Cholinergic-Muscarinic Dysfunction in Mood Disorders

التفاصيل البيبلوغرافية
العنوان: Cholinergic-Muscarinic Dysfunction in Mood Disorders
المؤلفون: David H. Overstreet, David S. Janowsky
المصدر: Medical Psychiatry ISBN: 142002115X
بيانات النشر: CRC Press, 2007.
سنة النشر: 2007
مصطلحات موضوعية: Physostigmine, medicine.medical_specialty, biology, business.industry, medicine.disease, Animal data, Endocrinology, Mood disorders, Internal medicine, Muscarinic acetylcholine receptor, medicine, biology.protein, Cholinergic, medicine.symptom, business, Mania, Acetylcholine, medicine.drug, Cholinesterase
الوصف: For more than a century, acetylcholine has been postulated to be a factor in the regulation and etiology of affect. In 1889, Willoughby (1) reported a case in which pilocarpine, now known to be a muscarinic cholinergic agonist, was used to alleviate acute mania. Subsequently, in the late 1940s, 1950s, and early 1960s, a number of authors observed the anergic, inhibitory, anxiety-enhancing and mood-depressing effects of centrally acting cholinesterase inhibitors, compounds that inhibit the breakdown of acetylcholine. The mood altering effects of these compounds, used as insecticides in the agriculture industry and as nerve agents by the military, were described naturalistically and as tested in experimental settings. The observations by Grob et al. (2), Gershon et al. (3,4), Bowers et al. (5), and Rowntree et al. (6) led to a series of reports suggesting that increases in central acetylcholine led to depression, anxiety, and anergia. In the early 1970s, based on the above studies and on animal data reported by Domino and Olds (7), Stark and Boyd (8), and Carlton (9), Janowsky et al. (10) developed an adrenergic-cholinergic balance hypothesis of manic depression. This hypothesis proposed that depression represents an overabundance of central acetylcholine, relative to central adrenergic neurochemicals, and that mania represents the converse. Part of the work of Janowsky et al. (10,11) involved infusing the short acting reversible central cholinesterase inhibitor physostigmine on one occasion and the noncentrally acting cholinesterase inhibitor, neostigmine on another. Comparing behavioral effects, Janowsky and colleagues used this paradigm in manics, depressives, schizophrenics, and normals and observed decreased manic and increased depressive symptoms only in their physostigmine treated subjects (11,12). This work was replicated during the 1970s and early 1980s by a variety of investigators. In the late 1970s Sitaram et al. (13) observed that shortening of the cholinergic-sensitive sleep parameter, rapid eye movement (REM) latency, by cholinomimetic drugs was exaggerated in affective disorder patients, suggesting cholinergic supersensitivity in these patients, a finding subsequently replicated in a number of studies. In the late 1970s and early 1980s, Davis and Davis (14) and Risch et al. (15) began a series of experiments in which they evaluated the effect of cholinergic influences on stress-sensitive neurohormones including ACTH, beta-endorphin
ردمك: 978-1-4200-2115-8
1-4200-2115-X
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ab584524dfc9beff506a8ee331910de5Test
https://doi.org/10.3109/9781420021158-7Test
رقم الانضمام: edsair.doi.dedup.....ab584524dfc9beff506a8ee331910de5
قاعدة البيانات: OpenAIRE