Electroconvulsive Shock Group Research Articles

Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat

BackgroundAlthough electroconvulsive therapy (ECT) is regarded as one of the efficient treatments for intractable psychiatric disorders, the mechanism of therapeutic action remains unclear. Recently, many studies indicate that ECT affects the immune-related cells, such as microglia, astrocytes, and lymphocytes. Moreover, microglial activation and astrocytic activation have been implicated in the postmortem brains of schizophrenia patients. We previously demonstrated that Gunn rats showed schizophrenia-like behavior and microglial activation in their brains. The present study examined the effects of electroconvulsive shock (ECS), an animal counterpart of ECT, on schizophrenia-like behavior, microgliosis, and astrogliosis in the brain of Gunn rats.MethodsThe rats were divided into four groups, i.e., Wistar sham, Wistar ECS, Gunn sham, and Gunn ECS. ECS groups received ECS once daily for six consecutive days. Subsequently, prepulse inhibition (PPI) test was performed, and immunohistochemistry analysis was carried out to determine the activation degree of microglia and astrocytes in the hippocampus by using anti-CD11b and anti-glial fibrillary acidic protein (GFAP) antibody, respectively.ResultsWe found PPI deficit in Gunn rats compared to Wistar rats, and it was significantly improved by ECS. Immunohistochemistry analysis revealed that immunoreactivity of CD11b and GFAP was significantly increased in Gunn rats compared to Wistar rats. ECS significantly attenuated the immunoreactivity of both CD11b and GFAP in Gunn rats.ConclusionsECS ameliorated schizophrenia-like behavior of Gunn rats and attenuated microgliosis and astrogliosis in the hippocampus of Gunn rats. Accordingly, therapeutic effects of ECT may be exerted, at least in part, by inhibition of glial activation. These results may provide crucial information to elucidate the role of activated glia in the pathogenesis of schizophrenia and to determine whether future therapeutic interventions should attempt to up-regulate or down-regulate glial functions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0688-2) contains supplementary material, which is available to authorized users.

Propofol Mitigates Learning and Memory Impairment After Electroconvulsive Shock in Depressed Rats by Inhibiting Autophagy in the Hippocampus.

BackgroundThe present study explored the effects of propofol on hippocampal autophagy and synaptophysin in depression-model rats undergoing electroconvulsive shock (ECS).Material/MethodsThe rat depression model was established by exposing Sprague-Dawley rats to stress for 28 consecutive days. Forty rats were assigned randomly into the depression group (group D; no treatment), the ECS group (group E), the propofol group (group P), and the propofol + ECS group (group PE). Open field tests and sucrose preference tests were applied to evaluate the depression behavior; and Morris water maze tests were used to assess the learning and memory function of the rats. Western blotting was used to detect the expression of Beclin-1 and LC3-II/I; and ELISA was applied to assess the expression of synaptophysin.ResultsRats in group E and group PE scored higher in the open field and sucrose preference tests compared with those in group D. Furthermore, rats in group E also had a longer escape latency, a shorter space exploration time, and increased expression of Beclin-1, LC3-II/I, and synaptophysin. Compared with group E, rats in group PE possessed a shorter escape latency, a longer space exploration time, reduced expression of Beclin-1, LC3-II/I, and synaptophysin.ConclusionsPropofol could inhibit excessive ECS-induced autophagy and synaptophysin overexpression in the hippocampus, thus protecting the learning and memory functions in depressed rats after ECS. The inhibitory effects of propofol on the overexpression of synaptophysin may result from its inhibitory effects on the excessive induction of autophagy.

Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats.

To explore the possible neurophysiologic mechanisms of propofol and N-methyl-D- aspartate (NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs. Models of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance, two intervention factors were included: electroconvulsive shock groups (with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal (ip) injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups (n=10 per group): ip injection of 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blot analysis. Propofol, MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels of phosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock. Electroconvulsive shock might reduce learning-memory impairment caused by protein Tau hyperphosphorylation in depressed rats by down-regulating glutamate content.

