Fear state induced by ethanol withdrawal may be due to the sensitization of the neural substrates of aversion in the dPAG

Cabral, Alícia; Isoardi, Nora A.; Salum, Cristiane; Macedo, Carlos Eduardo; Nobre, Manoel Jorge; Molina, Vı́ctor A.; Brandão, ML

doi:10.1016/j.expneurol.2006.02.004

Cited by 35 publications

(27 citation statements)

References 45 publications

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“…The same pattern of effects was observed in other studies that showed no influence of drug withdrawal on the processing of sensory information (Abduljawad et al, 1997;Cabral et al, 2006;Fendt and Mucha, 2001;Peleg-Raibstein et al, 2006). However, there was an unexpected enhancement of the PPI during withdrawal in both sucrose and diazepam groups.…”

Section: Discussionsupporting

confidence: 86%

“…The EPM was first validated as a test of anxiety-related behaviour for rats (Pellow and File, 1986) and it is frequently considered as a 'primer' test for measuring this type of behaviour. In our study, the interruption of the chronic oral regimen of diazepam caused an anxiogenic effect in the EPM test in the same fashion as those previously reported after abrupt interruption of alcohol chronic treatment (Cabral et al, 2006). In fact, withdrawn animals tend to spend more time inside and also to enter less The same pattern of results was obtained in the USV test.…”

Section: Discussionsupporting

confidence: 78%

“…The purpose of the procedures above was to determine the effects of the acclimitization to the continuous presentation of the prepulse, startle or prepulse + startle stimuli on the amplitude of startle responses. The inter-stimulus interval of 30 s used between trials was based on a previous study by our laboratory (Cabral et al, 2006;Nunes Mamede Rosa et al, 2005).…”

Section: Methodsmentioning

confidence: 99%

“…Startle response and PPI was tested in a simple paradigm routinely used in our laboratory (Cabral et al, 2006;Nunes Mamede Rosa et al, 2005) In this study, a pure tone was used as a prepulse stimulus since we have noted that the use of a white noise, but not a pure tone, activates both the affective and sensory channels, as this type of sound seems to promote aversion. The purpose of the procedures above was to determine the effects of the acclimitization to the continuous presentation of the prepulse, startle or prepulse + startle stimuli on the amplitude of startle responses.…”

Section: Methodsmentioning

confidence: 99%

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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: 86%

Section: Discussionsupporting

confidence: 78%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

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

Self Cite

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“…Our results demonstrating that DAT in the dBNST is unchanged during ethanol withdrawal raise the interesting possibility that there is divergent modulation of DA afferents to the BNST; with the VTA originating fibers having upregulated DAT expression with the PAG originating fibers having reduced DAT expression. Indeed, a sensitization of the PAG has been suggested to play a role in the negative states associated with ethanol withdrawal (Cabral et al, 2006). Alternatively, distinct target or terminal effects as outlined above could play a role.…”

Section: Dorsalateral Bnstmentioning

confidence: 99%

Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions

Healey

Winder

Kash

2008

Alcohol

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Neuroadaptations following chronic exposure to alcohol are hypothesized to play important roles in alcohol-induced alterations in behavior, in particular increased alcohol drinking and anxiety like behavior. Dopaminergic signaling plays a key role in reward-related behavior, with evidence suggesting it undergoes modification following exposure to drugs of abuse. A large literature indicates an involvement of dopaminergic signaling in response to alcohol. Using a chronic inhalation model of ethanol exposure in mice, we have begun to investigate the effects of alcohol intake on dopaminergic signaling by examining protein levels of tyrosine hydroxylase (TH) and the dopamine transporter (DAT), as well as monoamine metabolites in three different target fields of three different dopaminergic nuclei. We have focused on the dorsal lateral bed nucleus of the stria terminalis (dBNST) because of the reported involvement of dBNST dopamine in ethanol intake, and the nucleus accumbens (NAc) and dorsal striatum because of their dense dopaminergic innervation. After either a chronic intermittent exposure (CIE) or continuous exposure (CCE) regimen, mice were killed, and tissue punches collected from the dBNST, NAc and striatum for Western analysis. Strikingly, we found divergent regulation of TH and DAT protein levels across these three regions that was dependent upon the means of exposure. These data thus suggest that distinct populations of catecholamine neurons may be differentially regulated by ethanol, and that ethanol and withdrawal interact to produce differential adaptations in these systems.

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The autism diagnosis in translation: shared affect in children and mouse models of ASD

Bishop

Lahvis

2011

Autism Research

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In recent years, there have been significant improvements in assessment and diagnostic procedures for autism spectrum disorders (ASD). Standardized diagnostic instruments have been developed, promoting consistent diagnostic practices among clinicians. For clinical researchers, these instruments have facilitated collaborations across different sites by providing standardized metrics with which to evaluate ASD symptoms. Nevertheless, because ASD remains a diagnosis that is defined on the basis of behavior, there are significant challenges associated with modeling ASD social behaviors in laboratory animals. In order to more effectively study the causes of ASD symptoms and behaviors, there is a need to develop new ways of measuring social behaviors that can be applied to non-human species. Critically, while verbal dialogue between the clinician and patient is integral to clinical diagnoses, it cannot be employed for studies of animal models. However, observations of autistic-like social interactions can be modeled in animals. In this regard, communication between professionals in the clinical and basic sciences is necessary to break down the complex diagnosis into units of social impairment that can be more feasibly measured in different species. This paper presents a discussion between an animal researcher and a clinical psychologist. Using shared affect as an example, we explore potential avenues for increasing the utility of animal models to move us toward a better understanding of the mechanisms underlying social impairments in ASD. In the absence of molecular biomarkers that can be used to diagnose ASD, current diagnostic tools depend upon clinical assessments of behavior. Research efforts with human subjects have successfully utilized standardized diagnostic instruments, which include clinician interviews with parents and direct observation of the children themselves (Risi et al., 2006). However, because clinical instruments are semi-structured and rely heavily on dynamic social processes and clinical skill, scores from these measures do not necessarily lend themselves directly to experimental investigations into the causes of ASD. Studies of the neurobiology of autism require experimental animal models. Mice are particularly useful, in this regard, for elucidating genetic and toxicologjcal contributions to impairments in social function (Halladay et al., 2009). Behavioral tests have been developed that are relevant to autism (Crawley, 2004, 2007), including measures of repetitive behaviors (Lewis, Tanimura, Lee, & Bodfish, 2007; Moy et al., 2008), social behavior (Brodkin, 2007; Lijam et al., 1997; Moretti, Bouwknecht, Teague, Paylor, & Zoghbi, 2005), and vocal communication (Panksepp et al., 2007). Advances also include development of high-throughput measures of mouse sociability that can be used to reliably compare inbred mouse strains (Moy, et al., 2008; Nadler et al., 2004), as well as measures of social reward (Panksepp & Lahvis, 2007) and empathy (Chen, Panksepp, & Lahvis, 2009; Langford et al., 2006). ...

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Fear state induced by ethanol withdrawal may be due to the sensitization of the neural substrates of aversion in the dPAG

Cited by 35 publications

References 45 publications

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

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

Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions

The autism diagnosis in translation: shared affect in children and mouse models of ASD

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