Effects of histamine H 3 receptor ligands in experimental models of anxiety and depression

1999 ◽  
Vol 142 (2) ◽  
pp. 215-220 ◽  
Author(s):  
Carmen Pérez-García ◽  
Lydia Morales ◽  
M. Victoria Cano ◽  
Isabel Sancho ◽  
L. F. Alguacil
2014 ◽  
Vol 26 (5) ◽  
pp. 307-314 ◽  
Author(s):  
Fatma Sultan Kilic ◽  
Sule Ismailoglu ◽  
Bilgin Kaygisiz ◽  
Setenay Oner

BackgroundGabapentin, a third-generation antiepileptic drug, is a structural analogue of γ-aminobutyric acid, which is an important mediator of central nervous system. There is clinical data indicating its effectiveness in the treatment of psychiatric illnesses such as bipolar disorder and anxiety disorders.ObjectivesWe aimed to investigate the antidepressant and anxiolytic-like effects and mechanisms of gabapentin in rats.Material and MethodsFemale Spraque–Dawley rats weighing 250±20 g were used. A total of 13 groups were formed, each containing 8 rats: gabapentin (5, 10, 20, 40 mg/kg), amitriptyline (10 mg/kg), sertraline (5 mg/kg), diazepam (5 mg/kg), ketamine (10 mg/kg), gabapentin 20 mg/kg was also combined with amitriptyline (10 mg/kg), sertraline (5 mg/kg), diazepam (5 mg/kg) and ketamine (10 mg/kg). All the drugs were used intraperitoneally as single dose. Saline was administered to the control group. Elevated plus maze and forced swimming tests were used as experimental models of anxiety and depression, respectively.ResultsIt was observed that gabapentin showed an anxiolytic-like and antidepressant-like effect in all doses in rats. Its antidepressant effect was found to be the same as the antidepressant effects of amitriptyline and sertraline. There was no change in the antidepressant effect when gabapentin was combined with amitriptyline and ketamine, but there was an increase when combined with sertraline and diazepam. Gabapentin and amitriptyline showed similar anxiolytic effect, whereas ketamine and diazepam had more potent anxiolytic effect compared with them.ConclusionsThese data suggest that gabapentin may possess antidepressant- and anxiolytic-like effects.


2006 ◽  
Vol 34 (6) ◽  
pp. 1037-1040 ◽  
Author(s):  
V.A. Pavlov ◽  
K.J. Tracey

Innate immune responses and inflammation are regulated in part by neural mechanisms. In the present paper, we summarize experimental evidence that reveals that innate immunity and inflammation are controlled by the vagus nerve, previously known as a regulator of other vital physiological functions. Activation of vagus nerve cholinergic signalling inhibits TNF (tumour necrosis factor) and other pro-inflammatory cytokine overproduction through ‘immune’ α7 nicotinic receptor-mediated mechanisms. This efferent vagus nerve-based ‘cholinergic anti-inflammatory pathway’ has been elucidated as a critical regulator of inflammation in several experimental models of diseases. Our recent observations have shown that activation of central (brain) cholinergic transmission by selective muscarinic receptor ligands results in lower systemic TNF levels in rodents and indicate that the efferent vagus nerve may provide a functional brain-to-immune connection. Thus central cholinergic signalling is implicated in the activation of the cholinergic anti-inflammatory pathway. Electrical vagus nerve stimulation is clinically approved for the treatment of epilepsy and depression and current knowledge suggests that it could be utilized to control inflammation. Advances in understanding the receptor and molecular mechanisms of cholinergic anti-inflammatory signalling indicate that selective α7 nicotinic receptor agonists and centrally acting cholinergic enhancers can be used in the treatment of pathological conditions characterized by cytokine overproduction.


2012 ◽  
Vol 64 (1) ◽  
pp. 191-204 ◽  
Author(s):  
Mahmood Danish ◽  
Khanam Razia ◽  
Pillai Krishna Kolappa ◽  
Akhtar Mohd

Author(s):  
A. V. Kalueff ◽  
K. A. Demin ◽  
A. D. Volgin

Affective disorders — including anxiety and depression — are the most prevalent human brain diseases. Stress is the most common cause of these human psychopathologies, and is also often used to develop their experimental models in animals. In addition to genetic and environmental factors, genomic and epigenetic processes play an important role in affective pathogenesis. The aim of the present study is to examine the expression of brain genes in mice in the chronic 20-day social stress model developed by Prof. N.N. Kudryavtseva (Institute of Cytology and Genetics) and to experimentally test the hypothesis on ‘genes-integrators’ whose brain activity can specifically integrate anxiety-depressive mechanisms. The report will for the first time provide data on the existence of several such putative brain genes whose expression in the hippocampus and cortex changes dynamically as stress transitions from the «anxiety» (10 days) to the «depressive» phase (20 days), including a number of cytokine and cellular structural genes whose expression is specifically altered only in the «transitional» stage (15 days). The findings provide a new perspective on the complex genomics of the anxiety-depressive pathogenesis of the CNS, and can be translationally significant, including in terms of finding new potential targets for the therapy of anxiety and depression based on such ‘gene-integrators’.


2017 ◽  
Vol 36 (4) ◽  
pp. 215 ◽  
Author(s):  
AshokKumar Dubey ◽  
Snigdha Sharma ◽  
Shailendra Handu ◽  
Prashant Sharma ◽  
Pramod Mediratta ◽  
...  

2011 ◽  
Vol 49 (5) ◽  
pp. 477-483 ◽  
Author(s):  
Manavi Chatterjee ◽  
Pinki Verma ◽  
Rakesh Maurya ◽  
Gautam Palit

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