scholarly journals Glial Purinergic Signals and Psychiatric Disorders

2022 ◽  
Vol 15 ◽  
Author(s):  
Schuichi Koizumi
Keyword(s):  
Sleep Deprivation ◽  
Electroconvulsive Therapy ◽  
Atp Release ◽  
Fibroblast Growth Factor 2 ◽  
Therapeutic Effects ◽  
Drug Resistant ◽  
Glial Dysfunction ◽  
Resistant Depression ◽  
Antidepressive Effects

Emotion-related neural networks are regulated in part by the activity of glial cells, and glial dysfunction can be directly related to emotional diseases such as depression. Here, we discuss three different therapeutic strategies involving astrocytes that are effective for treating depression. First, the antidepressant, fluoxetine, acts on astrocytes and increases exocytosis of ATP. This has therapeutic effects via brain-derived neurotrophic factor-dependent mechanisms. Second, electroconvulsive therapy is a well-known treatment for drug-resistant depression. Electroconvulsive therapy releases ATP from astrocytes to induce leukemia inhibitory factors and fibroblast growth factor 2, which leads to antidepressive actions. Finally, sleep deprivation therapy is well-known to cause antidepressive effects. Sleep deprivation also increases release of ATP, whose metabolite, adenosine, has antidepressive effects. These independent treatments share the same mechanism, i.e., ATP release from astrocytes, indicating an essential role of glial purinergic signals in the pathogenesis of depression.

Electroconvulsive therapy increases glial cell-line derived neurotrophic factor (GDNF) serum levels in patients with drug-resistant depression

2009 ◽  
Vol 170 (2-3) ◽  
pp. 273-275 ◽  
Author(s):  
Xiaobin Zhang ◽  
Zhijun Zhang ◽  
Weiwei Sha ◽  
Chunming Xie ◽  
Guangjun Xi ◽  
...  
Keyword(s):  
Cell Line ◽  
Glial Cell ◽  
Electroconvulsive Therapy ◽  
Neurotrophic Factor ◽  
Serum Levels ◽  
Drug Resistant ◽  
Resistant Depression

scholarly journals Robust and Sustained Effect of Ketamine Infusions Coadministered with Conventional Antidepressants in a Patient with Refractory Major Depression

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
José Manuel Montes ◽  
Elena Luján ◽  
Fernado Pascual ◽  
Jose María Beleña ◽  
Jose Luis Perez-Santar ◽  
...  
Keyword(s):  
Major Depression ◽  
Transient Response ◽  
Electroconvulsive Therapy ◽  
Alternative Treatment ◽  
Potential Role ◽  
Antidepressant Treatments ◽  
Sustained Effect ◽  
Resistant Depression

Antidepressant treatments show low capacity to achieve full clinical remissions. Electroconvulsive therapy is an alternative treatment which has been shown to be more effective but it is not well tolerated and there are concerns regarding its safety. We present the case of a patient with resistant depression and modest and transient response to ECT and who showed a robust and maintained response after six i.v. ketamine (0.5 mg/kg) infusions without withdrawing her antidepressant regimen. Ketamine was very well tolerated. This case illustrates the potential role of ketamine as a booster to standard antidepressants.

scholarly journals Clozapine-resistant schizophrenia – non pharmacological augmentation methods

2017 ◽  
Vol 18 (4) ◽  
pp. 279-291
Author(s):  
Joanna Gałaszkiewicz ◽  
Krzysztof Rębisz ◽  
Justyna Morylowska-Topolska ◽  
Hanna Karakuła-Juchnowicz ◽  
Gustaw Kozak
Keyword(s):  
Electrical Stimulation ◽  
Transcranial Magnetic Stimulation ◽  
Electroconvulsive Therapy ◽  
Magnetic Stimulation ◽  
Transcranial Electrical Stimulation ◽  
Therapeutic Effects ◽  
Drug Resistant ◽  
Treatment Methods ◽  
Drug Of Choice ◽  
Pubmed Database

