Repeated ECS and fluoxetine administration have equivalent effects on hippocampal synaptic plasticity

Stewart, Caroline A.; Reid, Ian

doi:10.1007/s002130050045

Cited by 136 publications

(81 citation statements)

References 34 publications

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“…Different antidepressants and electroconvulsive therapy have been shown to effectively modulate synaptic plasticity in the dentate gyrus and the CA1 and in the neostriatum (De Murtas et al, 2004;Stewart and Reid, 2000). Here we found an impaired ability to induce LTP in a brain circuit that may be crucially involved in the pathophysiology of major depression (Nestler and Carlezon, 2006).…”

Section: Cms and Win55212-2 Effects On Plasticitymentioning

confidence: 55%

Cannabinoid Receptor Activation Prevents the Effects of Chronic Mild Stress on Emotional Learning and LTP in a Rat Model of Depression

Segev

Rubin

Abush

et al. 2013

Neuropsychopharmacol

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Most psychiatric disorders are characterized by emotional memory or learning disturbances. Chronic mild stress (CMS) is a common animal model for stress-induced depression. Here we examined whether 3 days of treatment using the CB1/2 receptor agonist WIN55,212-2 could ameliorate the effects of CMS on emotional learning (ie, conditioned avoidance and extinction), long-term potentiation (LTP) in the hippocampal-accumbens pathway, and depression-like symptoms (ie, coping with stress behavior, anhedonia, and weight changes). We also examined whether the ameliorating effects of WIN55,212-2 on behavior and physiology after CMS are mediated by CB1 and glucocorticoid receptors (GRs). Rats were exposed to CMS or handled on days 1-21. The agonist WIN55,212-2 or vehicle were administered on days 19-21 (IP; 0.5 mg/kg) and behavioral and electrophysiological measures were taken on days 23 and 28. The CB1 receptor antagonist AM251 (IP; 0.3 mg/kg) or the GR antagonist RU-38486 (IP; 10 mg/kg) were co-administered with WIN55,212-2. Our results show that CMS significantly modified physiological and behavioral reactions, as observed by the impairment in avoidance extinction and LTP in the hippocampal-accumbens pathway, and the alterations in depression-like symptoms, such as coping with stress behavior, weight gain, and sucrose consumption. The most significant effect observed in this study was that 3 days of WIN55,212-2 administration prevented the CMS-induced alterations in emotional memory (ie, extinction) and plasticity. This effect was mediated by CB1 receptors as the CB1 receptor antagonist AM251 prevented the ameliorating effects of WIN55,212-2 on extinction and LTP. The GR antagonist RU-38486 also prevented the CMS-induced alterations in extinction and plasticity, and when co-administered with WIN55,212-2, the preventive effects after CMS were maintained. The findings suggest that enhancing cannabinoid signaling could represent a novel approach to the treatment of cognitive deficits that accompany stress-related depression.

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Section: Cms and Win55212-2 Effects On Plasticitymentioning

confidence: 55%

Cannabinoid Receptor Activation Prevents the Effects of Chronic Mild Stress on Emotional Learning and LTP in a Rat Model of Depression

Segev

Rubin

Abush

et al. 2013

Neuropsychopharmacol

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“…A recent electrophysiological study has also demonstrated that chronic ADs increase the field excitatory postsynaptics potentials connectivity in the dentate gyrus, effects which could represent an increase in synaptic connections and number of new neurons in the dentate gyrus granule cell layer. 112 …”

Section: Influence Of Antidepressant Treatment On Cell Survival Pathwaysmentioning

confidence: 99%

Neuroplasticity and cellular resilience in mood disorders

et al. 2000

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Although mood disorders have traditionally been regarded as good prognosis diseases, a growing body of data suggests that the long-term outcome for many patients is often much less favorable than previously thought. Recent morphometric studies have been investigating potential structural brain changes in mood disorders, and there is now evidence from a variety of sources demonstrating significant reductions in regional CNS volume, as well as regional reductions in the numbers and/or sizes of glia and neurons. Furthermore, results from recent clinical and preclinical studies investigating the molecular and cellular targets of mood stabilizers and antidepressants suggest that a reconceptualization about the pathophysiology and optimal long-term treatment of recurrent mood disorders may be warranted. It is proposed that impairments of neuroplasticity and cellular resilience may underlie the pathophysiology of mood disorders, and further that optimal long-term treatment for these severe illnesses may only be achieved by the early and aggressive use of agents with neurotrophic/ neuroprotective effects. It is noteworthy that lithium, valproate and antidepressants indirectly regulate a number of factors involved in cell survival pathways including CREB, BDNF, bcl-2 and MAP kinases, and may thus bring about some of their delayed long-term beneficial effects via underappreciated neurotrophic effects. The development of novel treatments which more directly target molecules involved in critical CNS cell survival and cell death pathways have the potential to enhance neuroplasticity and cellular resilience, and thereby modulate the long-term course and trajectory of these devastating illnesses. Molecular Psychiatry (2000) 5, 578-593.Keywords: atrophy; cell death; neuroprotection; lithium; bcl-2; MAP kinase; neurite; neurotrophic; neurogenesis; N-acetylaspartate; gray matter There is mounting evidence that recurrent mood disorders-once considered 'good prognosis diseases'-are, in fact, often very severe and life-threatening illnesses. Recurrent mood disorders can have devastating long-term effects, and the cost of these illnesses in terms of human suffering, productivity and health care is enormous. Suicide is the cause of death in 10-20% of individuals, and in addition to suicide, mood disorders are associated with many other deleterious health-related effects. 1-5 Indeed, a recent study which controlled for physical illness, smoking and alcohol consumption found that the magnitude of the increased mortality risk conferred by the presence of high depressive symptoms was similar to that of stroke and congestive heart failure. 5 Not surprisingly, the costs associated with disability and premature death represent an economic burden of tens of billions of dollars annually in the United States alone. 1,6,7 It is now recognized that, for many patients, the long-term outCorrespondence: HK Manji, MD,

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“…43 To circumvent the potential problem of cognitive deficits with tricyclic antidepressant drugs, 44 we examined the effects of chronic fluoxetine, a selective serotonin reuptake inhibitor that does not impair cognitive function, on both hippocampal synaptic plasticity and spatial learning. 45 Rats were given a course of eight ECS treatments spaced at 48-h intervals or 15 days of daily injections with fluoxetine (1 mg kg −1 , IP). Control groups were given anaesthesia alone or vehicle injections.…”

Section: Molecular Mechanisms Underlying the Ecs Effectmentioning

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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Repeated ECS and fluoxetine administration have equivalent effects on hippocampal synaptic plasticity

Cited by 136 publications

References 34 publications

Cannabinoid Receptor Activation Prevents the Effects of Chronic Mild Stress on Emotional Learning and LTP in a Rat Model of Depression

Cannabinoid Receptor Activation Prevents the Effects of Chronic Mild Stress on Emotional Learning and LTP in a Rat Model of Depression

Neuroplasticity and cellular resilience in mood disorders

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

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