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.     

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A single electroconvulsive shock (ECS) or a sham ECS was administered to male 3-4-month-old Wistar rats 1, 2, and 4 h before training in an inhibitory avoidance test and in cued classical fear conditioning (measured by means of freezing time in a new environment). ECS impaired inhibitory avoidance at all times and, at 1 or 2 h before training, reduced freezing time before and after re-presentation of the ECS. These results are interpreted as a transient conditioned stimulus (CS)-induced anxiolytic or analgesic effect lasting about 2 h after a single treatment, in addition to the known amnesic effect of the stimulus. This suggests that the effect of anterograde learning impairment is demonstrated unequivocally only when the analgesic/anxiolytic effect is over (about 4 h after ECS administration) and that this impairment of learning is selective, affecting inhibitory avoidance but not classical fear conditioning to a discrete stimulus.     

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The effect of the Ca2+ blocker verapamil on amnesia induced by electroconvulsive shock (ECS) or by the alpha-adrenoceptor agonist clonidine was studied in male Wistar rats trained in passive avoidance task ("step down"). Clonidine (0.1 mg/kg, i.p.) and ECS induced a pronounced amnesia, significantly reducing the percentage of rats that had acquired the task upon retention tests, given 3 h, 24 h and 7 days after training. Verapamil (10 mg/kg) administered orally for 12 days (5 days before and 7 days after training) completely abolished the ECS- or clonidine-induced amnesia. These data suggest that calcium channel blocker verapamil has a protective effect against experimentally provoked memory deficit and might be useful for the treatment of cognitive disorders.     

Source of cues for cue-dependent amnesia in rats.

In 2 experiments 54 Sprague-Dawley male albino rats were given extensive training in a complicated appetitive maze and then handled extensively for 7 days. On the 7th day of the retention interval some Ss were exposed to the "cognitive" learning cues of the maze and some were not. Immediately afterward Ss were given ECS or sham ECS. To the extent that cognitive learning cues are assumed to activate memory, the ECS impaired retrieval of memory only for those Ss which had the cues reinstated prior to ECS administration. It appears that memory must be active at the time of ECS in order to obtain retrieval deficits. In a 3rd experiment with 36 Ss the intensity of hunger drive, manipulated by the amount of prefeeding, was not a cue for memory activation and subsequent cue-dependent amnesia. Arousal is therefore not believed to be crucial for the effect. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Electroconvulsive shock (ECS) does not facilitate the development of kindling

1. For many years it has been discussed whether repeated electroconvulsive shock (ECS) may induce a lasting epileptogenic effect on the brain (i.e. a kindling effect). In the present study the authors investigated whether weekly ECS do exert such an effect. 2. Bipolar electrodes were implanted in amygdala of 32 rats. Following a two to three week recovery period the rats were randomly allocated to two groups. One group received 12 weekly ECS, the other 12 weekly sham-ECS. 3. Three months after the last ECS/sham-ECS, kindling was initiated. Daily stimulation, eliciting an EEG-afterdischarge was given to all the rats. The animals received a total of 15 stimulations. 4. ECS-pretreated animals did not kindle faster than the sham-group. The two groups reached stage 4 (clonic rearing) after 5.8 (ECS-group) and 5.7 (sham-group) stimulations, respectively. 5. The authors did not find a facilitated development of kindling following ECS, instead they observed a slight, yet statistically significant inhibition of the development of the maximally generalized kindling-seizure--the stage 5 seizure--in the ECS-group. 6. In conclusion: The present study did not show a kindling effect of weekly ECS suggesting that kindling requires more than repeated elicitation of after-discharge.     

Effects of chronic lithium and electroconvulsive stimuli on cholecystokinin mRNA expression in the rat brain

This study compares the effect of lithium (Li+) and electroconvulsive stimuli (ECS), two treatments commonly used in the treatment of affective disorders, on CCK mRNA expression in the rat brain. Two groups of rats receiving either 4 week Li+ or vehicle food supplementation and two groups receiving 6 ECS or 6 sham ECS during 2 weeks were studied. A significant decrease in CCK mRNA levels was seen in the caudate putamen both after Li+ as compared to vehicle and ECS as compared to sham ECS, 27 and 25%, respectively. A small (10%), yet significant, decrease was also seen in the inner entorhinal cortex after Li+. The results indicate that both Li+ and ECS inhibit CCK synthesis in the caudate putamen and are consistent with other findings of presumed decreased dopaminergic action in this part of the brain following these treatments.     

Electroconvulsive shocks exacerbate the heightened acoustic startle response in stressed rats.

