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At least 19 recordsLinked to original sources
PubMed1995

Spatiotemporal selective effects on brain-derived neurotrophic factor and trkB messenger RNA in rat hippocampus by electroconvulsive shock.

Electroconvulsive therapy is used in the treatment of affective disorders and schizophrenia and experimental electroconvulsive shock may serve as an animal model for this treatment. The aim of this study was to investigate a possible role for neurotrophins in the mechanism of action of experimental electroconvulsive shock and thus in clinical electroconvulsive therapy. The effect of electroconvulsive shock on levels of messenger RNAs encoding the neurotrophin brain-derived neurotrophic factor and the receptor trkB in rat hippocampus was determined by in situ hybridization with RNA probes 1, 3, 9 and 27 h following the shock. Brain-derived neurotrophic factor messenger RNA levels were increased at 1, 3 and 9 h following the shock and normalized after 27 h. Granule cells of the dentate gyrus showed a more rapid response as compared to hilar cells and pyramidal cells of CA1. Total trkB messenger RNA levels, including the transcripts for both the truncated and full length trkB receptor protein (gp95trkB and gp145trkB, respectively), showed a pattern of increase very similar to that of the brain-derived neurotrophic factor messenger RNA. However, using a probe selective for the full length (gp145trkB) trkB messenger RNA, we determined a delayed pattern of activation with significant increase only at 3 and 9 h after the shock. In hippocampus total trkB messenger RNA was found to consist of approximately one-quarter of mRNA encoding gp145trkB and three-quarters encoding gp95trkB as revealed by RNAase protection. While brain-derived neurotrophic factor and the truncated trkB messenger RNAs appear to increase with a similar pattern, suggesting a similar mechanism of activation by electroconvulsive shock, full length receptor trkB messenger RNA appears to increase with a delayed pattern suggesting a separate mechanism of activation. Electroconvulsive shock-induced seizures seem to include activation of a brain neurotrophin known to be important for neuronal plasticity.

Animals↗
PubMed1987

On the mechanism of potentiation of apomorphine-induced stereotypy due to electroconvulsive shock.

Electroconvulsive shock-induced changes in the intensity of stereotype induced by apomorphine, the binding of [3H]spiroperidol in the corpus striatum, the accumulation of [3H]dopamine in brain and the permeability of the blood-brain barrier, were monitored in rats 30 min after single, or 24 hr after chronic (once daily for 7 days) electroconvulsive shock. There was significant potentiation in stereotypy induced by apomorphine after chronic electroconvulsive shock. The binding of [3H]spiroperidol did not show any change in the affinity (Kd) or density (Bmax) of receptors in the striatum after acute or chronic electroconvulsive shock. The accumulation of dopamine increased significantly in the hypothalamus after acute electroconvulsive shock and in the corpus striatum and hypothalamus after chronic electroconvulsive shock. A significant increase in the entry of sodium fluorescein into the hypothalamus occurred after acute electroconvulsive shock; it increased in all the regions of the brain after chronic electroconvulsive shock. Alteration in the blood-brain barrier (BBB) by electroconvulsive shock leading to increased accumulation of dopamine in the corpus striatum may be responsible for the potentiation of stereotypy.

Animals↗
PubMed1981

Cytophotometric and morphometric studies of postnatal rat hippocampal neurons and perineuronal gliocytes after electroconvulsive shock.

Electroconvulsive shock was evoked by transcorneal electric current (50 Hz, 50 mA; 3 times by 0.2s with 10-min pauses) in 10-day and 20-day old rats. 2 hours after the end of the convulsions, the total cytoplasmic RNA and protein content per cell in CA3 hippocampal neurons has been shown cytospectrophotometrically to increase markedly in 10-day old rats without statistically significant changes in 20-day old animals. No changes in the RNA and protein content were found in perineuronal neuroglia cells in the CA3 hippocampus in both age groups of rats. Morphometric determinations revealed a pronounced augmentation of volumes of the hippocampal neuronal bodies, nuclei, and cytoplasm as well as of nucleo-cytoplasmic ratio in 10-day old rats under effect of electroconvulsive shock. In 20-day old rats, the shock led to less marked increase in volumes of the hippocampal neurons, with no changes in nucleo-cytoplasmic ratio.

Aging↗
PubMed1967

Recovery of memory after amnesia induced by electroconvulsive shock.

Electroconvulsive shock given to rats immediately after one-trial avoidance learning produced a significant amnesic effect 24 hours later; this amnesia had largely disappeared in further retention tests 48 and 72 hours after treatment. This result puts in question a basic assumption implicit in most memory consolidation studies that such amnesic effects will be permanent.

