Disease relevance of Electroshock

• Release of tissue plasminogen activator (t-PA) and its interaction with plasma protease inhibitors were studied in two patients with massive defibrination, one after electroshock and soft tissue injury and the other after complicated labor; both had very severe hemorrhage [1].
• A memory trace in its active state is susceptible to interference by amnesic agents, such as hypothermia and electroconvulsive shock, and by NMDA receptor antagonists, suggesting that a time-dependent consolidation process occurs each time a memory is reactivated [2].
• In adult male rats, repeated electroshock seizures result in transient hypogonadism, characterized by decreased serum testosterone levels and lowered gonadal tissue weight [3].
• The compounds were tested in mice against seizures induced by electroshock and metrazole (pentylenetetrazole) and in the rotorod assay for neurologic deficit [4].
• To determine whether a single seizure permanently affects the brain's susceptibility to further seizures, 27-day-old rats were subjected to a single seizure induced by either an electroshock or the administration of pentylenetetrazol [5].

Psychiatry related information on Electroshock

• The cognition activating properties of lactams 4, 5, 6, and 10 were evaluated in enhancing retention for passive avoidance learning in rats without and after electroconvulsive shock (ECS); compounds 5 and 10 were found to be more potent than piracetam in the amnesia-reversal testing [6].
• A trend of recovery from amnesia was observed in the electroshock and leptazol groups when tested for retention 48-96 h posttreatment [7].
• Electroshock and leptazol seizures produced retrograde amnesia in all three paradigms, provided that seizures were maximal and retention was tested before 48 h [7].
• Repeated electroconvulsive shock enhanced the locomotor activity produced by either quipazine (25 mg/kg i.p.) or apomorphine (0.2 mg/kg s.c.) compared to sham-shocked controls [8].
• Methods. Dose- and time-response studies were done using two different seizure models: (1) maximal pentylenetetrazol seizures (MMT) and (2) maximal electroconvulsive shock (MES) seizures [9].

High impact information on Electroshock

• Presynaptic serotonin receptor-mediated response in mice attenuated by antidepressant drugs and electroconvulsive shock [10].
• When rats are given a series of electroconvulsive shocks (ECSs) over several days, they display enhanced behavioural responses to both serotonin- and dopamine-receptor agonists [11].
• The ability to associate odors with electroshock was abolished when Galphas* was targeted to MB, but not CC, structures, whereas sensorimotor responses to these stimuli remained normal [12].
• In the adult castrated male rat, exposure to inescapable, intermittent electroshocks inhibited the pulsatile pattern of luteinizing hormone release and markedly lowered its plasma concentrations [13].
• Activation of adenylate cyclase by a stable guanosine 5'-triphosphate analog was augmented in brain membrane preparations from rats treated on a long-term basis with tricyclic antidepressants or electroconvulsive shock [14].

Chemical compound and disease context of Electroshock

• Seizures induced in the rat by electroshock or by injections of pentylenetetrazol increase the specific binding of diazepam to putative receptor sites in cerebral cortical membranes [15].
• The onset and peak of anticonvulsant activity against maximal electroshock seizures directly paralleled the time course for the increase in GABA in nerve terminals, but was not positively correlated with that independent of the terminals [16].
• Amitriptyline potentiated this increase in cerebral permeability whereas lithium and electroconvulsive shock blunted this phenomenon [17].
• Electroconvulsive shock or frontal cortex stimulation administered to rats at 5 but not at 180 minutes after an initial administration of morphine sulfate disrupted the development of one-trial tolerance to the analgesic effects of morphine sulfate [18].
• Electroconvulsive shock and lidocaine reveal rapid consolidation of spatial working memory in the water maze [19].

Biological context of Electroshock

• Unaltered hippocampal dihydropyridine and omega-conotoxin GVIA binding sites after repeated electroconvulsive shock in rats [20].
• Effects of antidepressant drugs and electroconvulsive shock on pre- and postsynaptic alpha 2-adrenoceptor function in the brain: rapid down-regulation by sibutramine hydrochloride [21].
• On repeated administration, this latter effect is associated with an up-regulation of 5-HT2 receptors as it occurs after electroconvulsive shock [22].
• 1-Phenylcyclohexylamine (PCA) and its analogues 1-phenylcyclopentylamine (PPA) and 1-(3-fluorophenyl)cyclohexylamine (3-F-PCA) are potent anticonvulsants in the mouse maximal electroshock (MES) seizure test [23].
• Importantly, the 5-HT receptor antagonist, mesulergine (2 or 4 mg/kg), administered prior to electroshock testing, recapitulated the mutant phenotype in wild-type mice [24].

Anatomical context of Electroshock

• After repeated electroconvulsive shock treatment (once per day for 7 days), tyrosine hydroxylase activity increased significantly in the locus ceruleus, nucleus of the tractus solitarius, hippocampus, cerebellum, and frontal cortex and remained elevated for 4 to 8 days [25].
• Repeated electroconvulsive shock, applied to rats, induces a subsensitivity of dopamine autoreceptors located in the substantia nigra as indexed by single-unit electrophysiological techniques [26].
• Repeated electroconvulsive shock administration significantly enhanced PRAX1 expression in the CA1 subfield and dentate gyrus [27].
• The effect of a single electroconvulsive shock (ECS) (30 min and 24 h after treatment) and repeated ECS (10 once-daily) on the adenosine neuromodulatory system was investigated in rat cerebral cortex, cerebellum, hippocampus, and striatum [28].
• The response to noradrenaline was significantly increased in cortical slices from animals that had received either a single electroconvulsive shock (ECS) or a series of 10 daily ECS but was unchanged in caudate nucleus or hippocampal slices [29].

Gene context of Electroshock

• Administration of convulsant doses of Metrazole (pentylenetetrazol) and picrotoxin, as well as maximal electroshock, results in a rapid but transient increase in c-fos mRNA in mouse brain [30].
• Differential activation of c-Jun N-terminal protein kinase and p38 in rat hippocampus and cerebellum after electroconvulsive shock [31].
• Chronic electroconvulsive shock treatment elicits up-regulation of CRF and AVP mRNA in select populations of neuroendocrine neurons [32].
• Repeated electroconvulsive shock selectively increases the expression of the neuron specific enolase in piriform cortex [33].
• A role for some MAPKs (e.g., extracellular signal-regulated kinase, Erk1/2) has been documented in response to certain physiological stimuli, such as ischemia, visceral pain and electroconvulsive shock [34].

Analytical, diagnostic and therapeutic context of Electroshock

• In an attempt to determine whether the opioid peptides derived from prodynorphin participate in the effects of electroconvulsive shock (ECS), we used radioimmunoassay and immunocytochemistry to measure dynorphin-like immunoreactivity (DN-LI) in various rat brain regions after repeated ECS treatments [35].
• We investigated the expression of inositol 1,4,5-trisphosphate (InsP3) 3-kinase mRNA after a single electroconvulsive shock (ECS) with in situ hybridization histochemistry in rat brain [36].
• The seizures were evoked both by means of auditory stimulation in DBA/2 mice and by pentylenetetrazole or maximal electroshock in Swiss mice [37].
• Catalepsy and analgesia were found in varying degrees after maximal electroshock (MES), metrazol, picrotoxin, and Ro 5-3663 activated seizures [38].
• Two animal models which are known to be indicative of anticonvulsant efficacy in man are inhibition of maximal electroshock seizures (MES) and inhibition of pentylenetetrazol (PTZ) convulsions in either rats or mice [39].

References