Neuropsychopharmacology (2003) 28, S21S26. doi:10.1038/sj.npp.

1300135

ECT of Major Depressed Patients in Relation to Biological and Clinical Variables: A Brief Overview
Bjrn 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 least 3 months. A series of seizures further increased neurogenesis, indicating a dose-dependent mechanism, probably mediated by neurotrophic factors. Generation of new neurons in the hippocampus may be an important neurobiological element underlying the clinical effects of ECSs. An increase in the number of platelet 5-HT2 receptors after ECT was found in 12 major depressed patients (Stain-Malmgren et al, 1998). Serotonin (5-hydroxytryptaminergic (5-HT)) is one of the most important neurotransmitters involved in affective disorders. ECT alters serotonergic transmission as well 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 on GABAergic system (Bergsholm, 1999; Ishihara et al, 1999). Thus, ECT alters serotoninergic transmission considered as a characteristic of major depression as well as some receptor functions in noradrenergic and dopamnergic neurons decrease, resulting in an increase in the release of noradrenaline, dopamine, and other neurotransmitters (Ishihara et al, 1999).

Pada pasien schizophrenia (KAPLAN)

Dopamine Hypothesis

Kebanyakan hipotesis menyebutkan skizofrenia berasal dari aktivitas dopamine. Teori ini muncul dari dua observasi yaitu dari aksi dari antipsikotik (bekerja pada D2 reseptor) pada pasien skizofrenia dan meningkatnya aktivitas dopaminergik pada penggunaan amfetamin, kokain dan psikomimetik. Peningkatan dopamine ini selaras dengan beratnya gejala positif psikotik. Dari studi PET (Positron Emission Tomography) didapatkannya adanya peningkatan reseptor D2 di nucleus caudatus dan peningkatan konsentrasi dopamine di amygdale. Serotonin. Hipotesis mengenai serotonin adalah adanya peningkatan serotonin dapat menyebabkan gejala positif dan gejala negatif. Norepinephrine. A selective neuronal degeneration within the norepinephrine reward neural system could account for this aspect of schizophrenic symptomatology. However, biochemical and pharmacological data bearing on this proposal are inconclusive. GABA. The inhibitory amino acid neurotransmitter -aminobutyric acid (GABA) has been implicated in the pathophysiology of schizophrenia based on the finding that some patients with schizophrenia have a loss of GABAergic neurons in the hippocampus. GABA has a regulatory effect on dopamine activity, and the loss of inhibitory GABAergic neurons could lead to the hyperactivity of dopaminergic neurons. Neuropeptides. Neuropeptides, such as substance P and neurotensin, are localized with the catecholamine and indolamine neurotransmitters and influence the action of these neurotransmitters. Alteration in neuropeptide mechanisms could facilitate, inhibit, or otherwise alter the pattern of firing these neuronal systems. Glutamate. Glutamate has been implicated because ingestion of phencyclidine, a glutamate antagonist, produces an acute syndrome similar to schizophrenia. The hypotheses proposed about glutamate include those of hyperactivity, hypoactivity, and glutamate-induced neuro- toxicity. Acetylcholine and Nicotine. Postmortem studies in schizophrenia have demonstrated decreased muscarinic 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 systems involved in cognition, which is impaired in schizophrenia.