Effects of low-dose ketamine combined with propofol on phosphorylation of AMPA receptor GluR1 subunit and GABAA receptor in hippocampus of stressed rats receiving electroconvulsive shock.

To investigate the effects of low-dose ketamine combined with propofol on the antidepressant efficacy in stressed rats undergoing electroconvulsive shock (ECS) and its impact on phosphorylation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit glutamate receptor 1 (GluR1) and γ-aminobutyric acid receptor subunit A (GABAAR). Sprague-Dawley rats were stressed by chronic unpredictable mild stress. Fifty stressed rats were randomly divided into 5 groups (n = 10 per group): depression group (with no application, group D), ECS group (applied with ECS after intraperitoneal injection of isotonic sodium chloride solution, 8 mL/kg, group E), ketamine + ECS group (applied with ECS after intraperitoneal injection of ketamine, 10 mg/kg, group KE), propofol + ECS group (applied with ECS after intraperitoneal injection of propofol, 80 mg/kg, group PE), and ketamine + propofol + ECS group (applied with ECS after intraperitoneal injection of ketamine, 10 mg/kg, and propofol, 80 mg/kg, group KPE). All groups except group D underwent ECS once a day for 7 consecutive days. Sucrose preference test, open-field test, and Morris water maze were performed to assess the depressive behavior. Phosphorylation of GluR1 and GABAAR were evaluated by Western blot. Compared with group D, sucrose preference percentage and open-field scores were increased after ECS application in the 4 other groups; rats in group E reported prolonged escape latency and shortened space exploration time, whereas the escape latency were decreased and space exploration time were prolonged in group KPE; the ratio of p-GluR1/p-GABAAR in hippocampus were increased in the 4 other groups. When using group E as control, rats in group KPE exhibited higher sucrose preference percentage and open-field scores; the escape latency was shortened and space exploration time was prolonged in groups KE, PE, and KPE; the ratio of p-GluR1/p-GABAAR in the hippocampus was up-regulated in groups KE and KPE. When compared with groups KE and PE, the rats in group KPE exhibited higher sucrose preference percentage and open-field scores, the escape latency of group KPE was shortened and space exploration time was prolonged, the ratio of p-GluR1/p-GABAAR in the hippocampus of group KEP is between those of groups KE and PE. Low-dose ketamine combined with propofol may play a role in enhancing the antidepressant efficacy of ECS in stressed rats, ameliorating the cognitive impairment associated with ECS by balancing the expression of p-GluR1 and p-GABAAR in the hippocampus of stressed rats.

Effects of Propofol on Expression of Hippocampal Neuronal Nitric Oxide Synthase and Carboxy-Terminal PDZ Ligand of Neuronal Nitric Oxide Synthase in Stressed Rats Undergoing Electroconvulsive Shock

This study aimed at investigating the effects of propofol on the expression of hippocampal neuronal nitric oxide synthase (nNOS) and carboxy-terminal PDZ ligand of nNOS (CAPON) in stressed rats after electroconvulsive shock (ECS). Sprague-Dawley rats were stressed repeatedly for 28 days to establish a stressed model. Forty stressed rats were randomly divided into 4 groups (n = 10 for each group): the stressed group (unapplied group), propofol group (applied with intraperitoneal injection of propofol 80 mg/kg for 7 days), ECS group (applied with ECS and intraperitoneal injection of normal saline 8 mL/kg), or propofol + ECS group (applied with ECS and intraperitoneal injection of propofol 80 mg/kg). Sucrose preference test, open-field test, and Morris water maze were used to assess behavioral changes. Immunohistochemistry was carried out to measure the expression of nNOS and CAPON in hippocampal CA1, CA3, and DG areas. Rats in the ECS and propofol + ECS groups had higher sucrose preference percentages and open-field scores when compared with the stressed group. Rats in the ECS group exhibited longer escape latency, shorter space exploration time, up-regulated expression of nNOS, down-regulated expression of CAPON, and increased ratio of nNOS/CAPON in hippocampus. Compared with the ECS group, the propofol + ECS group exhibited shorter escape latency, longer space exploration time, down-regulated expression of nNOS, up-regulated expression of CAPON in hippocampus, and lower nNOS/CAPON values. Propofol may alleviate ECS-induced impairment of learning and memory in stressed rats by inhibiting excessive expression of nNOS and enhancing the expression of CAPON to maintain the balance between nNOS and CAPON in hippocampus.

