NDLI: TGFβ1 Treatment Reduces Hippocampal Damage, Spontaneous Recurrent Seizures, and Learning Memory Deficits in Pilocarpine-Treated Rats

Content Provider	Springer Nature Link
Author	Li, Liang Yong Li, Jia Lin Zhang, Hui Min Yang, Wen Ming Wang, Kai Fang, Yuan Wang, Yu
Copyright Year	2012
Abstract	Studies have demonstrated the neuroprotective activity of transforming growth factor beta-1 (TGFβ1), protecting neurons against different kinds of insults. However, the role of exogenous TGFβ1 in the neuronal damage following status epilepticus (SE) and the related spontaneous recurrent seizures (SRS) is unknown. The present study aimed to determine the effect of intranasal TGFβ1 administration on SRS and cognitive function following lithium–pilocarpine-induced SE and associated hippocampal damage. We found that intranasal TGFβ1 significantly attenuated the hippocampal insults marked by hematoxylin and eosin, terminal deoxynucleotidyl transferase dUTP nick end labeling, and Fluoro-Jade B staining by 24, 48, and 72 h after SE was induced. The expression of the apoptosis-suppressing protein, Bcl-2, was elevated, whereas the expression of the apoptosis-promoting proteins, Bax and Caspase-3, was suppressed in TGFβ1-treated rats compared to rats without TGFβ1 treatment by 24, 48, and 72 h following induction of SE. The seizure number, severity, and duration of SRS over a 1-month period of monitoring starting 15 days after SE induction as well as the cognitive deficits detected 45 days after SE induction were significantly reduced in TGFβ1-treated rats compared to those without TGFβ1 treatment. Our results indicate that intranasal delivery of TGFβ1 immediately after SE induction not only protected against SRS but also improved cognitive function. The anti-epileptogenic properties of TGFβ1 may be related to its effect of neuroprotection or to its effect of apoptosis pathway changes.
Starting Page	109
Ending Page	123
Page Count	15
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	50
Issue Number	1
e-ISSN	15591166
Language	English
Publisher	Humana Press Inc
Publisher Date	2012-08-31
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Apoptosis Cognitive function Neuronal degeneration Spontaneous recurrent seizures Transforming growth factor beta-1 Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Inhibition of miR-203 Reduces Spontaneous Recurrent Seizures in Mice

Carvacrol Attenuates Diabetes-Associated Cognitive Deficits in Rats

Chronic Trigeminal Nerve Stimulation Protects Against Seizures, Cognitive Impairments, Hippocampal Apoptosis, and Inflammatory Responses in Epileptic Rats

Hippocampal FGF-2 and BDNF overexpression attenuates epileptogenesis-associated neuroinflammation and reduces spontaneous recurrent seizures

Oxidative Stress Mediated Hippocampal Neuron Apoptosis Participated in Carbon Disulfide-Induced Rats Cognitive Dysfunction

Resistance Exercise Reduces Seizure Occurrence, Attenuates Memory Deficits and Restores BDNF Signaling in Rats with Chronic Epilepsy

HIF-1α Involves in Neuronal Apoptosis after Traumatic Brain Injury in Adult Rats

Hypothermia Reduces Brain Edema, Spontaneous Recurrent Seizure Attack, and Learning Memory Deficits in the Kainic Acid Treated Rats

Neuroinflammation-Induced Memory Deficits Are Amenable to Treatment with d-Cycloserine

TGFβ1 Treatment Reduces Hippocampal Damage, Spontaneous Recurrent Seizures, and Learning Memory Deficits in Pilocarpine-Treated Rats

Similar Documents

Inhibition of miR-203 Reduces Spontaneous Recurrent Seizures in Mice

Carvacrol Attenuates Diabetes-Associated Cognitive Deficits in Rats

Chronic Trigeminal Nerve Stimulation Protects Against Seizures, Cognitive Impairments, Hippocampal Apoptosis, and Inflammatory Responses in Epileptic Rats

Hippocampal FGF-2 and BDNF overexpression attenuates epileptogenesis-associated neuroinflammation and reduces spontaneous recurrent seizures

Oxidative Stress Mediated Hippocampal Neuron Apoptosis Participated in Carbon Disulfide-Induced Rats Cognitive Dysfunction

Resistance Exercise Reduces Seizure Occurrence, Attenuates Memory Deficits and Restores BDNF Signaling in Rats with Chronic Epilepsy

HIF-1α Involves in Neuronal Apoptosis after Traumatic Brain Injury in Adult Rats

Hypothermia Reduces Brain Edema, Spontaneous Recurrent Seizure Attack, and Learning Memory Deficits in the Kainic Acid Treated Rats

Neuroinflammation-Induced Memory Deficits Are Amenable to Treatment with d-Cycloserine

TGFβ1 Treatment Reduces Hippocampal Damage, Spontaneous Recurrent Seizures, and Learning Memory Deficits in Pilocarpine-Treated Rats