Amnesia↗
PubMed1966

Sleep: suppression of rapid eye movement phase in the cat after electroconvulsive shock.

Electroconvulsive shock, administered for 5 to 7 days, reduced the daily rapid eye movement sleep time of seven cats to as little as 28 percent of base line levels. After day 4, eye movements during periods of cortical activation without tonic electromyographic activity were greatlyreduced. Although partially deprived of rapid eye movements for as long as 7 days, the cats showed no compensatory rise in rapid eye movement time during the recovery period, but controls equally deprived gave significant rebounds. Rapid eye movement time of anesthetized cats was not affected by current that usually produces con vulsions; it was lowered in animals convulsed with metrazol, but the same dosage of this drug, administered so as to avoid convulsions, had little eflect. It appears that some aspect of the convulsion is responsible for lowering the rapid eye movement time.

Animals↗
PubMed1991

GABAA receptor mRNAs are increased after electroconvulsive shock.

Electroconvulsive shock (ECS) has been reported to alter brain second-messengers and neurotransmitter systems, including the gamma-aminobutyric acid (GABAergic) system, and to increase messenger ribonucleic acid (mRNA) for the proto-oncogene c-fos. We evaluated mRNA for the most abundant GABAA receptor subunits, alpha 1 and gamma 2, in brain regions after a single ECS in mice. Alpha 1 and gamma 2 mRNAs were unchanged from controls at 2 hrs after ECS, but both were significantly elevated in cerebellum and hippocampus after 4 hrs. This alteration persisted in cerebellum for alpha 1 mRNA at 8 hrs, but resolved for gamma 2 mRNA in cerebellum and for both subunit mRNAs in hippocampus. No changes in mRNA were observed in cortex for either subunit and no changes in either mRNA were observed in brain regions of sham-treated mice. Thus, ECS appears to be associated with a rapid, reversible increase in GABAA receptor subunit mRNAs in several brain regions.

Animals↗
PubMed2000

Differential changes in the expression of cyclic nucleotide phosphodiesterase isoforms in rat brains by chronic treatment with electroconvulsive shock.

Electroconvulsive shock (ECS) has been suggested to affect cAMP signaling pathways to exert therapeutic effects. ECS was recently reported to increase the expression of PDE4 isoforms in rat brain, however, these studies were limited to PDE4 family in the cerebral cortex and hippocampus. Thus, for comprehensive understanding of how ECS regulates PDE activity, the present study was performed to determine whether chronic ECS treatment induces differential changes in the expression of all the PDE isoforms in rat brains. We analyzed the mRNA expression of PDE isoforms in the rat hippocampus and striatum using reverse transcription polymerase chain reaction. We found chronic ECS treatment induced differential changes in the expression of PDE isoform 1, 2, 3, 4, 5 and 7 at the rat hippocampus and striatum. In the hippocampus, the expression of PDE1A/B (694%), PDE4A (158%), PDE4B (323 %), and PDE4D (181%) isoforms was increased from the controls, but the expression of PDE2 (62.8%) and PDE7 (37.8%) decreased by chronic ECS treatment. In the striatum, the expression of PDE1A/B (179%), PDE4A (223%), PDE4B (171%), and PDE4D (327%) was increased by chronic ECS treatment with the concomitant decrease in the expression of PDE2 (78.4%) and PDE3A (67.1%). In conclusion, chronic ECS treatment induces differential changes in the expression of most PDE isoforms including PDE1, PDE2, PDE3, PDE4, PDE5, and PDE7 in the rat hippocampus and striatum in an isoform- and brain region-specific manner. Such differential change is suggested to play an important role in regulation of the activity of PDE and cAMP system by ECS.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1986

Studies on the effects of opioid, noradrenergic and serotonergic antagonists on the antinociceptive effects of electroconvulsive shock.

Electroconvulsive shock (ECS) evoked a short-latencied elevation in the hot plate and tail flick response latencies. Naloxone administered before or immediately after ECS produced a dose-dependent antagonism of the antinociceptive effect measured at 7 min but not at 2 min after ECS. Intrathecally administered propranolol, methysergide or naloxone had no effect when administered either before or after ECS. In contrast, phentolamine given intrathecally produced a significant antagonism of the reflex latencies otherwise elevated after ECS. These effects appear mediated by an alpha 2-receptor as they were more readily antagonized by yohimbine than prazosin. These observations suggest the presence of two systems, one supraspinal and opioid in character and the other adrenergic with spinal receptors. The differential effects of injecting naloxone before and after ECS suggests that the opioid system is activated between 2 and 5 min after the ECS, while the adrenergic system, as examined by the effects of intrathecal alpha- and alpha 2-antagonists, appears to be activated immediately after the application of the ECS.

