author={Peter Zwanzger and Katharina Domschke and Jacques Bradwejn},
  journal={Depression and Anxiety},
Panic disorder (PD) is characterized by panic attacks, anticipatory anxiety and avoidance behavior. Its pathogenesis is complex and includes both neurobiological and psychological factors. With regard to neurobiological underpinnings, anxiety in humans seems to be mediated through a neuronal network, which involves several distinct brain regions, neuronal circuits and projections as well as neurotransmitters. 

Arousal and the attentional network in panic disorder

A multilevel model of arousal, attention and anxiety—including the norepinephrine, orexin, neuropeptide S and caffeine‐related adenosine systems—may be useful in integrating a range of data available on the pathogenesis of panic disorder.

A Novel Bio-Psychosocial-Behavioral Treatment Model of Panic Disorder

To conceptualize a novel bio-psychosocial-behavioral treatment model of panic disorder (PD), it is necessary to completely integrate behavioral, psychophysiological, neurobiological, and genetic

Cholecystokinin and Panic Disorder: Reflections on the History and Some Unsolved Questions

The history behind the discovery of the panicogenic effect of CCK-4 is described, and three unsettled questions about the involvement of cerebral CCK in the pathogenesis of anxiety and panic disorder are discussed, including therapeutic attempts with CCK2-receptor antagonists.

The role of cholecystokinin in the induction of aggressive behavior: a focus on the available experimental data (review).

The anatomical circuits through which CCK could potentially mediate all types of aggressive behavior are synopsized and the potential use of these experimental evidence in the current research quest for the clinical treatment of mood and anxiety disorders is highlighted.

Fear Network Model in Panic Disorder: The Past and the Future

The future delineation of advanced FNM model can be beneficial from more extensive and advanced studies focusing on the additional sensory regions of occipital, parietal and temporal cortex to confirm the role ofAdvanced FNM in the pathophysiology of PD.

Experimental Anxiety Model for Anxiety Disorders: Relevance to Drug Discovery.

  • M. Bourin
  • Psychology, Biology
    Advances in experimental medicine and biology
  • 2020
This chapter describes the various animal models that seem relevant to the development of anxiolytic drugs, as well as the human models of induced anxiety, or more precisely the panic inducers

Acute Shift in Glutamate Concentrations Following Experimentally Induced Panic with Cholecystokinin Tetrapeptide—A 3T-MRS Study in Healthy Subjects

According to preclinical studies, glutamate has been implicated in the pathogenesis of anxiety. In order to elucidate the role of glutamate in anxiety and panic in humans, brain glutamate+glutamine

Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition

  • B. BandelowD. Baldwin P. Riederer
  • Psychology, Biology
    The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry
  • 2017
Although at present, none of the putative biomarkers for anxiety disorders, obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD) is sufficient and specific as a diagnostic tool, an abundance of high quality research has accumulated that should improve understanding of the neurobiological causes of anxiety disorders.



Toward an integrated neurobiology of panic disorder.

An integrated neurobiology of panic disorder will provide a broader conceptual framework with which to tackle the complex questions about the pathophysiology and treatment of this condition.

Elevated plasma levels of neuropeptide Y in patients with panic disorder.

Higher plasma neuropeptide Y-like immunoreactivity suggests that this peptide may be implicated in the etiology or expression of symptoms of panic disorder.

Cholecystokinin-Tetrapeptide Induces Panic Attacks in Patients with Panic Disorder *

Cholecystokinin-tetrapeptide (CCK-4) and placebo were injected to 11 panic disorder patients. CCK-4 induced a panic attack identical to spontaneous panic attacks in all patients; placebo did not

Replication of action of cholecystokinin tetrapeptide in panic disorder: clinical and behavioral findings.

The effects of CCK-4 were consistent except symptom onset was more rapid with the second injection, which opens the doors for studies of the effects of drug treatment on CCk-4-induced panic.

Neuroanatomical circuits modulating fear and anxiety behaviors

  • D. Charney
  • Psychology, Medicine
    Acta psychiatrica Scandinavica. Supplementum
  • 2003
Objective:  Our understanding of the neurobiology of anxiety disorders, although not complete, has advanced significantly with the development and application of genetic, neuroimaging and

Imipramine antagonism of the panicogenic effects of cholecystokinin tetrapeptide in panic disorder patients.

It is demonstrated that imipramine can antagonize the panicogenic effects of CCK-4, and a marked reduction in the number and intensity of panic symptoms, duration of symptoms, frequency of panic attacks, and cardiovascular responsiveness.

Neuroanatomical hypothesis of panic disorder, revised.

Medications, particularly those that influence the serotonin system, are hypothesized to desensitize the fear network from the level of the amygdala through its projects to the hypothalamus and the brainstem, and effective psychosocial treatments may also reduce contextual fear and cognitive misattributions.

Neuropeptide S receptor gene — converging evidence for a role in panic disorder

Animal studies have suggested neuropeptide S (NPS) and its receptor (NPSR) to be involved in the pathogenesis of anxiety-related behavior. In this study, a multilevel approach was applied to further