Platelet [3H]Imipramine binding in generalized anxiety disorder, panic disorder, and agoraphobia with panic attacks

Schneider, Lon S.; Munjack, Dennis J.; Severson, James A.; Palmer, Ruby

doi:10.1016/0006-3223(87)90130-2

Cited by 35 publications

(15 citation statements)

References 35 publications

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“…Platelet imipramine binding (to a site related to the 5‐HT transporter site) did not differ in the PD group relative to those in the control group (149, 150). Another study reported reduced concentrations of circulating 5‐HT in PD compared with control samples (151), although this finding has not been replicated.…”

Section: Serotonergic Function In Anxiety Disordersmentioning

confidence: 94%

Neuroanatomical circuits modulating fear and anxiety behaviors

Charney

2003

Acta Psychiatr Scand

248

157

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Objective: Our understanding of the neurobiology of anxiety disorders, although not complete, has advanced significantly with the development and application of genetic, neuroimaging and neurochemical approaches. Method: The neuroanatomical basis of anxiety disorders is reviewed with particular focus on the amygdala and the temporal and prefrontal cortex. The functional anatomical correlates of anxiety disorders such as panic disorder, specific phobias and post‐traumatic stress disorder are also discussed. Results: Functional neuroimaging studies in patients with anxiety disorders have shown neurophysiological abnormalities during symptom provocation tests, implicating the limbic, paralimbic and sensory association regions. The involvement of neurotransmitters such as serotonin and norepinephrine in depressive disorders is well established. Antidepressants that affect these neurotransmitter systems have also been shown to be useful in the treatment and management of patients with anxiety disorders. The role of serotonin and norepinephrine in the pathophysiology of anxiety disorders is reviewed. In addition, the involvement of the stress hormone corticotropin‐releasing hormone, the peptide cholecystokinin and the amino acid transmitter γ‐amino butyric acid in anxiety disorders is reviewed. Conclusion: The inconsistency in the results of biologic investigations of anxiety disorders highlights the importance of addressing the neurobiologic heterogeneity inherent within criteria‐based, psychiatric diagnoses. Understanding of this heterogeneity will be facilitated by the continued development and application of genetic, neuroimaging and neurochemical approaches that can refine anxiety disorder phenotypes and elucidate the genotypes associated with these disorders. Application of these experimental approaches will also facilitate research aimed at clarifying the mechanisms of anti‐anxiety therapies.

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Section: Serotonergic Function In Anxiety Disordersmentioning

confidence: 94%

Neuroanatomical circuits modulating fear and anxiety behaviors

Charney

2003

Acta Psychiatr Scand

248

157

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“…Imipramine binding to platelets, a putative measure of the serotonin uptake site, appears to be normal (Davis et al, 1985;Roy-Byme & Uhde, 1985;Nutt & Fraser, 1987;Schneider et al, 1987;Uhde et al, 1987). Normal opiate receptor function is suggested by studies in which panic patients had responses to naloxone that were minimal and identical to those of control subjects (Hoehn-Saric & Masek, 1981;Liebowitz et al, 1984).…”

Section: Peripheral Receptor Statusmentioning

confidence: 99%

Systemic hormonal and physiological abnormalities in anxiety disorders

Cameron

Nesse

1988

Psychoneuroendocrinology

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Among the studies of systemic hormonal and physiological abnormalities associated with anxiety disorders, the most consistent and extensive findings suggest (a) peripheral adrenergic hyperactivity (including increases in norepinephrine but not epinephrine) and functional dysregulation, (b) increased incidence of mitral valve prolapse in panic patients, and (c) normal suppressibility of the hypothalamic-pituitary-adrenal cortical endocrine system with dexamethasone in panic patients. Other less-certain findings include (a) increased circulating concentrations of plasma ACTH and/or cortisol, and prolactin, in panic patients, (b) increased platelet monoamine oxidase activity in generalized anxiety and/or panic patients, (c) decreased gonadal axis activity in some anxious individuals, (d) decreased nighttime melatonin plasma concentrations in panic patients, and (e) peripheral alpha 2 and beta-adrenoreceptor down-regulation, with normal serotonin binding parameters. These findings, taken together, provide tentative support for dysfunction in adrenergic and GABAergic central nervous system mechanisms in people with anxiety disorders. Abnormal anxiety and normal stress both show evidence of adrenergic hyperactivity; however, there appear to be differences in hormonal profiles, especially the apparent lack of increase of epinephrine during panic attacks, as well as differences in the reactivity of the system, and in the "trigger" mechanisms which determine when the response occurs.

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“…. No changes are found in schizophrenia 130, panic attacks79,96 Alzheimer's or Parkinson's disease 109. Seasonal variations have been observed by most 7, 31, 111,125 but not by all 58 authors.…”

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confidence: 98%

“…Rather than clarify possible discrepancies, more have arisen: of the 9 studies with at least one year of data, five found seasonal changes 30, 31, 45, 91, 119 and four did not22,36,96,113. A number of studies have shown a variety of diurnal changes in either Vm.x or affinity or both 46'67' 85, 86,95, 126; no studies have used sufficient time points or subjects to provide a clear pattern (and a negative finding with two time points is not necessarily so 6).…”

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confidence: 99%

Platelet research in psychiatry

Wirz‐Justice

1988

Experientia

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The platelet is one of the most researched biological markers in psychiatry. Characteristics of MAO activity, 5-HT uptake, imipramine and alpha 2-adrenergic receptor binding, for example, are similar in platelet and CNS. Methodological factors are not negligible, and range from diagnostic specificity and drug effects to the normal physiological variability of age and hormone-related changes, circadian and seasonal rhythms. As yet, there are no clear state or trait platelet markers in affective disorders and schizophrenia that can be unequivocally used to detect vulnerability to the illness, predict therapeutic response, define clinical diagnostic entities or follow the course of the illness. However, platelet markers are increasingly being used in careful studies to monitor psychopharmacological effects (an in vivo assay of all active metabolites), different ligands can be specific markers for certain aspects of a psychiatric illness (e.g. alpha 2-adrenergic receptors and weight loss), and this homogeneous preparation of human cells is an increasingly important tool in studying mechanisms in pathophysiology. More longitudinal studies are required to establish functional relationships between platelet variables and psychopathology.

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Platelet [3H]Imipramine binding in generalized anxiety disorder, panic disorder, and agoraphobia with panic attacks

Cited by 35 publications

References 35 publications

Neuroanatomical circuits modulating fear and anxiety behaviors

Neuroanatomical circuits modulating fear and anxiety behaviors

Systemic hormonal and physiological abnormalities in anxiety disorders

Platelet research in psychiatry

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