Inhibitory Effects of Valproate on Impairment of Y-maze Alternation Behavior Induced by Repeated Electroconvulsive Seizures and c-Fos Protein Levels in Rat Brains

We previously showed that inhibition of repeated electroconvulsive shock (ECS)-induced seizures through 7-day administration of anti-epileptic drugs suppressed the impairment of spontaneous alternation behavior in the Y-maze test in rats. To clarify the precise mechanism(s), we investigated the effect of valproate on such impairment and examined the levels of brain-derived neurotrophic factor (BDNF) and c-Fos protein in the prefrontal cortex and the hippocampus 24h after the last administration of ECS. Seven-day intraperitoneal (i.p.) administration of valproate (400mg/kg) suppressed the impairment of spontaneous alternation behavior. Repeated ECS increased the BDNF protein levels in the hippocampus and prefrontal cortex in the presence or absence of valproate, indicating that the increase in BDNF protein levels resulted from electrical stimulation. c-Fos protein levels were significantly decreased in the hippocampal dentate gyrus after repeated ECS, but valproate had no significant effect on decreased c-Fos protein levels. Valproate＋ECS significantly increased the c-Fos protein levels of the prefrontal cortex compared with the ECS group. These findings suggest that the inhibitory effect of valproate on repeated ECS-induced impairment of spontaneous alternation behavior may be linked to the prefrontal cortex.

Evaluation of nootropic and neuroprotective effects of low dose aspirin in rats

Objective:To evaluate the nootropic and neuroprotective effects of aspirin in Sprague Dawley rats.Materials and Methods:Retention of conditioned avoidance response (CAR) and central 5-HT-mediated behavior (lithium-induced head twitches) were assessed using repeated electroconvulsive shock (ECS) in rats. Rats were divided into eight groups: control (pretreated with distilled water), scopolamine (0.5 mg/kg i.p.), ECS (150 V, 50 Hz sinusoidal with intensity of 210 mA for 0.5 s) pretreated, aspirin (6.75 mg/kg orally) pretreated, combined scopolamine and aspirin pretreated, ondansetron (0.36 mg/kg orally) pretreated, combined ECS and ondansetron pretreated and combined ECS and aspirin pretreated groups. Data was analyzed by the chi-square test and ANOVA.Results:Findings show that administration of single ECS daily for consecutive 8 days results in enhancement of 5-HT-mediated behavior (lithium-induced head twitches) and in disruption of the retention of CAR. Aspirin and ondansetron administration significantly increased the retention of conditioned avoidance response compared to control. Ondansetron and aspirin significantly prevented ECS-induced attenuation of the retention of conditioned avoidance response also. On the other hand, ondansetron and aspirin significantly retarded the ECS-induced enhancement of 5-HT-mediated behavior.Conclusion:Inhibition of the serotonergic transmission by aspirin is responsible for its nootropic and neuroprotective actions.

Confirmation of whole-brain kindling with repeated subthreshold electroconvulsive shocks: a controlled study.

Repeated, subconvulsive electroconvulsive shock (ECS) stimuli, administered a day apart, lower the ECS seizure threshold in rats. It is not known, however, whether this kindling results from the repeated subconvulsive stimulation or from the stress induced by the experimental procedures. Adult, male Wistar rats were randomized to receive a 3-mC ECS stimulus (n = 20), a 30-V (0.3-s) footpad shock (n = 20), or sham ECS and sham footpad shock (n = 20). All procedures were conducted once daily for 3 consecutive days. On the fourth day, all rats received a 3-mC ECS stimulus. At the end of the experiment, 85% of the rats in the ECS group but only 35% of the rats in each of the other two groups had experienced a seizure with the 3-mC stimulus (p < 0.001). The lowering of the ECS seizure threshold by repeated, once-daily subconvulsive stimuli is caused by the subconvulsive stimulation itself, not by experimental stress.

