fluvoxamine and Memory-Disorders

Rapid eye movement (REM) sleep has been considered important for consolidation of memories, particularly of skills. Contrary to expectations, we found that REM sleep suppression by administration of selective serotonin or norepinephrine re-uptake inhibitors after training did not impair consolidation of skills or word-pairs in healthy men but rather enhanced gains in finger tapping accuracy together with sleep spindles. Our results indicate that REM sleep as a unitary phenomenon is not required for skill-memory consolidation.

Topics: Adolescent; Adrenergic Uptake Inhibitors; Adult; Affect; Association Learning; Catecholamines; Cross-Over Studies; Double-Blind Method; Electroencephalography; Fluvoxamine; Humans; Hydrocortisone; Male; Memory Disorders; Morpholines; Motor Skills; Neuropsychological Tests; Photic Stimulation; Reaction Time; Reboxetine; Selective Serotonin Reuptake Inhibitors; Sleep, REM; Surveys and Questionnaires; Young Adult

Parkinson's disease (PD) is also associated with cognitive impairment and reduced extrinsic supply of dopamine (DA) to the prefrontal cortex (PFC). In the present study, we looked at whether exposure to early life stress reduces DA and serotonin (5-HT) concentration in the PFC thus leading to enhanced cognitive impairment in a Parkinsonian rat model. Maternal separation was the stressor used to develop an animal model for early life stress that has chronic effects on brain and behavior. Sprague-Dawley rats were treated with the antidepressant Fluvoxamine maleate (FM) prior to a unilateral 6-hydroxydopamine (6-OHDA) lesion to model motor deficits in rats. The Morris water maze (MWM) and the forelimb use asymmetry (cylinder) tests were used to assess learning and memory impairment and motor deficits respectively. Blood plasma was used to measure corticosterone concentration and prefrontal tissue was collected for lipid peroxidation, DA, and 5-HT analysis. Our results show that animals exposed to early life stress displayed learning and memory impairment as well as elevated basal plasma corticosterone concentration which were attenuated by treatment with FM. A 6-OHDA lesion effect was evidenced by impairment in the cylinder test as well as decreased DA and 5-HT concentration in the PFC. These effects were attenuated by FM treatment resulting in higher DA concentration in the PFC of treated animals than in non-treated animals. This study suggests that DA and 5-HT signaling in the PFC are responsive to FM and may reduce stress-induced cognitive impairment in PD.

Topics: Animals; Corticosterone; Dopamine; Fluvoxamine; Learning; Learning Disabilities; Lipid Peroxidation; Male; Maternal Deprivation; Memory; Memory Disorders; Neurotransmitter Agents; Nootropic Agents; Oxidopamine; Parkinsonian Disorders; Prefrontal Cortex; Random Allocation; Rats, Sprague-Dawley; Serotonin; Stress, Psychological

Cognitive deficits are a core symptom of schizophrenia. It is controversial whether antidepressants could improve cognitive symptoms in schizophrenia patients. The present study was designed to identify the therapeutic effect of antidepressants on cognitive deficits in schizophrenia. In the present study, adolescent rats were repeatedly exposed to dizocilpine, which can induce cognitive deficits associated with schizophrenia. Then these rats were treated by six antidepressants (fluvoxamine, sertraline, paroxetine, escitalopram, venlafaxine, mirtazapine) or vehicle. The rats in the control group were exposed to vehicle during the study. Lastly, all rats' spatial memory (a major part of cognition) was assessed using the Morris water maze (MWM) test, and the density of hippocampal parvalbumin (PV) interneurons was evaluated to explore possible mechanisms underlying spatial memory change in schizophrenia. The results of the present study supported the hypothesis of a therapeutic effect of fluvoxamine and escitalopram on spatial memory deficit induced by dizocilpine. Additionally, the data of the present study suggested that fluvoxamine and escitalopram remitted hippocampal PV interneuron reduction induced by dizocilpine. The neuroprotective effect of fluvoxamine and escitalopram may partly explain the therapeutic effect of antidepressants on spatial memory deficit in schizophrenia patients.

Topics: Animals; Antidepressive Agents; Cell Count; Citalopram; Cognition; Cognitive Dysfunction; Dizocilpine Maleate; Excitatory Amino Acid Antagonists; Fluvoxamine; Hippocampus; Interneurons; Male; Maze Learning; Memory Disorders; Mianserin; Mirtazapine; Paroxetine; Rats; Rats, Sprague-Dawley; Schizophrenia; Schizophrenic Psychology; Sertraline; Spatial Memory; Venlafaxine Hydrochloride

Topics: Alcohol Amnestic Disorder; Amnesia; Animals; Fluvoxamine; Humans; Memory Disorders; Oximes; Serotonin; Serotonin Antagonists