Clonidine in respiratory panic disorder subtype

Valença, Alexandre Martins; Nardi, Antônio Egídio; Mezzasalma, Marco A.; Nascimento, Isabella; Lopes, Fabiana L.; Zin, Walter A.; Versiani, Márcio

doi:10.1590/s0004-282x2004000300004

Cited by 7 publications

(5 citation statements)

References 21 publications

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“…Several studies have suggested that panic attacks might be the consequence of hyperactivity of LC noradrenergic cells (David Johnson, 2003; Valenca et al, 2004) and changes in the expression of neurotrophins and their receptors are essential for opiate-induced adaptations (Numan et al, 1998; Akbarian et al, 2001, 2002; Hatami et al, 2007). In the present work we observed profound abnormalities in LC neuronal responses in basal conditions and after chronic opiate exposure in TgNTRK3 mice.…”

Section: Discussionmentioning

confidence: 99%

Increased opioid dependence in a mouse model of panic disorder

Gallego

Murtra

Zamalloa

et al. 2009

Front. Behav. Neurosci.

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Panic disorder is a highly prevalent neuropsychiatric disorder that shows co-occurrence with substance abuse. Here, we demonstrate that TrkC, the high-affinity receptor for neurotrophin-3, is a key molecule involved in panic disorder and opiate dependence, using a transgenic mouse model (TgNTRK3). Constitutive TrkC overexpression in TgNTRK3 mice dramatically alters spontaneous firing rates of locus coeruleus (LC) neurons and the response of the noradrenergic system to chronic opiate exposure, possibly related to the altered regulation of neurotrophic peptides observed. Notably, TgNTRK3 LC neurons showed an increased firing rate in saline-treated conditions and profound abnormalities in their response to met5-enkephalin. Behaviorally, chronic morphine administration induced a significantly increased withdrawal syndrome in TgNTRK3 mice. In conclusion, we show here that the NT-3/TrkC system is an important regulator of neuronal firing in LC and could contribute to the adaptations of the noradrenergic system in response to chronic opiate exposure. Moreover, our results indicate that TrkC is involved in the molecular and cellular changes in noradrenergic neurons underlying both panic attacks and opiate dependence and support a functional endogenous opioid deficit in panic disorder patients.

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Section: Discussionmentioning

confidence: 99%

Increased opioid dependence in a mouse model of panic disorder

Gallego

Murtra

Zamalloa

et al. 2009

Front. Behav. Neurosci.

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“…While this novel direction for treatment of pathological anxiety in humans is promising, further work is needed to more directly target LC-NE system dysfunction with pharmacotherapies. One small study of three panic disorder patients showed that inhibition of the LC with the alpha2 agonist, clonidine, resulted in reduced panic and anxiety symptoms (Valenca et al, 2004).…”

Section: Anxiolyticsmentioning

confidence: 99%

The role of the locus coeruleus in the generation of pathological anxiety

Morris

McCall

Charney

et al. 2020

Brain and Neuroscience Advances

107

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This review aims to synthesise a large pre-clinical and clinical literature related to a hypothesised role of the locus coeruleus norepinephrine system in responses to acute and chronic threat, as well as the emergence of pathological anxiety. The locus coeruleus has widespread norepinephrine projections throughout the central nervous system, which act to globally modulate arousal states and adaptive behavior, crucially positioned to play a significant role in modulating both ascending visceral and descending cortical neurocognitive information. In response to threat or a stressor, the locus coeruleus–norepinephrine system globally modulates arousal, alerting and orienting functions and can have a powerful effect on the regulation of multiple memory systems. Chronic stress leads to amplification of locus coeruleus reactivity to subsequent stressors, which is coupled with the emergence of pathological anxiety-like behaviors in rodents. While direct in vivo evidence for locus coeruleus dysfunction in humans with pathological anxiety remains limited, recent advances in high-resolution 7-T magnetic resonance imaging and computational modeling approaches are starting to provide new insights into locus coeruleus characteristics.

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“…Notably, panic attacks triggered by respiratory symptoms are specifically responsive to clonidine, an a2-adrenergic agonist that silences LC (26).…”

mentioning

confidence: 99%

Breathing control center neurons that promote arousal in mice

Yackle

Schwarz

Kam

et al. 2017

Science

193

168

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Slow, controlled breathing has been used for centuries to promote mental calming, and it is used clinically to suppress excessive arousal such as panic attacks. However, the physiological and neural basis of the relationship between breathing and higher order brain activity is unknown. We found a neuronal subpopulation in the mouse preBötzinger Complex (preBötC), the primary breathing rhythm generator, which regulates the balance between calm and arousal behaviors. Conditional, bilateral genetic ablation of the ~175 Cdh9/Dbx1 double-positive preBötC neurons in adult mice left breathing intact but increased calm behaviors, and decreased time in aroused states. These neurons project to, synapse on, and positively regulate noradrenergic neurons in the locus coeruleus, a brain center implicated in attention, arousal and panic that projects throughout the brain.

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Clonidine in respiratory panic disorder subtype

Cited by 7 publications

References 21 publications

Increased opioid dependence in a mouse model of panic disorder

Increased opioid dependence in a mouse model of panic disorder

The role of the locus coeruleus in the generation of pathological anxiety

Breathing control center neurons that promote arousal in mice

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