Electroconvulsive therapy (ECT) has been successfully used in the treatment of depression, particularly when the illness is refractory to pharmacological therapy. A recent study has shown that ECT is also effective in reducing both depressive and posttraumatic stress disorder (PTSD) symptoms in patients with major depression (MDD) and co-occurring PTSD. This raises the possibility that ECT might be effective in the treatment of PTSD, a disease whose prevalence has increased substantially in recent years. A characteristic symptom of PTSD is an exaggerated reactivity to startling sounds (acoustic startle response; ASR). In the present study, we investigated the effects of electroconvulsive shocks (ECS) on the ASR, in a rat model of traumatic stress. The animals were subjected to a restraint/tailshock paradigm and then administered ECS. ASR measurements were obtained at several time points following ECS administration. Although ECS had no effect in control rats, it significantly exacerbated the already potentiated ASR in the stressed group. While ECT may prove to be an effective treatment for certain symptoms of co-occurring MDD/PTSD or PTSD alone, it may exacerbate heightened arousal associated with PTSD. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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Two once-daily electroconvulsive shocks (ECS) produced retrograde amnesia in rats trained on a Hebb-Williams maze; Verapamil (12.5 mg/kg, i.p.) or felodipine (10 mg/kg, p.o.) administered half an hour before each ECS attenuated this ECS-induced amnesia. Hence, these drugs may hold promise for the containment of amnesia induced by electroconvulsive therapy (ECT). Speculatively, one or more of several mechanisms may be involved: cerebral vasodilatation, enhancement of cholinergic tone, and inhibition of calcium-mediated impairment of neuronal function. These drugs may also act by attenuating the systolic surge in blood pressure during ECT, thereby decreasing edema due to cerebral hyperperfusion, as well as decreasing the possible transfer of potentially neurotoxic macromolecules through a putative breach in the blood-brain barrier.     

Effects of nimodipine, felodipine and amlodipine on electroconvulsive shock-induced amnesia in the rat

The effects of various doses (0.03, 0.1, 0.3 or 1.0 mg/kg) of the Ca2+ channel blockers nimodipine, felodipine and amlodipine on the learning ability of rats exposed to electroconvulsive shock were examined. The animals were trained in a passive avoidance procedure. The drugs tested were injected 30 min before the learning trial started. The electroconvulsive shock was given immediately after the learning trial response had been acquired. A passive avoidance retention test was performed 24 h later. It was found that electroconvulsive shock strongly impaired the retention of the passive avoidance response. Nimodipine, felodipine and amlodipine did not influence the passive avoidance behavior in the sham electroconvulsive shock group, but significantly improved the retention deficits in the animals exposed to electroconvulsive shock. These findings support the hypothesis that perturbations in Ca2+ homeostasis can contribute to the memory deficits associated with electroconvulsive shock. The antiamnestic effects of the substances tested make them interesting candidates for clinical trials in patients with cognitive impairment caused by electroconvulsive shock therapy.     

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A variety of neurotransmitter receptor changes occur after a course of electroconvulsive seizures (ECS) in rats, including an increased density of adenosine A1 sites. Adenosine antagonism has been related to the proconvulsant action of methylxanthines such as caffeine. We determined tonic-clonic seizure duration in rats given ECS with caffeine (0-175 mg/kg, IP) after a course of one or six daily ECS. A single day of ECS did not affect the dose-dependent proconvulsant action of caffeine. After six daily ECS, the proconvulsant action of caffeine was reduced. After nine daily ECS, an A1 antagonist (8-cyclopentyl-1,3-dipropylxanthine) and an A2A antagonist (1-allyl-3,7-dimethyl-8-p-sulfophenylxanthine) showed reduced proconvulsant activity. The results suggest that the reduced proconvulsant action of caffeine after chronic ECS depends on adenosine antagonism.     

Refractory hypothalamic adenylate cyclase in anorectic tumor-bearing rats: implications for NPY-induced feeding

Entorhinal-dentate evoked potentials were measured in rats before and after: (1) eight electroconvulsive shock (ECS) seizures, or (2) matched handling. In animals that received ECS, evoked potentials were significantly enhanced, as evidenced by a long-lasting increase in the amplitude of the population spike. This increase in population-spike amplitude lasted for at least 3 months after the last ECS trial. No evoked-potential changes were observed in the subjects that received matched handling. These data suggest that ECS seizures produce long-lasting, perhaps permanent, changes in the brain.     

