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Signal Transduction in Affective Disorders

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Title: Signal Transduction in Affective Disorders
by H. Ozawa, T. Saito, N. Takahata, Japan) (Cor)/ Symposium on Affective Disorders and Neuronal Signal Transduction (199 (Cor) Nihon Seishin Shinkei Gakkai Sokai 1996 Sapporo-Shi, Sapporo Neuroscience Meeting 1996), Nihon Seishin Shinkei Gakkai
ISBN: 4-431-70210-5
Publisher: Springer Verlag
Pub. Date: March, 1998
Format: Hardcover
Volumes: 1
List Price(USD): $128.00
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Average Customer Rating: 5 (1 review)

Customer Reviews

Rating: 5
Summary: Ah, I finally get to write a real scientific review
Comment: I read 41 different books (and over 500 journal articles) in preparing my new book, The Failures of American Medicine. All of the other books that I have reviewed, I have had to "talk down" to the lay-reader and try to explain in common sense terms why the book is good or bad. Now with this book (overpriced as it is), I finally can write a real scientific review. This book is very good, for what it is---the 5HT-2A signal transduction pathway. Yes, this is probably the main pathway that causes depression (besides HPA axis disregulation, although the 2A pathway is involved with HPA anyway). And it's also the main pathway that helps a person taking SSRI's overcome depression.

It explains that the 2A pathway shunts over to the noradrenaline (NA) pathway, thus providing energy and neuronal remodeling and dendrite regrowth. This is a discovery that had previously stumped researchers, because they realized that the 5HT and NA pathways must be interconnected, but they didn't know how they were. However, I think that this book brings to light an even more interesting discovery---patients with severe, suicidal depression have elevated intracellular calcium levels. Not only does the 2A pathway shunt over to the NA pathway, it also funnels into the "calcium" pathway, a complex and often redundant pathway that controls many different cellular functions, including muscle contraction. I believe that somehow the calcium pathway becomes dominant over the NA shunt, and (again, besides HPA axis disregulation) that's why patients become depressed. And certain calcium channel blockers (ex. Nimodopine) can act as antidepressants! Much more research is needed into the calcium field of brain research. The calcium pathway may also be involved in SSRI side effects, since this pathway may be stimulated in some patients, making things potentially worse, or possibly explaining why these patients are treatment-resistant. I have a chapter on this phenomenon in my book, if you care to read about it.

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