Panic Disorder

Panic Attack

Panic Disorder

Recurrent Panic Attacks

Anticipatory Anxiety

Agoraphobia

Hypochondriasis

Demoralisation

Epidemiology

Age of Onset

Situation of Onset

Stressful Life Events

Early Life Events

Maternal Over-Protection

Separation Anxiety

Short and Long-term Outcomes

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Panic Disorder: Pathogenesis

Biological Findings

Provocative Agents

Neurotransmitter Systems

Neuroanatomical Models

Brain Imaging

Psychological Models

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Areas of Controversy and Debate

The Evolutionary Perspective

Panic Disorder: Treatment

Pharmacotherapy

Benzodiazepines

Tricyclic Antidepressants

Monoamine Oxidase Inhibitors

Selective Serotonin Re-uptake Inhibitors

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Psychotherapy

Overcoming Anxiety (Home) > Panic Disorder > Neurotransmitter Systems

Neurotransmitter Systems

The neurotransmitter systems more studied in PD are the noradrenergic, serotoninergic and gamma-aminobutyric acid (GABA)-ergic ones. With regard to noradrenergic system, an hyperactivity of the locus coeruleus (LC), the main central noradrenergic nucleus, has been supposed the increasing firing rate of the LC may be due to a dysfunction of noradrenergic receptors.

The relationship between 5-HT and panic is complex. There are two opposing hypotheses attempting to explain PD based on a serotoninergic dysfunction: 5-HT excess and 5-HT defect. The 5-HT excess theory suggests that patients with PD either have an increased level of 5-HT release or a supersensitivity of postsynaptic receptors. The 5-HT deficit theory proposes that, in particular brain regions, 5-HT has a restraining effect on panic behaviour and, when there is a deficit of 5-HT, this restraint is reduced and panic ensues. With regard to the GABA-ergic system, in PD patients a shift of BDZ receptor in the inverse agonist direction or relative deficiency of an hypothetical anxiolytic ligand has been proposed.

Furthermore, dysfunction of dopaminergic system is indicated by panic attacks induced by dopaminergic agents. Involvement of the opioid system is suggested by observation of naltrexone-induced panic attacks. Cholinergic abnormalities could also be involved; Yergani et al. suggested that altered sympatovagal balance may contribute to panicogenic effects of lactate in PD patients. Moreover, an important role for neuromodulator systems, such as CCK and CRH systems, is emerging.

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