The effects of repeated minimal electroconvulsive shock exposure on levels of mRNA encoding fibroblast growth factor-2 and nerve growth factor in limbic regions

Chronic, but not acute, exposure to minimal electroconvulsive shock (ECS) has been shown to decrease vulnerability to neuronal cell death, without itself causing neuronal damage. One potential mechanism for the neuroprotective effect of ECS is the increase in fibroblast growth factor-2 (FGF-2) which occurs after chronic, but not acute, ECS exposure. This raises the possibility that repeated seizures over a period of several days may alter the transcriptional regulation of FGF-2. To test this hypothesis, the present study compared the effect of acute (1 day) vs. chronic (7 days) ECS treatment on levels of mRNA for FGF-2 in rhinal and frontal cortices, hippocampus, and olfactory bulbs. In addition, mRNA for another prominent neurotrophic factor, nerve growth factor (NGF), was assayed concurrently. At 8 h after acute ECS, mRNA levels increased by 60% for FGF-2 and 136% for NGF in rhinal cortex, 32% for FGF-2 and 36% for NGF in frontal cortex, and by 13% for NGF in hippocampus. After 7 days of ECS treatment the respective increases were 72% and 80%, 53% and 38%, and 28%. No increases were observed in olfactory bulbs after either treatment regimen. The peak increases in FGF-2 mRNA were consistently greater after chronic treatment, but the differences from those seen acutely reached significance in frontal cortex only. However, the duration over which mRNA for FGF-2 was elevated did not differ between the acute and chronic ECS groups. NGF mRNA induction was neither enhanced nor prolonged as a result of chronic ECS as compared to acute ECS treatment. These results suggest that chronic ECS treatment may lead to an enhanced rate of transcription of message for FGF-2 but not for NGF, in selected brain regions. At the same time, the results indicate that chronic ECS treatment induces FGF-2 and NGF mRNA expression in a tissue-specific manner and that this induction is maintained over the 7-day treatment period. The sustained increases in mRNAs for these trophic factors may contribute to the neuroprotective actions of chronic ECS treatment.

Potentiation of 5-HT 3 receptor functions in the hippocampal CA1 region of rats following repeated electroconvulsive shock treatments

Modulation of serotonin (5-HT) 3-receptor function by repeated electroconvulsive shock (ECS) treatment was investigated to elucidate the mechanism underlying the effectiveness of electroconvulsive therapy (ECT) which is clinically used for drug-resistant depression. ECS (100 V, 1 s) was applied once a day for 14 days via an electrode placed on the ears of rats (ECS group). For controls, rats were handled similar to the ECS-treated group except for the stimulation. Hippocampal slices (thickness, 450 μm) were prepared 24 h after the final ECS treatment when rats were 5–6 weeks old. Intracellular recordings were made from the neurons in the CA1 pyramidal cell layer. Activation of 5-HT 3 receptors increased spontaneous postsynaptic potentials (sPSP). Increased sPSP was mainly mediated by GABA. The 5-HT 3 receptor mediated increase in sPSP was potentiated in the ECS group compared with the control group. These findings suggest that the 5-HT 3 receptor function is potentiated by repeated ECS.

Enhancement of serotonin1A receptor function following repeated electroconvulsive shock in young rat hippocampal neurons in vitro

Effects of repeated electroconvulsive shock (ECS) treatment on 5-hydroxytryptamine (5-HT) response were investigated to elucidate the ECS-induced changes, which may be related to antidepressant effects, using electrophysiological methods with hippocampal slices in vitro. ECS was applied to Wistar rats once daily for 14 d from 3 wk of age (ECS group). Control animals did not receive ECS (control group). Twenty-four hours after the final ECS treatment, hippocampal slices were prepared for intracellular recording analysis. Application of 5-HT (0.1-30 µm) caused a dose-dependent hyperpolarization in hippocampal CA1 neurons. 5-HT-induced hyperpolarization in the ECS group was significantly greater than that in the control group. Furthermore, 8-OH-DPAT [8-hydroxy-2-(di-n-propylamino)tetralin], a 5-HT(1A) receptor agonist, also induced significantly larger hyperpolarization in the ECS group than in the control group. These results suggest that repeated ECS treatment enhances function of the 5-HT(1A) receptor for 5-HT. This supports the hypothesis that enhanced 5-HT(1A) receptor function, at least in part, contributes to the effectiveness of ECS treatment for depression directly and/or indirectly.

