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Query: UMLS:C0038454 (
stroke
)
147,016
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Serotonin
adipinate in a dose of 40-60 mg was injected by drip infusion to 30 patients with acute poisoning by psychotropic drugs for correcting circulatory disorders. The drug corrected hemodynamic disorders in the lesser and greater circulation by increasing the
stroke
volume and normalizing total peripheral vascular resistance and central blood volume.
...
PMID:[Use of serotonin adipinate in combined therapy of hemodynamic disorders in acute poisoning by psychopharmacological preparations]. 1005 Mar 32
Senescence is accompanied by the loss of neurons and synapses, and the maintenance of function depends on adaptive change at the levels of synaptic activity and cellular responsiveness. In the current study, we administered the neurotoxin MDMA, to young and aged mice and assessed the effects on indices of neuronal activity and cell signaling mediated through adenylyl cyclase. Young mice given MDMA showed 80% depletion of dopamine in the caudate and 30% depletion in the cerebral cortex; measurements of dopamine turnover indicated a compensatory upregulation of the activity of the remaining neurons in the caudate but downregulation in the cerebral cortex.
Serotonin
levels were comparatively less affected but serotonin turnover was decreased significantly in both regions. At the level of cell signaling, the young mice showed heterologous upregulation of adenylyl cyclase activity and a consequent enhancement of responses mediated through neurotransmitter receptors. In aged mice, MDMA treatment produced the same degree of lesioning but substantially different changes in neuronal activity and cell signaling. In the cerebral cortex, dopamine turnover was increased, and serotonin turnover decreased, effects opposite in direction to those seen in young mice. In the aged group, MDMA elicited heterologous loss of adenylyl cyclase responses instead of displaying the supersensitivity that had been seen in the young group. The aging brain thus displays maladaptation to the loss of monoaminergic input, effects that may augment the functional impairment associated with neurodegenerative disorders or
stroke
.
...
PMID:Cellular determinants of reduced adaptability of the aging brain: neurotransmitter utilization and cell signaling responses after MDMA lesions. 1101 Oct 18
It has recently been shown that
5-HT
(1A) receptor stimulation reduced the infarct volume after occlusion of the middle cerebral artery in rats. Since there is increasing evidence that apoptosis is involved in neurodegenerative diseases and
stroke
, we investigated whether the
5-HT
(1A) agonist Bay x 3702 could protect neurons against apoptotic damage in a rat model of transient forebrain cerebral ischemia. Bay x 3702 (4 microg/kg i.v.) caused a 10% reduction of neuronal damage in the hippocampal CA1 subfield. Higher doses of Bay x 3702 (40 and 12 microg/kg i.v.) did not cause any neuroprotective effect, most likely because of the strong reduction of mean arterial blood pressure during the period of Bay x 3702 infusion. Bay x 3702 (4 microg/kg i.v.) diminished DNA laddering in the hippocampus and striatum 4 days after 10 min forebrain ischemia. These results were confirmed by TUNEL-staining. The anti-apoptotic effect was abolished by additional treatment with the
5-HT
(1A) receptor antagonist WAY 100635 (1 mg/kg). Taken together, the results suggest that Bay x 3702 can rescue hippocampal as well as striatal neurons from apoptotic cell death in vivo via stimulation of
5-HT
(1A) receptors.
...
PMID:Stimulation of 5-HT(1A) receptors reduces apoptosis after transient forebrain ischemia in the rat. 1106 86
Brain ischemia provoked by
stroke
or traumatic brain injury induces a massive increase in neurotransmitter release, in particular of the excitotoxin glutamate. Glutamate triggers a cascade of events finally leading to widespread neuronal cell damage and death. The aminomethylchroman derivative BAY x 3702 is a novel neuroprotectant which shows pronounced beneficial effects in various animal models of ischemic brain injury. As shown previously BAY x 3702 binds to
5-HT
(1A) receptors of different species in subnanomolar range and is characterized as a full receptor agonist. In this study we investigated the influence of BAY x 3702 on potassium-evoked glutamate release in vitro and ischemia-induced glutamate release in vivo. In rat hippocampal slices BAY x 3702 inhibited evoked glutamate release in a dose-dependent manner (IC(50)=1 microM). This effect was blocked by the selective
5-HT
(1A) receptor antagonist WAY 100635, indicating that BAY x 3702 specifically acts via
5-HT
(1A) receptors. In vivo, release of endogenous aspartate and glutamate was measured in the cortex of rats by microdialysis before and after onset of permanent middle cerebral artery occlusion. Single dose administration of BAY x 3702 (1 microg/kg or 10 microg/kg i.v.) immediately after occlusion reduced the increase and total release of extracellular glutamate by about 50% compared to non-treated animals, whereas the extracellular aspartate levels were not significantly affected. Inhibition of glutamate release may therefore contribute to the pronounced neuroprotective efficacy of BAY x 3702 in various animal models of ischemic brain damage.
