Psychoneurochemical Investigations to Reveal Neurobiology of Memory Deficit in Epilepsy
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ORIGINAL PAPER
Psychoneurochemical Investigations to Reveal Neurobiology of Memory Deficit in Epilepsy Awanish Mishra • Rajesh Kumar Goel
Received: 25 July 2013 / Revised: 19 September 2013 / Accepted: 26 September 2013 / Published online: 8 October 2013 Ó Springer Science+Business Media New York 2013
Abstract Pentylenetetrazole-kindling induced memory deficit has been validated in our previous study. The present study attempts a neurochemical investigation to reveal possible targets for treatment of memory deficit associated with pentylenetetrazole-kindling. Kindling was induced by administering subconvulsive dose of pentylenetetrazole (35 mg/kg; i.p.) at an interval of 48 ± 2 h. Successfully kindled animals were divided into two groups (interictal and postictal group), while non-kindled (naive) animals served as naı¨ve group. In postictal group, animals were challenged with pentylenetetrazole (35 mg/kg) on days 5, 10, 15 and 20. Learning and memory were evaluated in all experimental groups using elevated plus maze and passive shock avoidance paradigm on days 5, 10, 15 and 20. After behavioral evaluations on day 20, all animals were sacrificed to remove their brains. Neurochemical (glutamate, GABA, norepinephrine, dopamine and serotonin) changes and acetylcholinesterase activity and total nitrite level were estimated using HPLC-FD methods and microplate reader method respectively, in discrete brain parts. The results of the neurochemical estimation demonstrated the imbalance in excitatory/inhibitory tone, reduction in monoamine level, elevated nitrosative and acetylcholinesterase activity in the cortex and hippocampus, as responsible factors for the pathobiology of learning and memory deficit in epilepsy. Restoration of these changes may be targeted for the management of memory deficit in epileptic patients.
A. Mishra R. K. Goel (&) Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala 147002, Punjab, India e-mail: [email protected]
Keywords Pentylenetetrazole-kindling Epileptic comorbidity Learning and memory deficit Neurotransmitters Post and interictal status
Introduction Epilepsy is a heterogeneous biomedical disorder, with enormous variations in etiology and clinical features, resulting in irregular episodic bursts of electrical activity in certain neurons, which may spread to the entire brain. It is one of the most common serious neurological disorders in the world [1]. Chronic epileptic patients are more often associated with one or more neurobehavioral comorbidities. Out of which, learning and memory deficit emerges as one of most debilitating neurobehavioral comorbidity of chronic epilepsy [2, 3] affecting around 30 % of patients with epilepsy [4] and greatly contribute to the major adverse effect on overall health and quality of life and substantially increase health care costs [5]. Cognitive functions in epileptic patients are as diverse as the epileptic condition itself by virtue of their origin, topography of epileptogenic foci, pathological mechanisms an
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