Exercise protects synaptic density in a rat model of Parkinson's disease

Parkinson's disease (PD) is characterized by Lewy body and neurite pathology associated with dopamine terminal dysfunction. Clinically, it motor slowing, rigidity, tremor. Postural instability pain are also features. Physical exercise benefits PD patients - possibly promoting neuroplasticity including synaptic regeneration. In a parkinsonian rat model, we test the hypotheses that exercise: (a) increases density reduces neuroinflammation (b) lowers nociceptive threshold increasing ?-opioid receptor expression. Brain autoradiography was performed on rats unilaterally injected either 6-hydroxydopamine (6-OHDA) or saline subjected to treadmill over 5 weeks. [3H]UCB-J used measure vesicle glycoprotein 2A (SV2A) density. Dopamine D2/3 availability were assessed [3H]Raclopride [3H]DAMGO, respectively, while detected 18kDA translocator protein (TSPO) marker [3H]PK11195. The determined prior throughout protocol. We confirmed dopaminegic deficit increased striatal reduced nigral tyrosine hydroxylase immunoreactivity in ipsilateral hemisphere of all 6-OHDA-injected rats. Sedentary lesioned 6-OHDA showed significant reduction substantia nigra binding [3H]PK11195 neuroinflammation. Lesioned who exercised had higher levels lower compared sedentary Striatal injections thalamic but subsequent restored binding. Exercise raised hippocampal SV2A rats, accompanied rise threshold. These data suggest protects integrity lesion model compensatory mechanisms. post lesioning altered opioid transmission resulting an