AbstractClozapine is the drug of choice for drug-resistant schizophrenia, but despite its use, 30-40% patients fail to achieve satisfactory therapeutic effects. In such situations, augmentation attempts are made by both pharmacological and non-pharmacological methods. To date, most of the work has been devoted to pharmacological strategies, much less to augemantation of clozapine with electroconvulsive therapy (C+ECT), transcranial direct current stimulation (tDCS) or transcranial magnetic stimulation (TMS).Aim: The aim of the work is to present biological, non-pharmacological augmentation treatment methods with clozapine.Material and methods: A review of the literature on non-pharmacological augmentation treatment methods with clozapine was made. PubMed database was searched using key words: drug-resistant schizophrenia, clozapine, ECT, transcranial magnetic stimulation, transcranial electrical stimulation and time descriptors: 1980-2017.Results: Most studies on the possibility of increasing the efficacy of clozapine was devoted to combination therapy with clozapine + electric treatments. They have shown improved efficacy when using these two methods simultaneously from 37.5 to 100%. The only randomized trial so far has also confirmed the effectiveness of this procedure. Despite the described side effects of tachycardia or prolonged seizures, most studies indicate the safety and efficacy of combined use of clozapine and electroconvulsive therapy. Transcranial magnetic stimulation also appears to be a safe method in patients treated with clozapine. However, further research is needed before ECT can be included in standard TRS treatment algorithms. The data for combining transcranial electrical stimulation with clozapine, come only from descriptions of cases and need to be confirmed in controlled studies.Conclusions: The results of studies on the possibility of increasing the effectiveness of clozapine using biological non-pharmacological treatment methods indicate a potentially beneficial effect of this type of methods in breaking the super-resistance in schizophrenia. Combination of clozapine and ECT can be considered as the most recommended strategy among these treatment methods.

Sleep Deprivation as a Diagnostic Instrument

1994 ◽  
Vol 164 (4) ◽  
pp. 554-556 ◽  
Author(s):  
C. J. Williams ◽  
J. D. I. Yeomans ◽  
A. K. Coughlan
Keyword(s):  
Cognitive Impairment ◽  
Sleep Deprivation ◽  
Electroconvulsive Therapy ◽  
Chronic Treatment ◽  
Depressive Illness ◽  
Psychometric Tests ◽  
Treatment Resistant Depression ◽  
Treatment Resistant ◽  
Severity Of Depression ◽  
Resistant Depression

A 59-year-old man with chronic treatment-resistant depression developed severe cognitive impairment. The severity of depression and the mode of presentation led to difficulty in diagnosis between a dementing disorder and a depressive illness. The diagnostic conundrum was resolved by the use of sleep deprivation (SD), which demonstrated clear subjective and objective improvements in his condition. These changes were quantified by a range of psychometric tests, which showed that initial deficits in cognitive performance improved temporarily after SD, and these improvements were maintained after effective treatment of the depression with electroconvulsive therapy.

Collagen-Induced Platelet Aggregation: -Evidence Against the Essential Role of Platelet Adenosine Diphosphate

1979 ◽  
Vol 42 (04) ◽  
pp. 1193-1206 ◽  
Author(s):  
Barbara Nunn
Keyword(s):  
Platelet Aggregation ◽  
Time Course ◽  
Essential Role ◽  
Atp Release ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
High Doses ◽  
Induced Aggregation

SummaryThe hypothesis that platelet ADP is responsible for collagen-induced aggregation has been re-examined. It was found that the concentration of ADP obtaining in human PRP at the onset of aggregation was not sufficient to account for that aggregation. Furthermore, the time-course of collagen-induced release in human PRP was the same as that in sheep PRP where ADP does not cause release. These findings are not consistent with claims that ADP alone perpetuates a collagen-initiated release-aggregation-release sequence. The effects of high doses of collagen, which released 4-5 μM ADP, were not inhibited by 500 pM adenosine, a concentration that greatly reduced the effect of 300 μM ADP. Collagen caused aggregation in ADP-refractory PRP and in platelet suspensions unresponsive to 1 mM ADP. Thus human platelets can aggregate in response to collagen under circumstances in which they cannot respond to ADP. Apyrase inhibited aggregation and ATP release in platelet suspensions but not in human PRP. Evidence is presented that the means currently used to examine the role of ADP in aggregation require investigation.

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