Dizocilpine antagonizes the effect of chronic imipramine on learned helplessness in rats

Meloni, Domenico; Gambarana, Carla; Montis, Maria Graziella De; Pra, P. Dal; Taddei, I; Tagliamonte, A.

doi:10.1016/0091-3057(93)90374-3

Cited by 89 publications

(42 citation statements)

References 18 publications

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“…The dose of dizocilpine used (0.1 mg/kg/24 h) does not produce apparent behavioral alterations, and it prevents the development of the protective effect of imipramine (Meloni et al 1993) and fluoxetine (Gambarana, unpublished results) on the behavioral and neurochemical sequelae of inescapable stress. Thus, the protective effect of ALCAR on stress appeared to be mediated by a process of neuronal plasticity dependent on NMDA receptor activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of Long-term Acetyl-L-carnitine Administration in Rats I. Increased Dopamine Output in Mesocorticolimbic Areas and Protection toward Acute Stress Exposure

Tolu

2002

Neuropsychopharmacology

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Section: Discussionmentioning

confidence: 99%

Effects of Long-term Acetyl-L-carnitine Administration in Rats I. Increased Dopamine Output in Mesocorticolimbic Areas and Protection toward Acute Stress Exposure

Tolu

2002

Neuropsychopharmacology

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“…41,42 Antagonists at the N-methyl-D-aspartate (NMDA) glutamate receptor have been shown to improve depressive symptoms in subjects diagnosed with major depression 43 and NMDA antagonists are effective in animal models of depression. 44,45 Dynorphin is known to inhibit excitatory glutamatergic neurotransmission (assessed primarily in the hippocampus). 46,47 Reduced prodynorphin mRNA levels, and possibly of dynorphin peptides, would be expected to increase glutamate tone in line with the theory of enhanced glutamateric circuits in depression.…”

Section: Discussionmentioning

confidence: 99%

Subjects with major depression or bipolar disorder show reduction of prodynorphin mRNA expression in discrete nuclei of the amygdaloid complex

Hurd

2002

Mol Psychiatry

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The dynorphin system has been associated with the regulation of mood. The expression of the prodynorphin mRNA was currently studied in the amygdaloid complex, a brain region critical for emotional processing, in subjects (14-15 per group) diagnosed with major depression, bipolar disorder, or schizophrenia and compared to normal controls. In situ hybridization histochemistry was used to characterize the anatomical distribution and expression levels of the prodynorphin mRNA within the amygdaloid complex. High prodynorphin mRNA levels were expressed in the parvicellular division of the accessory basal, posterior cortical, periamygdaloid cortex, and amygdalohippocampal area in normal subjects. Individuals with major depression had significantly reduced (41-68%) expression of the prodynorphin mRNA in the accessory basal (both parvicellular and magnocellular divisions; P Ͻ 0.01) and amygdalohippocampal area (P Ͻ 0.001) as compared to controls. The bipolar disorder group also showed a significant reduction (37-38%, P Ͻ 0.01) of the mRNA expression levels in the amygdalohippocampal area and in the parvicellular division of the accessory basal. No other amygdala nuclei studied showed any significant differences for the prodynorphin mRNA levels measured in the major depression and bipolar disorder subjects. Additionally, the prodynorphin mRNA expression levels did not differ significantly between the schizophrenic and normal control subjects in any of the amygdala areas examined. These findings indicate specific prodynorphin amygdala impairment in association with mood disorder. Molecular Psychiatry (2002) 7, 75-81.

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“…34,47 Both competitive and non-competitive NMDA receptor antagonists are active in the forced swimming test [77][78][79] and the learned helplessness model. 80 However, the relationship between NMDA blockade and antidepressant action is not clear-cut; in certain cases NMDA receptor antagonists can inhibit the action of clinically effective antidepressant treatments. 80 A preliminary clinical study has now suggested that the non-competitive NMDA receptor antagonist, ketamine, produced a rapid but reversible improvement in depressive symptoms following a single infusion.…”

Section: Antidepressant Action Of Nmda-receptor-directed Compoundsmentioning

confidence: 99%

“…80 However, the relationship between NMDA blockade and antidepressant action is not clear-cut; in certain cases NMDA receptor antagonists can inhibit the action of clinically effective antidepressant treatments. 80 A preliminary clinical study has now suggested that the non-competitive NMDA receptor antagonist, ketamine, produced a rapid but reversible improvement in depressive symptoms following a single infusion. There was a significant change in the Hamilton Depression Rating Scale within 72 h of intravenous ketamine hydrochloride that returned to baseline 1-2 weeks later.…”

Section: Antidepressant Action Of Nmda-receptor-directed Compoundsmentioning

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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Dizocilpine antagonizes the effect of chronic imipramine on learned helplessness in rats

Cited by 89 publications

References 18 publications

Effects of Long-term Acetyl-L-carnitine Administration in Rats I. Increased Dopamine Output in Mesocorticolimbic Areas and Protection toward Acute Stress Exposure

Effects of Long-term Acetyl-L-carnitine Administration in Rats I. Increased Dopamine Output in Mesocorticolimbic Areas and Protection toward Acute Stress Exposure

Subjects with major depression or bipolar disorder show reduction of prodynorphin mRNA expression in discrete nuclei of the amygdaloid complex

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

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