Effect of peripheral administration of cinnarizine and verapamil on the abstinence syndrome in diazepam-dependent rats

Chugh, Yati; Saha, Nilanjan; Sankaranarayanan, A; Sharma, Pankaj

doi:10.1007/bf02253599

Cited by 11 publications

(2 citation statements)

References 16 publications

(13 reference statements)

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“…The acoustic startle response is a reflexive neurobehavioural response mediated at the brain stem level (Koch, 1999;Lee et al, 1996) and is known to be affected by the withdrawal from chronic diazepam treatment (Chugh et al, 1992;Miczek and Vivian, 1993;Rasmussen et al, 1993). In our study rats withdrawn from oral diazepam intake increased their magnitude of startle response, in a similar manner to that verified during withdrawal from other drugs of abuse, such as alcohol (Chester et al, 2004;Pohorecky et al, 1976), morphine (Harris and Gewirtz, 2004;Kalinichev and Holtzman, 2003) and nicotine (Acri, 1994;Helton et al, 1993).…”

Section: Discussionsupporting

confidence: 76%

Analysis of the chronic intake of and withdrawal from diazepam on emotional reactivity and sensory information processing in rats

Ross

Castilho

Brandão

et al. 2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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It has been demonstrated that, on abrupt withdrawal, patients with chronic exposure can experience a number of symptoms indicative of a dependent state. In clinical patients, the earliest to arise and most persistent signal of withdrawal from chronic benzodiazepine (Bzp) treatment is anxiety. In laboratory animals, anxiety-like effects following abrupt interruption of chronic Bzp treatment can also be reproduced. In fact, signs that oscillate from irritability to extreme fear behaviours and seizures have been described already. As anxiety remains one of the most important symptoms of Bzp withdrawal, in this study we evaluated the anxiety levels of rats withdrawn from diazepam. Also studied were the effects on the motor performance and preattentive sensory gating process of rats under diazepam chronic treatment and upon 48-h withdrawal on three animal models of anxiety, the elevated plus-maze (EPM), ultrasonic vocalizations (USV) and startle + prepulse inhibition tests. Data obtained showed an anxiolytic-and anxiogenic-like profile of the chronic intake of and withdrawal from diazepam regimen in the EPM test, 22-KHz USV and startle reflex.Diazepam chronic effects or its withdrawal were ineffective in promoting any alteration in the prepulse inhibition (PPI). However, an increase of PPI was achieved in both sucrose and diazepam pretreated rats on 48-h withdrawal, suggesting a procedural rather than a specific effect of withdrawal on sensory gating processes. It is also possible that the prepulse can function as a conditioned stimulus to informing the delivery of an aversive event, as the auditory startling-eliciting stimulus. All these findings are indicative of a sensitization of the neural substrates of aversion in diazepam withdrawn animals without concomitant changes on the processing of sensory information.

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Section: Discussionsupporting

confidence: 76%

Analysis of the chronic intake of and withdrawal from diazepam on emotional reactivity and sensory information processing in rats

Ross

Castilho

Brandão

et al. 2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Modulation of calcium channels is another important factor in the pathophysiology of anxiety 55. In animal models of anxiety, calcium-channel blockers can abolish anxiety symptoms 63,64. Of the various subtypes of calcium channel, the highvoltage calcium channels, and particularly the N and P/Q types, control the release of excitatory neurotransmitters in synapses.…”

Section: Pathogenic Mechanisms Of Depression and Anxiety In Pwementioning

confidence: 99%

Depression and Anxiety in People with Epilepsy

2014

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Many recent epidemiological studies have found the prevalence of depression and anxiety to be higher in people with epilepsy (PWE) than in people without epilepsy. Furthermore, people with depression or anxiety have been more likely to suffer from epilepsy than those without depression or anxiety. Almost one-third of PWE suffer from depression and anxiety, which is similar to the prevalence of drug-refractory epilepsy. Various brain areas, including the frontal, temporal, and limbic regions, are associated with the biological pathogenesis of depression in PWE. It has been suggested that structural abnormalities, monoamine pathways, cerebral glucose metabolism, the hypothalamic-pituitary-adrenal axis, and interleukin-1b are associated with the pathogenesis of depression in PWE. The amygdala and the hippocampus are important anatomical structures related to anxiety, and γ-aminobutyric acid and serotonin are associated with its pathogenesis. Depression and anxiety may lead to suicidal ideation or attempts and feelings of stigmatization. These experiences are also likely to increase the adverse effects associated with antiepileptic drugs and have been related to poor responses to pharmacological and surgical treatments. Ultimately, the quality of life is likely to be worse in PWE with depression and anxiety than in PWE without these disorders, which makes the early detection and appropriate management of depression and anxiety in PWE indispensable. Simple screening instruments may be helpful for in this regard, particularly in busy epilepsy clinics. Although both medical and psychobehavioral therapies may ameliorate these conditions, randomized controlled trials are needed to confirm that.

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