Pharmacological modulation of cortical plasticity following kainic acid lesion in rat barrel cortex.
OBJECTIVE
The brain shows remarkable capacity for plasticity in response to injury. To maximize the benefits of current neurological treatment and to minimize the impact of injury, the authors examined the ability of commonly administered drugs, dextroamphetamine (D-amphetamine) and phenytoin, to positively or negatively affect the functional recovery of the cerebral cortex following excitotoxic injury.


METHODS
Previous work from the same laboratory has demonstrated reorganization of whisker functional responses (WFRs) in the rat barrel cortex after excitotoxic lesions were created with kainic acid (KA). In the present study, WFRs were mapped using intrinsic optical signal imaging before and 9 days after creation of the KA lesions. During the post-lesion survival period, animals were either treated with intraperitoneal D-amphetamine, phenytoin, or saline or received no treatment. Following the survival period, WFRs were again measured and compared with prelesion data.


RESULTS
The findings suggest that KA lesions cause increases in WFR areas when compared with controls. Treatment with D-amphetamine further increased the WFR area (p < 0.05) while phenytoin-treated rats showed decreases in WFR areas. There was also a statistically significant difference (p < 0.05) between the D-amphetamine and phenytoin groups.


CONCLUSIONS
These results show that 2 commonly used drugs, D-amphetamine and phenytoin, have opposite effects in the functional recovery/plasticity of injured cerebral cortex. The authors' findings emphasize the complex nature of the cortical response to injury and have implications for understanding the biology of the effects of different medications on eventual functional brain recovery.
Darbar
Aneela
A
Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, New York 13210, USA. darbara@upstate.edu
Stevens
Richard T
RT
Siddiqui
Adnan H
AH
McCasland
James S
JS
Hodge
Charles J
CJ
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology* / Q000627:therapeutic use; D001930:Brain Injuries / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D000697:Central Nervous System Stimulants / Q000494:pharmacology* / Q000627:therapeutic use; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology; D003913:Dextroamphetamine / Q000494:pharmacology* / Q000627:therapeutic use; D007608:Kainic Acid; D009473:Neuronal Plasticity / Q000187:drug effects*; D010672:Phenytoin / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D014738:Vibrissae / Q000187:drug effects / Q000502:physiology
D000927:Anticonvulsants; D000697:Central Nervous System Stimulants; D010672:Phenytoin; D007608:Kainic Acid; D003913:Dextroamphetamine