Background: The aim of this study was to evaluate antidepressant-like effect (Porsolt test), locomotor activity and motor coordination of joint administration of tramadol (TRM) and venlafaxine (VEN) in rats.
Methods: The tests were performed on male Wistar rats after single and chronic treatment (7 and 14 days) with TRM intraperitoneally (ip) and VEN orally (po) administered once a day. The controls were given 0.
Recent research has suggested that cognitive disorders are a persistent trait of mental illnesses such as schizophrenia. Cognitive deficits in the course of schizophrenia may be due to the disease and/or drug therapy, especially with old-generation drugs. Several clinical experiments have indicated the beneficial effects of new-generation antipsychotics on cognitive processes in patients treated for mental disorders.
View Article and Find Full Text PDFAs shown in clinical studies, combinations of first generation normothymics (carbamazepine - CBZ) with atypical neuroleptics (olanzapine - OLA) lead to improvements in approximately half of patients treated for relapses of bipolar affective disease. Our previous studies have shown OLA to have an antidepressant effect when administered at a dose of 0.5 mg/kg only upon single administration; the effect did not last throughout chronic administration, whereas CBZ administered at a dose of 30 mg/kg showed an antidepressant effect only after 7 days of administration.
View Article and Find Full Text PDFCognitive disorders in the course of mental illnesses are one of the most important and most difficult therapeutic problems related to those illnesses and they regard attention, memory, learning and sensory modulation. The limited number of nicotinic receptors (subtypes alpha7 and alpha4beta2) seems to cause the incidence and exacerbation of cognitive deficits in such patients. In patients with schizophrenia, the impairment of cognitive processes is also a side-effect of neuroleptics.
View Article and Find Full Text PDFArzneimittelforschung
October 2010
Deficits of cognitive functions are perceived as an important pathogenic factor of many neurological and psychiatric diseases. Such symptoms can be a result of a disease process or appear due to applied medication. Epilepsy is a disease in which cognitive deficits can occur before first seizures, during seizures and remissions.
View Article and Find Full Text PDFEpileptic patients are at risk of experiencing cognitive deficits as a result of pharmacotherapy as well as etiology of epilepsy. Antiepileptic drugs increase inhibitory neurotransmission and reduce the responsiveness of neurons, and thereby may have a negative impact on memory. The enriched environment intensifies exploration of the new area behavior, which may have a positive impact on spatial memory in rats.
View Article and Find Full Text PDFMany patients undergoing long-term treatment of epilepsy complain of memory disorders, which entail worse quality of life. The risk factors generating memory disorders include: morphological brain damage, the duration and course of epileptic seizures (conscience disorders), the time of diagnosis (the risk is greater if epileptic seizures start early in life), drug resistance, the presence of interseizure changes in the EEG in the form of sharp-wave discharges or sharp spike-wave/ slow spike-wave complexes and improper pharmacotherapy (exceeding the admissible concentration of drugs in blood serum, polytherapy). GABAergic neurotransmission of older antiepileptic drugs (barbiturates, benzodiazepines) makes them particularly prone to produce modest, but statistically significant disruption of cognitive processes.
View Article and Find Full Text PDFBrain-derived neurotrophic factor (BDNF) is a key neurotrophic factor in the brain. It plays an important role in the etiopathogenesis and pharmacotherapy of mental disorders, such as depression or schizophrenia. In recent years, studies have shown that cognitive processes, which are impaired in the course of mental disorders, significantly change BDNF levels in the brain.
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