The benzodiazepine antagonist flumazenil blocks the effects of CCK receptor agonists and antagonists in the elevated plus-maze

Chopin, Philippe; Briley, Mike

doi:10.1007/bf02244646

Cited by 63 publications

(23 citation statements)

References 33 publications

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“…Consequently, it is likely that the behavioral responses to di¤erent anxiogenic stimuli are di¤erentially a¤ected by similar doses of the same anxiolytic agent. This hypothesis is sustained by other Þndings, showing that the minimum e¤ective dose may vary among animal model predictive of anxiolysis (Chopin and Briley 1993;Griebel et al 1994;Wieland et al 1995;Singh et al 1996).…”

Section: Discussionmentioning

confidence: 43%

Adenosine A 1 receptors modulate anxiety in CD1 mice

et al. 1998

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The effect of the selective adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) was investigated in CD1 mice by the elevated plus-maze and the light/dark test, two models for measuring anxiety in rodents. CCPA, administered i.p., had an anxiolytic effect at 0.3 nmol/kg in the elevated plus-maze and at 1 nmol/kg in the light/dark test. Brain levels of 22 nM were found after administration of 100 nmol/kg CCPA, as measured by ex vivo binding experiments. These values are consistent with the occupancy of adenosine A1 but not A2 receptors by CCPA, and suggest that the anxiolytic-like action of CCPA may be mediated by centrally located adenosine A1 receptors. Both CPT, a selective adenosine A1 receptor antagonist, and IBMX, a non-selective adenosine antagonist, had an anxiogenic effect in the two tests. It is thus possible that purinergic neurons may be involved in the tonic modulation of affective state in mice.

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Section: Discussionmentioning

confidence: 43%

Adenosine A 1 receptors modulate anxiety in CD1 mice

et al. 1998

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“…It has earlier been shown that CCK B receptor antagonists (L-365 260) can block the anxiogenic effects of CCK8 in animal models (Chopin and Briley 1993), and that of CCK4 (Bradwejn et al 1994) and pentagastrin (Lines et al 1995) in human studies. De Montigny describes panicogenic action of CCK4 in healthy individuals, panic attacks being provoked in doses ranging from 20 to 100 µg (de Montigny 1989).…”

Section: Cck B Receptors and Discomfortmentioning

confidence: 42%

Anxiogenic effects of the CCK B agonist pentagastrin in humans and dose-dependent increase in plasma C-peptide levels

et al. 2002

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“…In contrast, the selective CCK 2 agonist, CCK-4, induces anxiety in nonhuman subjects [20,305] and promotes panic in panic patients and normal subjects [21,23]. The differential propensity of CCK-8S and CCK-4 to provoke anxiety and/or panic in human subjects as well as rats and mice may be attributable to species variations [306], differential brain region sensitivity (e.g., amygdala, prefrontal cortex and nucleus accumbens, [307,308]), drug route [309,310] and/or paradigm specificity [308]. Clearly, discrepancies between clinical and nonhuman studies necessitate examination of methodological variables including drug schedule and experiential factors that influence sensitivity to CCK challenge and anxiety (panic) induction.…”

Section: Cholecystokinin Anxiety and Panic Attackssupporting

confidence: 41%

“…In rats, flumazenil (4 mg/kg i.p.) significantly antagonized the anxiogenic effects of the CCK 2 agonist, CCK-8S and the anxiolytic-like effects of the CCK 2 antagonist, L-365, 260 [310]. Moreover, rats rated anxious with respect to performance in the elevated plus maze exhibited a reduced benzodiazepine receptor density and increased CCK-8S binding in the frontal cortex relative to non-anxious counter-parts [315].…”

Section: Cholecystokinin Induced Anxiety: Nonhuman Modelssupporting

confidence: 41%

The Myth of Panic Spontaneity: Consideration of Behavioral and Neurochemical Sensitization

Hebb¹,

Anger²,

Mendella³

et al. 2007

TOPJ

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Panic disorder is characterized by a progression of panic symptom severity with repeated attacks. Repeated panic episodes evoke heightened anticipatory anxiety, phobic avoidance and are typically associated with comorbid symptoms of depression. Due to the heterogeneity of the disorder, reliable neurochemical correlates attending panic have not been identified. However, variable neuropeptide interfacing with major and minor transmitter systems may modulate individual vulnerability to panic and account for variable panic profiles. The extensive colocalization of cholecystokinin (CCK) with other neurotransmitters, including dopamine (DA), enkephalin (ENK) and GABA, in specific central sites may influence various aspects of anxiety and panic. The behavioral correlates attending panic likely follow from variable neurochemical release and conditioning/sensitization. Clinicians maintain that recurrent panic attacks are spontaneous (unexpected, uncued) and fail to acknowledge the wealth of information implicating a prominent role for stressful life events in panic. Conditioning and sensitization of both behavior (e.g., fear-motivated) and neurochemical events (e.g., DA and CCK) in response to uncontrollable stressors parallel the diverse heterogeneity of panic amongst clinical samples. Cholecystokinin-4, pentagastrin, lactate acid, and CO 2 induce panic attacks that are dependent on subjective history, expectancy measures and panic profiles. Panic disorder is associated with chronic illness and familial sick-role modeling exacerbates the course of the illness. The current review outlines the evidence in support of a conditioning/sensitization model for panic, a model that may explain the variable efficacies of pharmacological interventions.

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The benzodiazepine antagonist flumazenil blocks the effects of CCK receptor agonists and antagonists in the elevated plus-maze

Cited by 63 publications

References 33 publications

Adenosine A 1 receptors modulate anxiety in CD1 mice

Adenosine A 1 receptors modulate anxiety in CD1 mice

Anxiogenic effects of the CCK B agonist pentagastrin in humans and dose-dependent increase in plasma C-peptide levels

The Myth of Panic Spontaneity: Consideration of Behavioral and Neurochemical Sensitization

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