Proactive and retroactive effects of repeated electroconvulsive shock on passive avoidance retention in rats

Lerer, Bernard; Stanley, Michael; Keegan, Michael; Altman, Harvey J.

doi:10.1016/0031-9384(86)90317-3

Cited by 16 publications

(2 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…11 In animal models, impairment to avoidance learning has been shown to last up to 21 days. 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.…”

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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…This is in line with ECS studies on retrograde amnesia using another memory test (the passive avoidance task, taxing both hippocampus-dependent contextual memory and amygdala-dependent emotional memory (47)), where retrograde amnesia was seen 24 h after three, but not after one or two, ECS treatments (48). Other researchers using the passive avoidance task have also failed to observe retrograde amnesia after one ECS, but observed a significant memory loss after multiple (seven) ECS treatments (49). We conclude that an extended delay (7 days) after a single ECS is not in itself sufficient to cause retrograde amnesia.…”

Section: Discussionmentioning

confidence: 99%