Neuro Psychopharmacology

of 2

Please download to get full document.

View again

All materials on our website are shared by users. If you have any questions about copyright issues, please report us to resolve them. We are always happy to assist you.
PDF
2 pages
0 downs
3 views
Share
Description
Neuropsychopharmacology (2003) 28, S21–S26. doi:10.1038/sj.npp.1300135 ECT of Major Depressed Patients in Relation to Biological and Clinical Variables: A Brief Overview Björn Wahlund1 and Dietrich von Rosen1 -BDNF increases the formation of new serotonergic synapses, and the metabolism of serotonin and noradrenaline (Bergsholm, 1999). Madsen et al (2000) showed on rats that a single ECS significantly increased the number of newborn nerve cells in the dentate gyrus. These cells survived for at
Tags
Transcript
     Neuropsychopharmacology (2003) 28, S21  –  S26. doi:10.1038/sj.npp.1300135 ECT of Major Depressed Patients in Relation to Biologicaland Clinical Variables: A Brief Overview Björn Wahlund 1  and Dietrich von Rosen 1  -BDNF increases the formation of new serotonergic synapses, and the metabolism of serotoninand noradrenaline(Bergsholm, 1999). Madsen et al (2000) showed on rats that a single ECS significantly increased the number of newborn nerve cells in the dentate gyrus. These cells survived for at least 3 months. A series of seizures further increased neurogenesis, indicating a dose-dependent mechanism, probablymediated by neurotrophic factors. Generation of new neurons in the hippocampus may be animportant neurobiological element underlying the clinical effects of ECSs.-   An increase in the number of platelet 5-HT 2 receptors after ECT was found in 12 majordepressed patients(Stain-Malmgren et al , 1998).-   Serotonin (5-hydroxytryptaminergic (5-HT)) is one of the most importantneurotransmitters involved in affective disorders. ECT alters serotonergic transmission aswell as several subtypes of 5-HT-receptors in CNS(Bergsholm, 1999; Ishihara et al ,1999).-   ECS also have an effect on the cholinergic and glutaminergic system as well as onGABAergic system(Bergsholm, 1999; Ishihara et al , 1999).-   Thus, ECT alters serotoninergic transmission considered as a characteristic of majordepression as well as some receptor functions in noradrenergic and dopamnergic neuronsdecrease, resulting in an increase in the release of noradrenaline, dopamine, and otherneurotransmitters(Ishihara et al , 1999). Pada pasien schizophrenia (KAPLAN) Dopamine Hypothesis  Kebanyakan hipotesis menyebutkan skizofrenia berasal dari aktivitas dopamine. Teori inimuncul dari dua observasi yaitu dari aksi dari antipsikotik (bekerja pada D 2  reseptor) pada pasienskizofrenia dan meningkatnya aktivitas dopaminergik pada penggunaan amfetamin, kokain danpsikomimetik. Peningkatan dopamine ini selaras dengan beratnya gejala positif psikotik. Daristudi PET ( Positron Emission Tomography ) didapatkannya adanya peningkatan reseptor D 2 dinucleus caudatus dan peningkatan konsentrasi dopamine di amygdale. Serotonin . Hipotesis mengenai serotonin adalah adanya peningkatan serotonin dapatmenyebabkan gejala positif dan gejala negatif. Norepinephrine . A selective neuronal degeneration within the norepinephrine reward neuralsystem could account for this aspect of schizophrenic symptomatology. However, biochemicaland pharmacological data bearing on this proposal are inconclusive. GABA. The inhibitory amino acid neurotransmitter γ-aminobutyric acid (GABA) has beenimplicated in the pathophysiology of schizophrenia based on the finding that some patients withschizophrenia have a loss of GABAergic neurons in the hippocampus. GABA has a regulatoryeffect on dopamine activity, and the loss of inhibitory GABAergic neurons could lead to thehyperactivity of dopaminergic neurons. Neuropeptides . Neuropeptides, such as substance P and neurotensin, are localized with thecatecholamine and indolamine neurotransmitters and influence the action of theseneurotransmitters. Alteration in neuropeptide mechanisms could facilitate, inhibit, or otherwisealter the pattern of firing these neuronal systems. Glutamate . Glutamate has been implicated because ingestion of phencyclidine, a glutamateantagonist, produces an acute syndrome similar to schizophrenia. The hypotheses proposed aboutglutamate include those of hyperactivity, hypoactivity, and glutamate-induced neuro- toxicity. Acetylcholine and Nicotine . Postmortem studies in schizophrenia have demonstrated decreasedmuscarinic and nicotinic receptors in the caudate-putamen, hippocampus, and selected regions of the prefrontal cortex. These receptors play a role in the regulation of neurotransmitter systemsinvolved in cognition, which is impaired in schizophrenia.
Related Search
We Need Your Support
Thank you for visiting our website and your interest in our free products and services. We are nonprofit website to share and download documents. To the running of this website, we need your help to support us.

Thanks to everyone for your continued support.

No, Thanks