Changes in markers of neuronal and glial plasticity after cortical injury induced by food restriction

• Published in: Experimental neurology 2009-11, Vol.220 (1), p.198-206
• Main Authors: Lončarević-Vasiljković, Nataša, Pešić, Vesna, Tanić, Nikola, Milanović, Desanka, Popić, Jelena, Kanazir, Selma, Ruždijić, Sabera
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Biomarkers - analysis; Biomarkers - metabolism; Blood Glucose - physiology; Brain Injuries - diet therapy; Brain Injuries - metabolism; Brain Injuries - physiopathology; Cerebral Cortex - injuries; Cerebral Cortex - metabolism; Cerebral Cortex - physiopathology; Cortical injury; Corticosterone; Corticosterone - blood; Food Deprivation - physiology; Food restriction; GAP-43; GAP-43 Protein - genetics; GAP-43 Protein - metabolism; GFAP; Glial Fibrillary Acidic Protein - genetics; Glial Fibrillary Acidic Protein - metabolism; Gliosis - diet therapy; Gliosis - metabolism; Gliosis - physiopathology; Glucose; Growth Cones - metabolism; Growth Cones - ultrastructure; Immunohistochemistry; Injuries of the nervous system and the skull. Diseases due to physical agents; Male; Medical sciences; Nerve Regeneration - physiology; Neuroglia - metabolism; Neurology; Neuronal Plasticity - physiology; Neurons - metabolism; Plasticity; Rats; Rats, Wistar; Recovery; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - analysis; RNA, Messenger - metabolism; Synaptophysin; Synaptophysin - genetics; Synaptophysin - metabolism; Traumas. Diseases due to physical agents
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/j.expneurol.2009.08.024

The regenerative capacity of the adult central nervous system is limited. We investigated whether short-term food restriction (FR; 50% of the daily food intake lasting 3 months) modulates processes of brain plasticity after cortical injury. Quantitative changes of growth-associated protein 43 (GAP-43) and synaptophysin (SYP) mRNA levels in the ipsilateral cortex of the adult rat during the recovery period (from 2 to 28 days) after injury were investigated by real-time RT-PCR. Using Western blot and immunohistochemical analyses we examined the levels and localization of proteins involved in neuronal plasticity, SYP and GAP-43, as well as glial fibrillary acidic protein (GFAP), a marker of glial plasticity. A marked rise in GAP-43 and SYP immunoreactivity observed in the FR group on the 7th day after injury pointed to increases in axonal branching and synapses in the cortex surrounding the lesion. The appearance of reactive astrocytes was accompanied by the absence of immunoreactivity for GAP-43 and SYP in ad libitum fed animals. This finding supports the hypothesis that morphological hypertrophy of astrocytes associated with GFAP synthesis is responsible either directly or indirectly for the inhibitory role of activated glia on axonal regeneration. Examination of the effects of FR on serum corticosterone and glucose concentrations and GAP-43, SYP and GFAP expression revealed that FR facilitated recovery of the injured region by attenuating reactive astrogliosis and enhancing the expression of neuronal plasticity markers.