Analgesia↗
PubMed1999

Differential activation of c-Jun N-terminal protein kinase and p38 in rat hippocampus and cerebellum after electroconvulsive shock.

Electroconvulsive shock (ECS), an effective treatment for psychiatric diseases, has been reported to induce immediate-early genes (IEGs) and to activate p42 and p44 MAPKs (ERK-1 and ERK-2) in rat brain. In this study, we examined the activation of the other members of MAPK family, c-Jun N-terminal protein kinase (JNK/SAPK) and p38. Following ECS, the phosphorylation of p38 was substantially increased in both hippocampus and cerebellum, but the increase of JNK phosphorylation was observed only in hippocampus. We also investigated the phosphorylation of their upstream kinases, SEK-1, MKK6 and MKK3. In both hippocampus and cerebellum, the phosphorylation of MKK6 showed closer correlation with p38 phosphorylation than that of MKK3. However, SEK-1, known as upstream kinase of JNK and p38 in vitro, corresponded with none of MAPKs. These results, with previous reports on the activation of ERK, indicate that ECS activates three MAPKs differentially in rat hippocampus and cerebellum, and suggest the possibility that unknown MAPKK may be involved in the activation of JNK in rat brain after ECS.

Animals↗
PubMedDate not supplied

Pre-test administration of beta-endorphin, or of electroconvulsive shock reverses the memory disruptive effect of posttraining electroconvulsive shock.

Memory disruption by posttraining electroconvulsive shock was studied in adult Wistar rats using three different tasks: step-down inhibitory avoidance, two-way active avoidance, and habituation of rearing to an open field. The animals were given training and test sessions 24 hours apart in each of these tasks. Immediate posttraining transcorneal, 15 mA, 60 Hz, 2 sec electroconvulsive shock disrupted memory of the three tasks. The effect was completely reversed by the IP administration of beta-endorphin (2.0 micrograms/kg), 6 min prior to testing, or of another electroconvulsive shock, 30 min prior to testing. These findings indicate that the posttraining electroconvulsive shock did not affect memory storage. In view of the fact that electroconvulsive shock has been previously shown to cause a pronounced decrease of brain beta-endorphin immunoreactivity, attributable to a release of the peptide, the present findings can be interpreted as showing that memory disruption by posttraining electroconvulsive shock results from the induction of state dependency on beta-endorphin.

Animals↗
PubMed1983

Alteration of electroconvulsive threshold by cerebrospinal fluid from cats tolerant to electroconvulsive shock.

Daily electroconvulsive shocks for 22 days resulted in a progressive elevation of electroconvulsive threshold. When these shocks were discontinued, the thresholds returned to untreated levels in approximately 20 days. Cerebrospinal fluid collected from cats with elevated thresholds and repeatedly transferred to the ventricular space of untreated animals elevated the electroconvulsive threshold of the recipient. This finding demonstrates that a substance present in the cerebrospinal fluid of cats with elevated electroconvulsive threshold can alter the threshold of untreated animals.

Animals↗
PubMed2000

Neurogenesis in the dentate gyrus of the rat following electroconvulsive shock seizures.

Electroconvulsive shock (ECS) seizures provide an animal model of electroconvulsive therapy (ECT) in humans. Recent evidence indicates that repeated ECS seizures can induce long-term structural and functional changes in the brain, similar to those found in other seizure models. We have examined the effects of ECS on neurogenesis in the dentate gyrus of the adult rat using bromodeoxyuridine (BrdU) immunohistochemistry, which identifies newly generated cells. Cells have also been labeled for neuronal nuclear protein (NeuN) to identify neurons. One month following eight ECS seizures, ECS-treated rats had approximately twice as many BrdU-positive cells as sham-treated controls. Eighty-eight percent of newly generated cells colabeled with NeuN in ECS-treated subjects, compared to 83% in sham-treated controls. These data suggest that there is a net increase in neurogenesis within the hippocampal dentate gyrus following ECS treatment. Similar increases have been reported following kindling and kainic acid- or pilocarpine-induced status epilepticus. Increased neurogenesis appears to be a general response to seizure activity and may play a role in the therapeutic effects of ECT.

Animals↗
PubMed2001

Regulation of expression and enzymatic activities of tyrosine and tryptophan hydroxylases in rat brain after acute electroconvulsive shock.