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1. The effect of electroconvulsive shock (ECS) on the extracellular concentration of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) was examined in the frontal cortex of rats with the use of in vivo microdialysis. 2. The extracellular concentration of DOPAC, HVA and 5-HIAA was largely increased after the first ECS treatment. The increase after the eighth ECS treatment tended to be attenuated or was significantly attenuated as compared to that after the first ECS treatment. The baseline concentration of DOPAC and 5-HIAA was significantly increased after repeated ECS, though that of DA and HVA did not show any significant change after repeated ECS. 3. These results suggest that the activating effect of repeated ECT on 5-hydroxytryptaminergic (5-HT) and DA neurotransmission, (especially on 5-HT neurotransmission), is significant in improving depression both in patients with Parkinson's disease (PD) and in those who do not suffer from PD.     

Passive avoidance behavior in rats after electroconvulsive shock: Facilitative effect of response retardation.

In 3 experiments, a total of 178 male Wistar rats were trained in a one-trial passive avoidance task and then were submitted to electroconvulsive shock (ECS) or to sham ECS. 24 hrs later they were tested for retention, with the door opened either immediately or 30 sec after the beginning of the test. Ss initially forced to avoid for 30 sec continued to avoid for the entire test, but the others had the usual low step-through latencies seen with ECS-treated Ss. Activity measures for those Ss stepping through differentiated groups having received footshock from those not having footshock and ECS. A retest 5-10 min later showed "recovery" in the amnestic Ss and continued avoidance behavior for those that avoided on the first test. Results are taken as evidence that ECS effects are not on memory storage but on the capacity of the animal to organize information effectively and quickly in order to produce an adaptive response. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Preliminary comparison of behavioral and biochemical effects of chronic transcranial magnetic stimulation and electroconvulsive shock in the rat

To confirm the assumption that repetitive rapid-rate transcranial magnetic stimulation (TMS) induces the functional and structural changes analogous to those which are evoked during electroconvulsive shock (ECS), we compared now the effects of treatments with TMS and ECS on the behavioral responses in rats. We also tested the reactivity of the cyclic adenosine monophosphate (AMP) generating system in cerebral cortical slices. TMS similarly to ECS shortened the immobility time in the forced swimming test and produced a depression of responsiveness of the noradrenaline-stimulated cyclic AMP generating system, although the significance of the latter effect was borderline. In contrast to ECT, TMS produced no such immediate behavioral effects as analgesia and depression of the early phase of locomotor activity. The data suggest that TMS produces in rats some responses that are regarded as predictive for antidepressant activity, similar to those produced by ECS, but less adverse effects.     

Seizures, memory and synaptic plasticity

Electrophysiological studies of the rodent hippocampus show that repeated seizure activity has a profound, deleterious effect on an important form of synaptic plasticity (long-term potentiation, LTP) which has been suggested to underlie memory formation. It appears that seizure activity incrementally causes an indiscriminate and widespread induction of long-term potentiation, consuming and thereby reducing overall hippocampal plasticity available for information processing. Consistent with this finding, severe deficits in a form of learning known to be mediated by hippocampal function are observed in rat subjected to repeated electroconvulsive seizures (ECS). The effect on synaptic function gradually resolves over a period of around 40 days, paralleling the time course of the transitory cognitive impairment seen following electrical seizure induction (ECT) in humans being treated for severe affective disorder. The effect is likely to be mediated by NMDA receptor activation during seizure activity, as the phenomenon can be prevented by the administration of a non-competitive NMDA receptor associated channel blocker (ketamine) immediately before seizure induction. The mechanisms described may account for the inter-ictal cognitive disturbance observed in patients suffering from poorly controlled epilepsy.     

An experimental model of acute encephalopathy after total body irradiation in the rat: effect of liposome-entrapped Cu/Zn superoxide dismutase

PURPOSE: To develop an experimental model of acute encephalopathy following total body irradiation in rats and to define the therapeutic effect of liposome-entrapped Cu/Zn superoxide dismutase. METHODS AND MATERIALS: A total of 120 4-month-old rats received 4.5 Gy total body irradiation (TBI) while 120 rats received sham irradiation. A behavioral study based on a conditioning test of negative reinforcement, the one-way avoidance test, was performed 5 hours before irradiation and repeated the following days. Subcutaneous treatment was started 1 hour after irradiation and repeated daily for 2 weeks. In both the irradiated and sham group, three subgroups were defined according to the treatment received: liposome-entrapped Cu/Zn superoxide dismutase (0.5 mg/kg), liposomes only, normal saline. RESULTS: This work comprised two consecutive studies. In study A (90 rats) the one-way avoidance test was administered daily from day 0 to day 4 with a recall session at day 14. In study B (validation phase in 150 rats) the behavioral test was performed only from day 0 to day 6. Before irradiation, all rats showed a similar behavioral response. Study A (6 groups of 15 rats): Following TBI, irradiated rats treated with liposomes only or saline demonstrated a significant delay in learning the one-way avoidance test in comparison with sham-irradiated rats (0.05 < p <0.001 depending upon the day of evaluation and the subgroup type). In contrast, irradiated rats treated with liposome-entrapped Cu/Zn superoxide dismutase did not differ from sham-irradiated rats. Study B (6 groups of 25 rats): The results were the same as those in study A, demonstrating a significant delay in the learning of the test in the liposome and saline-treated irradiated rats in comparison with sham-irradiated rats (0.02 < p < 0.001). The irradiated rats, treated with liposome-entrapped Cu/Zn superoxide dismutase did not differ from the sham-irradiated controls. CONCLUSION: This study indicates that a relatively low dose of total body irradiation induces a substantial acute learning dysfunction in the rat. This effect is prevented by the administration of liposome-entrapped Cu/Zn superoxide dismutase.     