...
PMID:Inhibition of evoked glutamate release by the neuroprotective 5-HT(1A) receptor agonist BAY x 3702 in vitro and in vivo. 1114 61
The effects of aniracetam on extracellular levels of dopamine (DA), serotonin (
5-HT
) and their metabolites were examined in five brain regions in freely moving
stroke
-prone spontaneously hypertensive rats (SHRSP) using in vivo microdialysis. Basal DA release in SHRSP was uniformly lower in all regions tested than that in age-matched control Wistar Kyoto rats. 3,4-Dihydroxyphenylacetic acid and homovanillic acid levels were altered in the basolateral amygdala, dorsal hippocampus and prefrontal cortex of SHRSP. While basal
5-HT
release decreased in the striatum and increased in the basolateral amygdala, there was no associated change in 5-hydroxyindoleacetic acid levels. Systemic administration of aniracetam to SHRSP enhanced both DA and
5-HT
release with partly associated change in their metabolite levels in the prefrontal cortex, basolateral amygdala and dorsal hippocampus, but not in the striatum and nucleus accumbens shell, in a dose-dependent manner (30 and/or 100 mg/kg p.o.). Microinjection (1 and 10 ng) of aniracetam or its metabolites (N-anisoyl-GABA and 2-pyrrolidinone) into the nucleus accumbens shell produced no turning behavior. These findings indicate that SHRSP have a dopaminergic hypofunction throughout the brain and that aniracetam elicits a site-specific activation in mesocorticolimbic dopaminergic and serotonergic pathways in SHRSP, possibly via nicotinic acetylcholine receptors in the ventral tegmental area and raphe nuclei. The physiological roles in the aniracetam-sensitive brain regions may closely link with their clinical efficacy towards emotional disturbances appearing after cerebral infarction.
...
PMID:Site-specific activation of dopamine and serotonin transmission by aniracetam in the mesocorticolimbic pathway of rats. 1128 61
Late-life depression is a serious health problem that is challenging to manage but generally responds well to pharmacotherapy. Selective serotonin (5-hydroxytryptamine:
5-HT
) reuptake inhibitors (SSRIs), the most commonly prescribed antidepressants, are usually used as first-line agents for elderly patients with depression. Like most drugs, SSRIs have not been widely tested in clinical trials that approximate 'real-life' geriatric situations. However, studies completed to date provide valuable information about the efficacy, safety and tolerability of this class of antidepressants among older patients with depression, including those with depression secondary to
stroke
or dementia and those with other comorbid physical disorders. Although one SSRI may be more efficacious or better tolerated by elderly patients than another, existing data do not support such claims. However, other distinguishing features may influence the choice of agent. For example, fluoxetine, fluvoxamine and paroxetine are more likely to be involved in significant drug-drug interactions than are citalopram or sertraline. In contrast to the other SSRIs, fluoxetine has a half-life well in excess of 1 day, which can be an advantage when weaning the patient off therapy in that it may reduce the incidence of discontinuation symptoms, but a significant disadvantage if the patient cannot tolerate the drug or experiences an adverse drug-drug interaction.
...
PMID:Selective serotonin reuptake inhibitors for late-life depression: a comparative review. 1139 44
Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (
5-HT
) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in
stroke
-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and
5-HT
release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and
5-HT
release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl-gamma-aminobutyric acid [corrected] (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and
5-HT
release in the same region, respectively. These results indicate that aniracetam enhances DA and
5-HT
release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors.
...