Acute electroconvulsive shock (ECS) causes a significant increase of protein synthesis in depressive patients and such an increase raises the possibility that the regulation of specific proteins and enzymatic activities in the brain might be one of the mechanisms required for the induction of long-term adaptive neurochemical changes after electroconvulsive therapy. In current studies, we investigated and compared simultaneously the short- and long-term effects of an acute ECS on the expression and enzymatic activities of both tyrosine and tryptophan hydroxylases (TH and TpOH, respectively) in different rat brain areas. Our results demonstrated that an acute ECS produced: (1) a long-lasting decrease in TH and TpOH protein levels in locus ceruleus (LC), ventral tegmental area (VTA) and in TpOH protein level in the raphe centralis (RC), maximal at 72 h, with concomitant changes in mRNA levels and enzymatic activities in the LC only; (2) large increase of TpOH protein levels in the frontal cortex (Cxf) (+145%) and increase of TH protein levels in the hippocampus (Hip) (+207%), maximal at 72 h and 7 days which was not accompanied by corresponding increase of in vivo enzymatic activities. Furthermore, a second ECS increased in vivo TpOH activity in the Cxf (+19%) while decreasing K(m) value (-50%) for tetrahydrobiopterin cofactor. A stability of the observed findings on TpOH activity in the Cxf after repeated ECS might be one of the mechanisms for the antidepressant effects of electroconvulsive therapy.

5-Hydroxytryptophan↗
PubMed1977

Intensification of the alcohol withdrawal syndrome following periodic electroconvulsive shocks.

Repeated electroconvulsive shocks (ECSs) administered once every 3 days to rats at either of two current intensities led to a progressive intensification of the motor seizure pattern. Moreover, the incidence of convulsive symptoms elicited by subsequent alcohol exposure and withdrawal was greatly increased by prior exposure to the repeated ECSs. These results illustrate a treatment--drug interaction which could have hazardous consequences for patients undergoing electroconvulsive therapy. Thus, until the appropriate tests can be conducted on human patients, drug intake following electroconvulsive therapy should be carefully regulated.

Alcoholism↗
PubMed2001

Isoform-specific changes of adenylate cyclase mRNA expression in rat brains following chronic electroconvulsive shock.

1. Electroconvulsive shock (ECS) has been reported to regulate the cAMP signaling system at various levels, suggesting that the cAMP system is involved in the therapeutic mechanism. 2. Chronic ECS has been suggested to change the expressions of adenylate cyclase (AC) genes, which constitute at least 9 families. However, little is known about its effect on the expression of AC. Therefore, to understand how chronic ECS alters the expression of AC genes in the brain, the authors analyzed the expression of 9 AC isoforms at the transcriptional level in rat hippocampus and cerebellum by quantitative RT-PCR following chronic ECS treatment. 3. Chronic ECS treatment was found to induce differential changes in the expression of AC isoforms in an isoform- and brain region-specific manner in the rat hippocampus and cerebellum. 4. Thus, it is concluded that chronic ECS induces differential changes in the expression of AC isoform mRNA in an isoform- and brain region-specific manner in the rat hippocampus and cerebellum. This suggests that the differential expression of AC isoforms might be an important mechanism by which chronic ECS treatment regulates the cAMP signaling system in rat brains.

Adenylyl Cyclases↗
PubMed1984

Reversible motor paralysis in rats after repeated electroconvulsive shock.

Repeated electroconvulsive shocks (ECS) delivered at brief (10 to 15 min) intervals through earclip electrodes, induced a reversible motor paralysis in 35% of treated rats. Paralysis was characterized by loss of locomotor activity without apparent loss of sensory functions. It occurred after 10 to 13 shocks regardless of whether stimulation was of subthreshold (40 to 60 mA) or suprathreshold (65 mA) intensity. This phenomenon may provide a useful animal model for the investigation of reversible injury to the spinal cord.

Animals↗
PubMed1994

Role of seizure activity in the decreased pineal response to isoproterenol in rats chronically treated with electroconvulsive shock.

Chronic electroconvulsive shock (ECS) has been previously reported to blunt the melatonin response to acute isoproterenol administration in rats. To assess whether electrically induced seizures are indeed required for the appearance of the blunted pineal response to isoproterenol, pineal and serum melatonin levels were measured after isoproterenol stimulation in rats treated with ECS (80 mA, 0.5 sec), subconvulsive shock (15 mA, 0.5 sec), or sham-ECS once per day at 11:30-12:00 h for 8 days. In ECS-treated rats, both pineal and serum melatonin levels after isoproterenol administration were significantly lower than those in sham-treated animals and in rats receiving subconvulsive shock. Moreover, as compared with sham treatment, chronic subconvulsive shock did not affect the melatonin response to isoproterenol. These data show that seizure activity is indeed required for the ECS-induced decrease in the pineal response to acute beta-adrenergic stimulation.

Animals↗