs, such as riluzole and nipecotic acid. Neuroprotection was assessed through histological markers for cell density (Nissl), astrocytic reactivity (GFAP) and cell death labeling (TUNEL), which were performed 24 h and 72 h after SE. Parawixin2 treatment resulted in neuroprotective effects in a dose dependent manner at 24 h and 72 h after SE, as well as reduced reactive astrocytes and apoptotic cell death. Based on these findings, Parawixin2 has a great potential to be used as a tool for neuroscience research and as a probe to the development of novel GABAergic neuroprotective agents.


2019 ◽  
Vol 33 (7) ◽  
pp. 986-995 ◽  
Author(s):  
Elizabeth Stewart ◽  
Cathy Catroppa ◽  
Linda Gonzalez ◽  
Deepak Gill ◽  
Richard Webster ◽  
...  

2012 ◽  
Vol 43 (01) ◽  
Author(s):  
VE Bernedo Paredes ◽  
H Schwartz ◽  
M Gartenschläger ◽  
M Gartenschläger ◽  
HG Buchholz ◽  
...  

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