Browsing by Subject "neuroplastisuus"

The syndrome of cerebral palsy (CP) includes motor impairments that results from a brain lesion occurring pre-, intra- or postnatally. Setting diagnosis of CP is usually happened during first years of life, and the more accurate is the diagnosis the more probably are the chances of individual’s rehabilitation. There are many ways of classifying a subtype of CP. Anyways concerning with rehabilitation the main focus may be among neuroplastic factors. The better the usable interventions are based on the supporting of neuroplasticity, the more efficient are the methods which are used within rehabilitation of CP, probably. This review concerns of neural plasticity and the special features of it during pathology of CP. The invasive and non-invasive interventions supporting neural plasticity among CP are the core features in this review. There has been used main index words during literature search, like ”cerebral palsy”, ”neurorehabilitation”, ”neuroplasticity”, ”pharmacology” and ”neonatal”. The main outcomes of literature search pointed that extreme intensive, a great number of repetitions was the key factor for the efficient interventions with parameters of neuroplasticity and general functioning and these findings were ensured with computerized scanning methods among central nervous system. Especially constraint-induced movement interventions pointed to be important factor with the role of neural plasticity. In the other words, the stronger limb was restricted and the functions must be performed with more weaker limb. There were also obtained some promising early phase interventions: pharmacological therapies, progenitor cells, hypothermia and the role of predisposing genetic variants (preventive method). Selective serotonin reuptake inhibitors could be useful with supporting of neural plasticity, and the progenitor cells could probably fix some already progressed, harmful neural connections. Hypothermia has probably the key role of restricting the lesion size and with some other factors during an acute phase (like apoptosis and encephalopathy). Some selective genetic variants could help of preparing prenatally for the chance of pathology of CP. There is some evidence that magnesium sulphate has some neuroprotective effects, but the newest results are challenging this hypothesis. There are no identical clinical outcomes of effects of maternal magnesium sulphate medication, thus much more research must be conducted in the future. The interventions within the syndrome of CP probably will develop with more selective ways in the future. The evolution of technics will also be making possible some whole new research methods. Despite the great evolution of the health care system during 20th and 21st century, the prevalence has not been declined. This points out that our methods we are using nowadays cannot inhibit the pathology of CP, but there will be much potential developing among neurosupportive interventions. Anyways, the latest methods will need much more research so that we can somehow exactly operationalize the harm-benefit ratios of interventions among human beings.

Currently, there is an undeniable need for more effective treatments of depression. The efficacy of traditional antidepressant drugs becomes apparent after multiple weeks of treatment. New advancements in depression treatments have been made, as glutamatergic NMDA-receptor antagonist ketamine is seen to ameliorate symptoms rapidly, even only hours after drug administration. Understanding ketamine’s mechanism of action as an antidepressant could enable the development of more effective antidepressant drugs. The critical molecular level component in ketamine’s antidepressant effect is considered to be the activation of TrkB tyrosine receptor kinase B, which subsequently leads to the initiation of signaling pathways, which regulate synaptic plasticity. So far, it has not been examined; whether there is a difference in ketamine’s antidepressant effect based on the dosing-time of day. The aim of the present study was to find out if there is a variation between ketamine’s effect on synaptic plasticity and the circadian phase in which the drug is administered. Ketamine’s (200 or 50 mg/kg, i.p.) effects were studied in C57BL/6J–mice during light phase (mouse’s inactive phase) and dark phase (mouse’s active phase) of the day. The phase of the day didn’t affect the activity of TrkB signaling in its related parts (pTrkBTyr816, pGSK3βSer9, p-p70S6KTyr421/Ser424 and p-p44/42MAPKThr202/Tyr204) in prefrontal cortex samples which were analysed in Western blot assay. Ketamine increased dose-dependently the phosphorylation of GSK3βSer9 and p70S6KTyr421/Ser424 as well as decreased p-p44/42MAPKThr202/Tyr204 at 30 minutes after drug administration in both phases of the day. Ketamine (200 mg/kg, i.p.) also lowered the glucose concentration measured from the trunk blood. To examine the effect of hypoglycemia on the activity of TrkB signaling another experiment was conducted. The hypoglycemia induced by insulin detemir (6 IU/kg, i.p.) didn’t affect any measured protein phosphorylation at 60 minutes after drug administration. The results of this study support the notion of ketamine’s rapid and dosedependent induction of neuroplasticity. The possible role of hypoglycemia in ketamine's neuropharmacology should be investigated in future studies.