Factors in the modification by isolation of electroconvulsive shock-produced retrograde amnesia in the rat.

Cites earlier research which demonstrated that placing rats in a sensory-restricted environment during the electroconvulsive shock- (ECS) retention interval following 1-trial appetitive learning will prevent or eliminate ECS-produced retrograde amnesia. Exp I replicated this finding using 32 male Dublin albino rats in a 1-trial aversive learning task, indicating that this effect is not task specific. Exp II attempted to determine whether illumination or the restricted environment was the crucial factor in this phenomenon. 64 male Sprague-Dawley rats placed in the light during the ECS-retention interval, whether restricted or in the colony, demonstrated retrograde amnesia after ECS. However, Ss left in the dark during this interval demonstrated little, if any, retention deficit particularly if this condition was combined with sensory isolation. These studies further indicate that manipulation of S's general environment after ECS can alter ECS-produced retention losses. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Retrograde effects of electroconvulsive shock on learned responses.

Indicates that electroconvulsive shock (ECS) has 3 different effects on responses learned prior to its administration. 1st, the aversive effect of ECS, demonstrable in 1 trial but usually found after repeated presentations, can produce a delay-of-punishment gradient. 2nd, ECS apparently differentially affects memory depending upon the learning-ECS interval, an effect which can be interpreted as disruption of memory consolidation. The postlearning interval during which ECS produces temporally graded memory effects is very brief, probably well under 1 min. The 3rd effect of ECS is the halting of the incubation, i.e., the development over time, of a punishment-produced conditioned emotional response. In the passive avoidance learning situation, incubation disruption and memory disruption have identical behavioral consequences in that in both cases Ss tend to repeat the previously punished response. The postpunishment time course of incubation is relatively long, with maximum response suppression occurring between 1 and 4 hr. after punishment. The ECS disruption of the long-term incubation process has frequently been misinterpreted as ECS disruption of a long-term memory consolidation process. (60 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Autobiographical memory and mood: Effects of electroconvulsive therapy.

An Autobiographical Memory Interview (AMI) was administered to 75 depressed inpatients and 16 nondepressed controls. Patients were randomized to 1 of 4 forms of electroconvulsive therapy (ECT) that varied in electrode placement and stimulus intensity. Short-term retrograde amnesia was assessed during the week following the randomized phase. Bilateral ECT produced more marked deficits than right unilateral ECT. At a 2-mo follow-up, persistent amnesic deficits were related to having received a second ECT course and, to a lesser extent, bilateral ECT during the randomized phase. The magnitude of clinical improvement was not associated with amnesia scores at either time point. There were no differential amnesic effects as a function of the affective valence of memories. It appears that retrograde amnesia for autobiographical information after ECT and mood congruence effects on recall are independent phenomena. The magnitude and persistence of retrograde amnesia is related to how ECT is performed and not to changes in clinical state or the affective valence of memories. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

ECS in one-trial appetitive learning of rats: Retention and amnesia.

Conducted 4 experiments with 214 male hooded rats to assess the kind and degree of amnesia induced by ECS following a 1-trial appetitive learning experience. Exp I (n = 30) and II (n = 60) show that although there is a definite amnesia that cannot be explained as an artifact of ECS-induced aversiveness, some memory of the experience does survive the ECS. Exp III (n = 96) suggests that this memory is for the novelty aspects of the learning experience, while there is at least a partial amnesia for the positive reinforcement received. Results of a 4th experiment (n = 28) suggest that the ECS has the effect of interrupting or preventing the classification of a novel object as reinforcing or nonreinforcing. (PsycINFO Database Record (c) 2010 APA, all rights reserved)