Reversible loss of hippocampal long term potentiation following electroconvulsive seizures

Hesse, Gary W.; Teyler, Timothy J.

doi:10.1038/264562a0

Cited by 78 publications

(38 citation statements)

References 17 publications

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“…These burst-like responses resemble activity recorded during seizures. In fact, in vitro studies showed that seizure activity or seizure-like extracellular conditions induced depotentiation (Harrison and Alger 1993;Hesse and Teyler 1976;Moore et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Protein Phosphatases Mediate Depotentiation Induced by High-Intensity Theta-Burst Stimulation

Kang-Park¹,

Sarda²,

Jones³

et al. 2003

Journal of Neurophysiology

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Wilson. Protein phosphatases mediate depotentiation induced by highintensity theta-burst stimulation. J Neurophysiol 89: 684 -690, 2003; 10.1152/jn.01041.2001. We have previously reported that varying stimulus intensity produces qualitatively different types of synaptic plasticity in area CA1 of hippocampal slices: brief low-intensity (LI) theta-burst (TB) stimuli induce long-term potentiation (LTP), but if the stimulus intensity is increased (to mimic conditions that may exist during seizures), LTP is not induced; instead, high-intensity (HI) TB stimuli erase previously induced LTP ("TB depotentiation"). We now have explored the mechanisms underlying TB depotentiation using extracellular field recordings with pharmacological manipulations. We found that TB depotentiation was blocked by okadaic acid and calyculin A (inhibitors of serine/threonine protein phosphatases PP1 and PP2A), FK506 (a specific blocker of calcineurin, a Ca 2ϩ /calmodulin (CaM) protein phosphatase), and 8-Br-cAMP (an activator of protein kinase A) with 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor). These results suggest that protein phosphatase pathways are involved in the TB depotentiation similar to other type of down-regulating synaptic plasticity such as low-frequency stimulation (LFS)-induced long-term depression (LTD) and depotentiation in the rat hippocampus. However, TB depotentiation and LFS depotentiation could have differential functional significance.

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Section: Discussionmentioning

confidence: 99%

Protein Phosphatases Mediate Depotentiation Induced by High-Intensity Theta-Burst Stimulation

Kang-Park¹,

Sarda²,

Jones³

et al. 2003

Journal of Neurophysiology

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“…Although early preclinical research has demonstrated that postictal dendritic swelling could be reversible (Hesse and Teyler, 1976), and the transient intra-ictal breach in the blood-brain barrier (Andrade and Bolwig, 2014) might facilitate local swelling, there is evidence suggesting that edema is unlikely to be the primary cause of the observed volume changes (Kunigiri et al, 2007;Szabo et al, 2007;Nordanskog et al, 2010;Jorgensen et al, 2015).…”

Section: Alternative Processes Accounting For Hippocampal Volume Chanmentioning

confidence: 99%

Relationship Between Hippocampal Volume, Serum BDNF, and Depression Severity Following Electroconvulsive Therapy in Late-Life Depression

Bouckaert

Dols

Emsell

et al. 2016

Neuropsychopharmacol

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Recent structural imaging studies have described hippocampal volume changes following electroconvulsive therapy (ECT). It has been proposed that serum brain-derived neurotrophic factor (sBDNF)-mediated neuroplasticity contributes critically to brain changes following antidepressant treatment. To date no studies have investigated the relationship between changes in hippocampal volume, mood, and sBDNF following ECT. Here, we combine these measurements in a longitudinal study of severe late-life unipolar depression (LLD). We treated 88 elderly patients with severe LLD twice weekly until remission (Montgomery-Åsberg Depression Rating Scale (MADRS) o10). sBDNF and MADRS were obtained before ECT (T0), after the sixth ECT (T1), 1 week after the last ECT (T2), 4 weeks after the last ECT (T3), and 6 months after the last ECT (T4). Hippocampal volumes were quantified by manual segmentation of 3T structural magnetic resonance images in 66 patients at T0 and T2 and in 23 patients at T0, T2, and T4. Linear mixed models (LMM) were used to examine the evolution of MADRS, sBDNF, and hippocampal volume over time. Following ECT, there was a significant decrease in MADRS scores and a significant increase in hippocampal volume. Hippocampal volume decreased back to baseline values at T4. Compared with T0, sBDNF levels remained unchanged at T1, T2, and T3. There was no coevolution between changes in MADRS scores, hippocampal volume, and sBDNF. Hippocampal volume increase following ECT is an independent neurobiological effect unrelated to sBDNF and depressive symptomatology, suggesting a complex mechanism of action of ECT in LLD.

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“…12 Early studies suggested that the memory impairments could be due to alterations in hippocampal synaptic plasticity. Hesse and Teyler 13 found that locally generated seizure activity could reverse previously induced long-term potentiation in the hippocampus. Subsequently, Anwyl et al 14 gave rats a course of 10 electroconvulsive stimulation (ECS) treatments and then found that the induction of LTP by high-frequency stimulation to the Schaffer collateral/commissural fibres was impaired in the CA1 field of hippocampal slices.…”

Section: Electroconvulsive Stimulation and Hippocampal Synaptic Plastmentioning

confidence: 99%

Antidepressant mechanisms: functional and molecular correlates of excitatory amino acid neurotransmission

Stewart

Reid

2002

Mol Psychiatry

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Specific targeting of the serotonergic and noradrenergic systems for the development of antidepressant compounds has resulted in drugs with more favourable side-effect profiles but essentially no greater efficacy than those compounds discovered more than 40 years ago. Alternative targets are now being considered in the hope that they will have a faster onset of action and be useful for those patients currently unresponsive to conventional treatments. Excitatory amino acid neurotransmission has been attributed various roles in both normal and abnormal brain function. The N-methyl-D-aspartate receptor in particular has long been postulated to play a role in the formation of memories. Major depressive disorder is characterised by alterations in cognitive function, as well as affect. Although there is evidence that early adverse events and stress can have a causal influence on depression, the underlying neurobiology of the disorder is poorly understood. This review will document current evidence for the involvement of excitatory amino acid neurotransmission in the pathophysiology of the affective disorders. The preclinical literature suggests that both electroconvulsive stimulation and antidepressant drugs can affect hippocampal long-term potentiation and the expression of excitatory amino acid receptor subtypes. Exposing animals to stress, including the kind that produces learned helplessness, can also affect synaptic plasticity in the hippocampus. There is clinical evidence that patients with chronic depression have structural brain abnormalities, including hippocampal atrophy, and a preliminary study has shown that an N-methyl-D-aspartate receptor antagonist may have antidepressant efficacy. Molecular Psychiatry (2002) 7, S15-S22.

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Reversible loss of hippocampal long term potentiation following electroconvulsive seizures

Cited by 78 publications

References 17 publications

Protein Phosphatases Mediate Depotentiation Induced by High-Intensity Theta-Burst Stimulation

Protein Phosphatases Mediate Depotentiation Induced by High-Intensity Theta-Burst Stimulation

Relationship Between Hippocampal Volume, Serum BDNF, and Depression Severity Following Electroconvulsive Therapy in Late-Life Depression

Antidepressant mechanisms: functional and molecular correlates of excitatory amino acid neurotransmission

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