Long-term enhancement of entorhinal-dentate evoked potentials following `modified' ECS in the rat

Electroconvulsive therapy (ECT) is widely used as a treatment for drug-resistant depression. The animal analogue of ECT is electroconvulsive shock (ECS) seizures. We have recently shown that repeated ECS seizures cause a long-lasting, perhaps permanent, enhancement in entorhinal-dentate evoked potentials in the rat. Our study, however, involved `unmodified' ECS, whereas in clinical practice ECT is now usually given in its `modified' form (with near-threshold currents, a short-acting barbiturate, muscle relaxant and oxygen). We have therefore repeated our experiments using modified ECS. Entorhinal-dentate evoked potentials were measured in Long–Evans rats before and after: (1) eight modified ECS seizures; or (2) eight sham modified ECS trials. Despite the use of the modified procedure, a significant and long-lasting enhancement in population spike amplitude was seen in the ECS group. We conclude that the modified procedure does not protect rats against the long-lasting enhancement of evoked potentials. Similar changes may be occurring in the brains of patients subjected to modified ECT.

Seizure threshold to lidocaine is decreased following repeated ECS (electroconvulsive shock).

Seizure susceptibility to lidocaine was investigated in rats which had received repeated ECS (electroconvulsive shock). In the first experiment three groups of rats received an ECS daily for 18 days, an ECS weekly for 18 weeks, and 18 sham treatments, respectively. Twelve weeks after the last ECS all rats received a lidocaine challenge (LC) in the form of an intraperitoneal (IP) injection of lidocaine (65 mg/kg). After the injection the animals were observed for occurrence of motor seizures. A total of 67% (10/15), 47% (7/15), and 0% (0/18) of the daily, weekly, and sham groups, respectively, had motor seizures in response to the LC. In the second experiment five groups of rats received an ECS daily for 0, 1, 6, 18, and 36 days, respectively. Eighteen weeks after the last ECS all rats received an LC and 0% (0/15), 13% (2/15), 20% (3/15), 53% (8/15), and 58% (7/12), respectively, developed seizures in response to the LC. In the third experiment two groups of rats received daily ECS and sham-ECS, respectively. Twenty-four hours after the last ECS all rats received an LC. A total of 60% (9/15) of the ECS group and 0% (0/10) of the sham-ECS group had seizures in response to the LC.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chronic electroconvulsive shock on interstitial concentrations of dopamine in the nucleus accumbens

There is accumulating evidence that chronic electroconvulsive shock (ECS) can increase the functional output of central dopaminergic systems. The present experiments investigated the effects of acute and chronic ECS on interstitial concentrations of dopamine (DA) in the nucleus accumbens (NAC) using in vivo microdialysis in awake freely moving rats. ECS (150 V, 0.75 s) increased interstitial concentrations of DA, DOPAC and HVA to approximately 130% of baseline values. The magnitude of the ECS-induced increase in DA was not affected by chronic ECS. In contrast, the response of the DA metabolites was attenuated in the chronic ECS group. Chronic ECS did not influence apomorphine (25 micrograms/kg, SC)-induced decreases in extracellular concentrations of DA or its metabolites in the NAC, thus providing no support for the hypothesis that chronic ECS produces subsensitivity of DA autoreceptors. d-Amphetamine (1.5 mg/kg SC)-induced increases in extracellular DA were significantly prolonged in the NAC of the chronic ECS group. In accordance with previous reports, the locomotor stimulant effects of d-amphetamine were also enhanced in the chronic ECS group. These data provide further evidence that chronic ECS can increase certain behavioral and neurochemical indices of meso-accumbens DA function.

