Article

Paroxetine influences respiration in rats: implications for the treatment of panic disorder.

Department of Pharmacology, Göteborg University, Box 431, SE 405 30 Göteborg, Sweden.
European Neuropsychopharmacology (impact factor: 4.05). 02/2004; 14(1):29-37. pp.29-37
Source: PubMed

ABSTRACT Since hyperventilation and shortness of breath are characteristic features of panic attacks, and since the attacks can be elicited by CO(2) inhalation, an involvement of central or peripheral chemoreceptors in the pathophysiology of panic disorder has been suggested. Prompted by clinical reports suggesting that the susceptibility to spontaneous as well as CO(2)-induced anxiety and hyperventilation is attenuated by serotonin reuptake inhibitors (SRIs), we undertook the present study in order to explore the possible effect of an SRI, paroxetine, on baseline respiration and CO(2)-induced hyperventilation in freely moving Wistar rats. A significant increase in baseline respiratory rate was seen both after 5 and 15 weeks of treatment with paroxetine. CO(2) exposure induced a dose-dependent increase in respiratory rate, but not tidal volume, in both paroxetine-treated rats and controls; this response was reduced after 15 weeks of paroxetine treatment, but not after 5 weeks of treatment. We suggest that an influence on the regulation of respiration may be of importance for the anti-panic effect of SRIs.

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    Article: Anxiety and panic: from human studies to animal research and back.
    Marco Battaglia, Anna Ogliari
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    ABSTRACT: The role of learning and conditioning varies across human anxiety disorders, and distinguishing between fear and panic is important to guide investigation in panic disorder. By reminding that some psychological and psychobiological theories view panic attacks as false alarms of unconditioned biological origin, we suggest that employing endophenotypes of biological and evolutionary relevance--such as the respiratory responses to suffocative stimuli--can be fruitful for both human research and animal models of panic, and can help keeping unconditioned components of the clinical picture separate from the conditioned components in the experimental setting. We present a review of a model of panic disorder by which idiosyncratic environmental adverse events can promote unconditioned and unexpected spells of physical alarm. Along the proposed causal pathway the alternative splicing expression of polymorphic genes of the cholinergic system play an important role. The overproduction of the Acetylcholinesterase readthrough splice variant after minor stress can promote passive avoidance and learning through action at the level of the corticolimbic circuitries, as well as heightened sensitivity to suffocative stimuli by action upon the cholinergic components of chemoception. When a component of anticipatory anxiety complicates the clinical picture of recurrent panic attacks, and the HPA becomes activated, the glucocorticoid response element 17 kb upstream of the Acetylcholinesterase gene transcription initiation site may sustain sensitivity to suffocative stimuli for prolonged time. Finally, we review how animal models of human panic based on unconditioned provocation of alarm reactions by the same respiratory panicogens that are employed in man are viable and promising.
    Neuroscience & Biobehavioral Reviews 03/2005; 29(1):169-79. · 8.65 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

5 weeks
 
anti-panic effect
 
baseline respiration
 
baseline respiratory rate
 
clinical reports
 
CO(2)-induced anxiety
 
CO(2)-induced hyperventilation
 
dose-dependent increase
 
panic attacks
 
panic disorder
 
paroxetine treatment
 
paroxetine-treated rats
 
peripheral chemoreceptors
 
possible effect
 
respiration
 
respiratory rate
 
serotonin reuptake inhibitors
 
SRI
 
tidal volume
 
Wistar rats