Dorsal periaqueductal gray matter-evoked panic-like behaviors are markedly inhibited by a low peripheral dose of thyrotropin releasing hormone

Siqueira, Carla Coelho; Rossoni, Renzo Roldi; Schenberg, Luiz Carlos

doi:10.1016/j.psyneuen.2009.06.021

Cited by 5 publications

(2 citation statements)

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“…produced significant increases in the thresholds of DPAG-evoked responses of immobility (40%), trotting (33%), galloping (34%), jumping (39%) and exophthalmus (43%). In contrast, TRH had no effects on EPM arm exploration (Siqueira, Rossoni, & Schenberg, 2010). In another study, the effects of the anti-thyroid agent methimazole (MTZ) were evaluated either on the panic-like behaviors induced by electrical stimulation of DPAG or the anxiety-like behaviors of rats exposed to the EPM.…”

Section: Translational Modelling Of Panic Attacksmentioning

confidence: 93%

“…A third group of experiments examined the effects of hypothyroidism in DPAG-evoked defensive responses (Siqueira, Rossoni, & Schenberg, 2010; Siqueira, Rossoni, Tiengo, Tufik, & Schenberg, 2010). The relationship between panic attacks and hormone imbalance was originally suggested by Klein (1964) in his pioneering study of the pharmacotherapy of panic and anxiety disorders.…”

Section: Translational Modelling Of Panic Attacksmentioning

confidence: 99%

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Towards a translational model of panic attack.

Schenberg

2010

Psychology & Neuroscience

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About 20 years ago, Deakin and Graeff proposed that whereas generalized anxiety disorder is produced by the overactivity of 5-HT excitatory projections from dorsal raphe nucleus to the areas of prefrontal cortex and amygdala which process distal threat, panic attacks are a dysfunction of 5-HT inhibitory projections from dorsal raphe nucleus to the dorsal periaqueductal gray matter, thereby releasing the responses to proximal threat, innate fear or anoxia. Besides, they suggested that the decrease in 5-HT1A neurotransmission in the hippocampus results in learned helplessness and depression. Accordingly, the Deakin Graeff hypothesis provided a unified frame to the widespread use of 5-HT selective reuptake inhibitors in generalized anxiety, panic disorder and depression. Competitor hypotheses implicate panic attacks with the abnormal functioning of locus coeruleus, basolateral amygdala, dorsomedial hypothalamus or an as-yet-unknown suffocation alarm system. Conversely, cognitive psychologists suggest that panic attacks result from the catastrophic (cortical) interpretation of bodily symptoms. In any event, translational models of panic attack are expected to reproduce the main features of clinical panic, namely, the patient's higher sensitivity to both lactate and CO2, the drug specific sensitivity, the lack of stress hormone responses during panic attacks, the higher vulnerability of women and the high comorbidity with agoraphobia, major depression and childhood separation anxiety. Therefore, here we review the main steps in the experimental approach to anxiety disorders which are paving the route towards a translational model of panic attack.

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Section: Translational Modelling Of Panic Attacksmentioning

confidence: 93%