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Immunolesions of medial septal GABAergic neurons

Jaime S, Perez Cordova MG, Hernandez S, Colom L (2009) Immunolesions of medial septal GABAergic neurons. Neuroscience 2009 Abstracts 241.8/I15. Society for Neuroscience, Chicago, IL.

Summary: Epilepsy is a neurodegenerative condition characterized by spontaneous recurrent seizures that are triggered by excessive electrical activity due to changes in neurological functions. One of the most common forms of epilepsy is Temporal Lobe Epilepsy (TLE) in which seizures originate in limbic structures as hippocampal and/or para-hippocampal areas. Principal cell (i.e. pyramidal cells) activity is indirectly regulated by rhythmic inputs from GABAergic neurons in the septal region of the basal forebrain which selectively innervate inhibitory hippocampal interneurons. In previous studies, using the pilocarpine model of TLE, we have demonstrated that the septum plays an antiepileptic role and that medial septum GABAergic neurons degenerate in the epilepsy process. Thus, damage of medial septum GABAergic neurons may contribute to epileptogenesis. The purpose of this study is to investigate the role of medial septum GABAergic neurons in excitability control and epileptic activity generation. For this purpose, anti-GAT1-SAP (3µL at 325ng/µL) was stereotaxically injected in the medial septum of Sprague Dawley male rats to selectively destroy this neuronal population and investigate the subsequent functional changes. Analysis was performed using stereological approaches which revealed a significant reduction in cell count between treated (anti-GAT1-SAP) and saline-injected control rats (8591.38±941.65 and 25609.87±407.73 respectively; (Student’s t-test; p<0.05). In conclusion, our preliminary results show that the single injections of anti-GAT1-SAP selectively lesions most of the medial septum GABAergic neurons, providing a powerful tool to study the role of these neurons in the control of hyperexcitability states. Studies underway involve the investigation of the functional alterations produced by the selective destruction of MS GABAergic neurons.

Related Products: GAT1-SAP (Cat. #IT-32)

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