Protein Synthesis Inhibition in the Peri-Infarct Cortex Slows Motor Recovery in Rats
نویسندگان
چکیده
Neuroplasticity and reorganization of brain motor networks are thought to enable recovery of motor function after ischemic stroke. Especially in the cortex surrounding the ischemic scar (i.e., peri-infarct cortex), evidence for lasting reorganization has been found at the level of neurons and networks. This reorganization depends on expression of specific genes and subsequent protein synthesis. To test the functional relevance of the peri-infarct cortex for recovery we assessed the effect of protein synthesis inhibition within this region after experimental stroke. Long-Evans rats were trained to perform a skilled-reaching task (SRT) until they reached plateau performance. A photothrombotic stroke was induced in the forelimb representation of the primary motor cortex (M1) contralateral to the trained paw. The SRT was re-trained after stroke while the protein synthesis inhibitor anisomycin (ANI) or saline were injected into the peri-infarct cortex through implanted cannulas. ANI injections reduced protein synthesis within the peri-infarct cortex by 69% and significantly impaired recovery of reaching performance through re-training. Improvement of motor performance within a single training session remained intact, while improvement between training sessions was impaired. ANI injections did not affect infarct size. Thus, protein synthesis inhibition within the peri-infarct cortex impairs recovery of motor deficits after ischemic stroke by interfering with consolidation of motor memory between training sessions but not short-term improvements within one session.
منابع مشابه
Maladaptive effects of learning with the less-affected forelimb after focal cortical infarcts in rats.
It is common following stroke to focus early rehabilitation efforts on developing compensatory use of the less-affected body side. Here we used a rat model of focal cortical infarct to examine how motor skill acquisition with the less-affected ("intact") forelimb influences sensorimotor function of the infarct-impaired forelimb and neural activity in peri-infarct cortex. Rats proficient in skil...
متن کاملBrain excitability in stroke: the yin and yang of stroke progression.
There is no current medical therapy for stroke recovery. Principles of physiological plasticity have been identified during recovery in both animal models and human stroke. Stroke produces a loss of physiological brain maps in adjacent peri-infarct cortex and then a remapping of motor and sensory functions in this region. This remapping of function in peri-infarct cortex correlates closely with...
متن کاملMotor recovery mechanisms in patients with middle cerebral artery infarct: a mini-review.
Previous studies on the mechanisms of motor recovery in patients with middle cerebral artery (MCA) infarct except for the studies on cortical peri-infarct reorganization after primary motor cortex infarct were reviewed. Eight studies were classified and reviewed by the following four motor recovery mechanisms: contribution of premotor cortex, subcortical peri-infarct reorganization, ipsilateral...
متن کاملReducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke
Stroke is a leading cause of disability, but no pharmacological therapy is currently available for promoting recovery. The brain region adjacent to stroke damage—the peri-infarct zone—is critical for rehabilitation, as it shows heightened neuroplasticity, allowing sensorimotor functions to re-map from damaged areas. Thus, understanding the neuronal properties constraining this plasticity is imp...
متن کاملAssociative Diaschisis and Skilled Rehabilitation-induced Behavioral Recovery following Focal Ischemic Infarct
The time course of peri-infarct diaschisis following a focal ischemic infarct and the effects of delayed rehabilitation on behavioral and functional recovery were examined. Intracortical microstimulation (ICMS) was used to derive topographical maps of forelimb representations within the rat motor cortex and ischemia was induced via bipolar coagulation of surface vasculature. At one hour there w...
متن کامل