title: Focal photothrombotic lesion of the rat motor cortex increases BDNF levels in motor-sensory cortical areas not accompanied by recovery of forelimb motor skills.
abstract: Brain infarct triggers neurodegeneration that often shades spontaneous plasticity, occurring in the areas related anatomically and functionally to the infarcted structures. Neurotrophins which promote neuronal survival and plasticity, may protect neurons and enhance remodeling of the remaining circuits, leading to restoration of function. In particular, the crucial role of brain-derived neurotrophic factor (BDNF) in cortical function is well documented. Since BDNF was implicated in the mechanism of postinfarct recovery, we investigated whether focal photothrombosis in the motor cortex of adult rats modifies cortical BDNF protein levels in a time- and region-dependent fashion. In parallel, we aimed to establish, which cortical cells respond with altered BDNF expression and whether these alterations are reflected by forelimb motor skill impairment and recovery, evaluated up to 1 month postinfarct. The distribution of BDNF protein was visualized immunohistochemically and BDNF tissue levels were evaluated with enzyme-linked immunosorbent assay (ELISA). Ipsilateral to the infarct, an increase in BDNF levels occurred both in injured and neighboring regions already 24 h after photothrombosis. This increase was sustained up to postlesion day 7 in the motor cortex and reduced at 28 days. No BDNF changes were detected in homotopic regions of the contralateral cortex. The time-course of enhanced neurotrophic expression was paralleled by bilateral deficits in skilled reaching, which was the only clear and measurable motor impairment observed in the study. We conclude that the spontaneous increase of BDNF is not sufficient to protect neurons from degeneration in the lesion proximity whereas plasticity reported in the adjacent regions may be attributable to enhanced BDNF-related stimuli, which do not counteract the impairment of skilled reaching but might be, at least in part, responsible for the absence of deficits in other functional/behavioral tests.
authors: Nencki Institute of Experimental Biology [corrected] Polish Academy of Sciences, Warsaw, Poland.
authors: Dorota
authors: D
authors: Sulejczak
authors: Ewelina
authors: E
authors: Ziemlińska
authors: Julita
authors: J
authors: Czarkowska-Bauch
authors: Ewa
authors: E
authors: Nosecka
authors: Ryszard
authors: R
authors: Strzalkowski
authors: Malgorzata
authors: M
authors: Skup
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005552:Forelimb; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009044:Motor Cortex / Q000378:metabolism*; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology*; D013997:Time Factors
chemical_list: D019208:Brain-Derived Neurotrophic Factor