Privação de sono REM em um modelo experimental da doença de Parkinson

Abstract

Parkinson's disease (PD) is a common neurological condition all over the world. Most of the cases are considered to be the result of a degenerative process affecting mainly nigrostriatal dopamine neurons, leading to a marked dopamine deficiency in the striatum. Other neurotransmitter abnormalities occur in several different regions of the brain, but, by far, the dopamine depletion is the more striking feature of the disease. Twenty years after the introduction of L-Dopa as a treatment for PD and after other new pharmacological strategies, mainly using direct dopamine agonists (bromocriptine, lisuride, pergolide) this condition still offers a great treatment challenge. showed that REM sleep deprived (REM SD) rats displayed aggressive behavior after receiving amphetamine. Non-deprived control animals which received a similar dose of the drug did not display aggressiveness. Carlini & Lindsey 3 had observed that REM SD rats receiving apomorphine (a potent direct dopamine receptor agonist) also showed the same aggressive behavior, whereas non-deprived animals did not. This effect could not be blocked by pretreatment with alpha-MPT, a tyrosine-hydro ¬ xilase inhibitor 15or by administration of L-Dopa, and was enhanced by using bromocriptine and piribedil (direct receptor agonists)i5. These findings suggest that REM SD may be acting by producing supersensitivity of the post-synaptic dopamine receptors, both in the striatum and cortical-limbic areas. Pflug & Tolled made the first attempt at using total SD in depressed patients, reporting improvement.Since then many others have been using the same procedure 2,4,9,16 . Endogenous depression has been considered as the consequence of monoamine decreased function in CNS. Although noradrenaline and serotonin may be the major neurotransmitters involved, dopamine undoubtly plays a role in the pathophysiology, since improvement of this condition is

Chronic sleep restriction in the rotenone Parkinson’s disease model in rats reveals peripheral early-phase biomarkers

“…Similarly, 24 h of total sleep deprivation produced the same outcome, without changes in plasma corticosterone, suggesting that the increase in locomotor activity was not a consequence of the hypothalamic-pituitary-adrenal stress response 51 . REM sleep deprivation is also able to augment locomotion 39 and counterbalance PD model-induced hypokinesia 52 , a compensatory effect considered to be due to supersensitivity of brain dopamine receptors 53 , specifically, through D2 receptor up-regulation 54 . Therefore, total SR can lead to a substantial loss of REM sleep, enough to compensate for the motor impairment produced by ROT lesion.…”