Seizures and sensory stimulation result in different patterns of brain derived neurotrophic factor protein expression in the barrel cortex and hippocampus.
Brain-derived neurotrophic factor (BDNF) is important for the development and trophic support of neurons, and may be involved in controlling axonal sprouting and synaptic plasticity. In order to investigate the activity-dependent regulation of the BDNF gene, BDNF expression was examined within the rat somatosensory cortex (SSC) and hippocampus following vibrissae stimulation, kainic acid induced seizure, and pentylenetetrazol (PTZ) induced seizure. The specific goals of this study were to determine the time course and magnitude of BDNF's activity-dependent expression, and to compare the expression patterns of three commonly used neuronal activation paradigms. Our results demonstrate three novel observations. First, the patterns of BDNF protein expression are dependent upon the neuronal stimulation model used. Both unilateral whisker stimulation (a model of experience dependent plasticity) and kainic acid induced seizure were able to increase the levels of BDNF protein within the SSC and hippocampus. In contrast, PTZ induced seizure did not increase BDNF protein levels in either tissue. Second, there is a dissociation between BDNF mRNA and protein levels following PTZ induced seizure. PTZ seizures resulted in strong increases of BDNF mRNA levels without corresponding increases of the protein. Finally, whisker stimulation resulted in an unexpected increase in BDNF mRNA and protein levels within the hippocampus. These results suggest specific types of neuronal activity can regulate gene expression differently. Furthermore, temporal and spatial differences between the expression of BDNF protein and mRNA levels suggest that the BDNF gene is regulated at the level of translation as well as transcription.
Nanda
S A
SA
Neuroscience Training Program and Waisman Center, University of Wisconsin, Room 707 Waisman Center, 1500 Highland Ave., Madison, WI 53705, USA.
Mack
K J
KJ
D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D003292:Convulsants; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology*; D018690:Excitatory Amino Acid Agonists; D015870:Gene Expression / Q000502:physiology; D006624:Hippocampus / Q000737:chemistry / Q000378:metabolism / Q000503:physiopathology*; D007608:Kainic Acid; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology; D010433:Pentylenetetrazole; D010812:Physical Stimulation; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000139:chemically induced / Q000503:physiopathology; D013003:Somatosensory Cortex / Q000737:chemistry / Q000378:metabolism / Q000503:physiopathology*; D014110:Touch / Q000502:physiology*; D014738:Vibrissae / Q000294:innervation / Q000502:physiology
D019208:Brain-Derived Neurotrophic Factor; D003292:Convulsants; D018690:Excitatory Amino Acid Agonists; D012333:RNA, Messenger; D007608:Kainic Acid; D010433:Pentylenetetrazole