Electroconvulsive shock stimulates polyphosphoinositide degradation and inositol trisphosphate accumulation in rat cerebrum: lithium pretreatment does not potentiate these changes

Using an in vivo model, we explored the acute effects of electroconvulsive shock (ECS) and lithium on rat cerebral polyphosphoinositides and inositol phosphates. ECS was shown to increase the [ 3H]inositol trisphosphate ([ 3H]IP 3) by 75%, decrease the endogenous mass of phosphatidylinositol 4,5-bisphosphate (PIP 2) by 23%, and enhance [ 3H] myo-inositol labeling into the polyphosphoinositides. In contrast, lithium pretreatment 20–24 h prior to ECS appeared to attenuate the ECS-induced [ 3H]IP 3 increase and the decrease in mass of PIP 2; [ 3H]inositol monophosphate ([ 3H]IP 1) levels demonstrated no differences between the lithium ECS and lithium-alone groups. These results indicate that ECS stimulates the inositol lipid cycle in brain possibly due to neurotransmitter release. Moreover, the effects of lithium suggest other possible sites of action of this cation on inositol lipid metabolism in addition to an inhibition of inositol-1-phosphatase.

Repeated electroconvulsive shock (ECS) and morphine tolerance: Demonstration of cross-sensitivity in the rat

In a complementary set of studies, we found that nine days of electroconvulsive shock (ECS) sensitized opiate-naive rats to the acute effects of a single morphine injection and, conversely, the induction of morphine tolerance by morphine pellet implantation sensitized ECS-naive rats to the acute opiate-like effects of a single ECS. Colonic temperatures were significantly elevated and body weight gains were significantly diminished in the repeated ECS group 24 hrs following the final ECS treatment. Likewise, morphine pellet implantation for three days resulted in significantly elevated colonic temperatures and decreased body weight gains. The cross-sensitivity between repeated ECS and morphine tolerance as well as the common effects of these two procedures on body weight and colonic temperature suggests that the physiological changes following repeated ECS and the induction of morphine tolerance may share common neurobiological mechanisms.

Alterations of amygdaloid kindling phenomenon following repeated electroconvulsive shocks in rats.

In this study we investigated the effect of the electroconvulsive shock (ECS) soon after each amygdaloid stimulation (KS) upon the development of a kindling phenomenon. Thirty male Wistar albino rats were used in this study. Once daily stimulation of 200 microA, 1 msec, 60 Hz, 2 sec train by the right amygdaloid stimulation electrodes and the recording of the EEG were done. Rats of the Kindling + ECS group received the ECS through the clipped ears for five minutes after the KS. Behavioral manifestations, the duration of afterdischarge and the numbers of spikes were counted for five minutes at the time of every stimulation. The numbers of times the KS required to develop each stage were stage 1:4.8, stage 2:8, stage 3:8.6, stage 4:9.6, stage 5:12.6, respectively, on the kindling group. On the ECS-treated group, those were stage 1:8, stage 2:17, stage 3:18, stage 4: more than 20. The ECS soon after the amygdaloid stimulation retarded the process of kindling significantly. This result is consistent with the hypothesis that the electroconvulsive shocks disturb the information of the synaptic pathway before the consolidation of a central neuroplastic change underlying kindling.

The effect of electroconvulsive shock on body weight, food intake and water intake in the rat

Body weight, food intake, fecal boli and water intake were measured every 12 hr for 6 days before and 6 days after the administration of a single 50 mA electroconvulsive shock (ECS) to male albino rats. The ECS group showed reduced levels on all measures during the 24 hr following ECS, and began to regain control values for food intake, fecal boli and water intake within 3–4 days. Body weights, however, remained depressed 6 days after ECS. These findings confirm and extend previous research indicating that ECS has effects on basic parameters not associated with amnesia for acquired responses.

Effect of Electroconvulsive Shock (ECS) on Extinction of an Approach Response

Aversive effects of ECS were studied by comparing the effect of ECS on the extinction of a well developed approach response under two conditions. Rats pretrained to run a straight alley were given ECS immediately after (5 sec.), or 1 hr. after entering the goal box. No significant differences occurred until the fifth trial when the Immediate ECS group showed significantly longer approach latencies.