title: The role of neuronal activity in upregulating GFAP mRNA levels after electrolytic lesions of the entorhinal cortex.
abstract: This study evaluates whether the rapid transient increases in glial fibrillary acidic protein (GFAP) mRNA in the hippocampus after electrolytic lesions of the entorhinal cortex (EC) are triggered by lesion-induced changes in hippocampal neuronal activity (either the decreases that result from loss of afferent drive or transient increases that occur during lesion production). To evaluate the role of activity, we carried out four experiments: (1) tetrodotoxin (TTX) was injected into the EC to mimic the decreases in afferent drive that occur after lesion; (2) TTX was injected into the EC or hippocampus before producing electrolytic lesions to block any abnormal activity induced during lesion production; (3) the EC was destroyed by aspiration, thus creating a lesion comparable in size to the electrolytic lesion, without passing direct current; (4) seizures were elicited by stimulating the EC of anesthetized rats, to examine whether electrographic seizures alone can induce the same type of increases in GFAP mRNA as lesions. Our results demonstrated that: (1) TTX injections into the EC did not induce the same increases in GFAP mRNA levels that occurred after EC lesions; (2) animals that received TTX injections into the EC prior to lesions exhibited increases in hippocampal GFAP mRNA that were nearly as great as following EC lesions alone; (3) aspiration lesions of the EC resulted in increases in GFAP mRNA that were comparable to those observed after electrolytic lesions; and (4) seizure-inducing stimulation of the EC resulted in 2-fold increases in GFAP mRNA in the hippocampus 24 hr after stimulation rather than the 5-13-fold increases observed after lesions. These results suggest that lesion-induced changes in hippocampal neuronal activity are not solely responsible for inducing the rapid transient increases in GFAP mRNA levels in the hippocampus ipsilateral to EC lesions.
authors.affiliation: Department of Neuroscience, University of Virginia, Charlottesville 22908.
authors.forename: M S
authors.initials: MS
authors.lastname: Kelley
authors.forename: O
authors.initials: O
authors.lastname: Steward
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology*; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis*; D006624:Hippocampus / Q000166:cytology / Q000502:physiology; D007696:Kindling, Neurologic / Q000502:physiology; D008297:Male; D009410:Nerve Degeneration / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009693:Nucleic Acid Hybridization; D015347:RNA Probes; D012333:RNA, Messenger / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000503:physiopathology; D013779:Tetrodotoxin / Q000494:pharmacology; D015854:Up-Regulation / Q000502:physiology*
chemical_list: D005904:Glial Fibrillary Acidic Protein; D015347:RNA Probes; D012333:RNA, Messenger; D013779:Tetrodotoxin