Behavioral, neurochemical, anatomical and electrophysiological correlates of panic disorder: multiple transmitter interaction and neuropeptide colocalization

Zacharko, Robert M.; Koszycki, Diana; Mendella, Paul D.; Bradwejn, Jacques

doi:10.1016/0301-0082(95)80007-u

Cited by 30 publications

(5 citation statements)

References 687 publications

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“…Actions in this model may be related to the control of panic attacks, and experimental models of this disorder employing electrical stimulation of the dorsomedial hypothalamus and periaqueductal grey showed that activation of 5-HT 2C receptors was effective Millan 2003;Graeff 2004). In line with this notion, panic attacks may be linked to abrupt and transient over-activation of adrenergic pathways which are inhibited and excited by 5-HT 2C agonists and antagonists, respectively (Zacharko et al 1995;Singewald and Sharp 2000;Millan et al 2000b;Millan 2003). Thus, anxiolyticlike actions of 5-HT 2C receptor antagonists, transduced in the amygdala and hippocampus (Menard and Treit 1999;Campbell and Merchant 2003;Millan 2003;Alves et al 2004), may be expressed against certain forms of clinical anxiety, such as "generalized anxiety disorder"-but not all, such as panic attacks.…”

Section: Modulation Of Frontocortical Monoaminergic Transmissionmentioning

confidence: 56%

S32006, a novel 5-HT2C receptor antagonist displaying broad-based antidepressant and anxiolytic properties in rodent models

et al. 2008

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Section: Modulation Of Frontocortical Monoaminergic Transmissionmentioning

confidence: 56%

S32006, a novel 5-HT2C receptor antagonist displaying broad-based antidepressant and anxiolytic properties in rodent models

et al. 2008

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“…Research over the past two decades using challenge studies and a variety of panicogenic agents has suggested a network model involving dysregulation of multiple neuronal systems, including monoamine and neuropeptide [1]. In addition, the results of…”

Section: Introductionmentioning

confidence: 99%

Association Study of a Brain-Derived Neurotrophic Factor (Val66Met) Genetic Polymorphism and Panic Disorder

et al. 2004

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Brain-derived neurotrophic factor (BDNF), a member of the neurotrophic factor family, plays an important role in the development, maintenance and function of several neuronal systems. Recent studies have demonstrated that antidepressants, commonly used for panic disorder treatment, can increase central BDNF. In addition, animals with BDNF deficits have higher levels of anxiety when exposed to stressors in comparison to normal controls. The present study tested the hypothesis that the BDNF gene Val66Met polymorphism is associated with panic disorder. In this study, therefore, the incidence of this polymorphism was compared in 103 panic disorder patients and 180 normal controls. The genotype and allele frequencies for the BDNF gene Val66Met polymorphism did not differ comparing the two groups. Furthermore, no association was demonstrated between this BDNF polymorphism and either mitral valve prolapse or agoraphobia in panic disorder patients. These findings suggest that the investigated BDNF polymorphism does not play a major role in the pathogenesis of panic disorder in this Chinese population. Further studies exploring the relationship between genetic variations of BDNF and the cerebral atrophy associated with, and antidepressant treatment response in, panic disorder may be appropriate.

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“…[6][7][8] The noradrenaline and serotonin transmitter hypotheses provide explanations for the efficacy of antidepressants, however, antipanic treatment with antidepressants is characterized by an initial worsening of the symptoms, 9 and requires long-term drug administration to achieve clinical improvement. 10 This initial exacerbation of symptoms, in a time frame which corresponds to the rapid elevation in brain monoamine levels, contrasts to what would be expected if abnormalities in the monoaminergic systems were primarily involved in the pathophysiology of PD.…”

Section: Introductionmentioning

confidence: 99%

Common effects of chronically administered antipanic drugs on brainstem GABAA receptor subunit gene expression

et al. 2001

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Panic disorder is an anxiety disorder that can be treated by long-term administration of tricyclic antidepressants such as imipramine, monoamine oxidase inhibitors such as phenelzine, or the selective serotonin reuptake inhibitor (SSRI) antidepressants. Clinical data also indicate that some benzodiazepines, such as alprazolam, are effective antipanic agents, and that their therapeutic onset is faster than that of antidepressants. Benzodiazepines are well known for their action at GABA A receptors, and preclinical data indicate that imipramine and phenelzine also interfere with the GABAergic system. In addition some clinical data lend support to decreased benzodiazepine-sensitive receptor function in panic disorder patients. Using imipramine, phenelzine and alprazolam, we investigated, in rats, the possibility that the therapeutic efficacy of antipanic agents stems from the remodeling of GABAergic transmission in the pons-medulla region. Of the 12 GABA A receptor subunit (␣1-6, ␤1-3, ␥1-3) steady-state mRNA levels investigated, we observed an increase in the levels of the ␣3-, ␤1-and ␥2-subunit transcripts with all three antipanic agents tested. The effects of imipramine and phenelzine on these subunits occurred after 21 days of treatment, while alprazolam effects were observed after 3 days of administration. Histochemical data suggest that the ␣3␤1␥2 subunits comprise a receptor subtype in the pons-medulla region. Therefore, we conclude that these molecular events parallel the therapeutic profile of the drugs examined. We further propose that these events may correspond to a remodeling of the GABA A receptor population, and may be useful markers for investigation of the antipanic properties of drugs. Molecular Psychiatry (2001) 6, 404-412.

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Behavioral, neurochemical, anatomical and electrophysiological correlates of panic disorder: multiple transmitter interaction and neuropeptide colocalization

Cited by 30 publications

References 687 publications

S32006, a novel 5-HT2C receptor antagonist displaying broad-based antidepressant and anxiolytic properties in rodent models

S32006, a novel 5-HT2C receptor antagonist displaying broad-based antidepressant and anxiolytic properties in rodent models

Association Study of a Brain-Derived Neurotrophic Factor (Val66Met) Genetic Polymorphism and Panic Disorder

Common effects of chronically administered antipanic drugs on brainstem GABAA receptor subunit gene expression

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