PMID:Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP. 1159 8
Depression occurs at least temporarily in up to 30 - 40 % of all patients that have experienced a
stroke
. In the literature the term of a "Poststroke Depression" (PSD) has already been established. However standardised criteria for this diagnoses do not exist to this day. In most cases the DSM or ICD classification system is applied. Other investigators used various psychiatric rating scales. Even though it is generally acknowledged that there is a high prevalence, the occurrence of depression in combination with a
stroke
fails in most cases to be diagnosed or is left untreated. The need for treatment is even more pronounced by studies showing that a combination of
stroke
and depression will result in a less favourable outcome, particularly pertaining to that of functional treatment (motor skills, independent participation in activities of daily life). This difference in impairment between a depressed
stroke
patient and a not depressed
stroke
patient could be proven in studies that have been conducted over years. Despite the necessity of treatment that can be concluded from such a finding, the recent literature does not offer consistent information as to the ideal point of time for intervention nor the kind and intensity necessitated. According to singular studies, that have rarely been conducted under controlled conditions, there have been positive outcomes after early treatment. Along with psychostimulants that were most predominantly applied in the USA, as well as conventional tricyclic antidepressants, the group of the "Selective
Serotonin
Reuptake Inhibitors, SSRIs" have resulted in particularly favourable clinical outcomes.
...
PMID:[Post-stroke depression: diagnosis and therapy]. 1175 47
Since serotonin (
5-HT
) stimulates motor function, pharmacological potentiation of
5-HT
neurotransmission may improve motor function in healthy subjects and, possibly, recovery in post-
stroke
patients. Indeed, fluoxetine, a selective serotonin reuptake inhibitor (SSRI), increased activation in executive motor areas of healthy subjects as fenozolone, a releaser of monoamines (including noradrenaline, dopamine, and serotonin) from intracellular stores. This study is intended to test the hypothesis that paroxetine can likewise modulate brain motor activity in a dose-dependent manner in healthy subjects. In a double-blind counterbalanced study, six subjects underwent functional MRI examinations on three sessions 1 week apart (E1, E2, and E3) at the time of peak plasma concentrations (5 h after drug intake, i.e., either 20 or 60 mg of paroxetine or placebo) with a complex sequential opposition task. Rest and activation alternated in a block design. During activation, subjects performed, with the right hand, a 1-Hz-paced task that alternated two fist closings with a sequential opposition task. Paroxetine elicited effects similar to those reported for fluoxetine; notable changes were hyperactivation in the contralateral S1/M1, and posterior SMA and widespread hypoactivation of basal ganglia and cerebellum. There was an inverse correlation between dose and effect: significantly greater effects were observed with the 20-mg dose compared with 60 mg. Paroxetine dose-dependently modulates activation of the entire motor pathway in a way that favors motor output. Thus, a single dose of the SSRI paroxetine reorganized motor processing.
...
PMID:A single dose of the serotonin neurotransmission agonist paroxetine enhances motor output: double-blind, placebo-controlled, fMRI study in healthy subjects. 1177 71
Serotonin
is a potent pulmonary vasoconstrictor actively accumulated by mammalian platelets and avian thrombocytes and released into the plasma during platelet or thrombocyte aggregation.
Serotonin
has been implicated in the mechanisms responsible for pulmonary hypertension in several human and animal studies. However, the role of serotonin in pulmonary hypertension syndrome (PHS, ascites) in broilers previously had not been evaluated. In the present study we evaluated the pulmonary hemodynamic responses of broilers to intravenous infusions of serotonin dissolved in 2.5% (wt/vol) mannitol solution (carrier vehicle). Carrier vehicle infusion alone had no influence on any of the hemodynamic variables.
Serotonin
infusion triggered rapid increases in pulmonary arterial pressure to approximately 50% above pre-infusion baseline values, accompanied by decreases in mean systemic arterial pressure and cardiac output. The peak pulmonary arterial pressure response occurred within approximately 70 s after the start of serotonin infusion and remained elevated above baseline values over the course of a 10-min infusion period. Pulmonary arterial pressure and cardiac output returned to pre-infusion baseline values upon cessation of serotonin infusion, whereas mean systemic arterial pressure returned toward pre-infusion base-line values. Pulmonary hypertensive responses were associated with increased pulmonary vascular resistance (pulmonary vasoconstriction). The peak pulmonary arterial pressure attainable was inadequate to propel the normal cardiac output through the elevated pulmonary vascular resistance. Consequently, the impeded venous return to the left ventricle caused dependent reductions in
stroke
volume, cardiac output, and mean systemic arterial pressure. Reductions in cardiac output were associated with reductions in
stroke
volume but not heart rate. Any factor that reduces the pulmonary vascular capacity or increases the pulmonary vascular resistance theoretically can increase the incidence of PHS. The present study provides direct evidence that serotonin can trigger pulmonary vasoconstriction and pulmonary hypertension in broilers.
...
PMID:Hemodynamic responses of broiler pulmonary vasculature to intravenously infused serotonin. 1187 32
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