serotonina powstaje w jelicie!!!

[szewcmiki1]

wg najnowszych badan 95% serotoniny powstaje w jelitach,

[dala.tata]

poprosze o link do tych badan.

to żadna nowość

[neuroleptyk]

Nie wiem więc czemu autor o tym pisze. Co jest dla niego w tym
problematyczne?

www3.interscience.wiley.com/journal/120714741/abstract?CRETRY=1&SRETRY=0

Nigdy nie słyszeliście o prokinetycznym leku cisaprid? Agonista
receptora 5-HT4?

en.wikipedia.org/wiki/Enterochromaffin_cell
Autor prawdopodobnie wziął informację z wikipedii.

Nie będę wyszukiwał specjalnie abstraktów, a to, że serotonina jest
istotnym neurotransmiterem poza mózgiem nie jest żadnym nowum. Ale
by nie być pustosłownym coś jednak zamieszczę.

Res Commun Mol Pathol Pharmacol. 2003;113-114:115-31.

Effects of fluvoxamine, a selective serotonin re-uptake
inhibitor, on serotonin release from the mouse isolated ileum.

Minami M, Taguchi S, Kikuchi T, Endo T, Hamaue N, Hiroshige T, Liu
Y, Yue W, Hirafuji M.

Department of Pharmacology, Health Sciences University of Hokkaido,
Ishikari-Tobetsu, Hokkaido 061-0293, Japan. [e-mail]

The presence of nausea and vomiting is problematic for all selective
serotonin re-uptake inhibitors (SSRIs), and their usefulness as anti-
depressants is limited in this respect. In an attempt to examine the
background of SSRI-induced emesis, the present study aims to
describe the role of 5-hydroxytryptamine (serotonin:5-HT) from the
viewpoint of 5-HT release in the mouse-isolated ileum. In this
study, it was demonstrated that 5-HT release from the mouse-isolated
ileum was significantly increased by fluvoxamine at a concentration
of 10(-6) M. Also, it was demonstrated that granisetron, a 5-HT3
receptor antagonist, inhibited significantly the increase in
fluvoxamine (10(-6) M) -induced 5-HT release. The effect of
granisetron on fluvoxamine-induced 5-HT release was occurred in a
concentration-dependent manner. The present study demonstrated for
the first time that the SSRI-induced increase in 5-HT release from
the isolated ileum was significantly inhibited by 5-HT3 receptor
antagonist. These results suggest that 5-HT3 receptors might be
involved in SSRI-induced 5-HT release from the mouse isolated ileal
tissue. Fluvoxamine (10(-6) M)-induced 5-HT release was inhibited
concentration -dependently by the concomitant perfusion of
diltiazem. The results suggest that L-type calcium channel might be
also involved in SSRI-induced 5-HT release from the isolated ileum.
Furthermore, tetrodotoxin (10(-6) M) completely inhibited the
increase in 5-HT release induced by fluvoxamine. This finding
suggests that the increase of 5-HT induced by fluvoxamine involves
enterochromaffin (EC) cell stimulation via an inter-neuron pathway
in the gastrointestinal tract (GI). SSRI initiates an increase in
the concentration of 5-HT in the GI tract. 5-HT released from the EC
cells of the intestinal mucosa may stimulate the 5-HT3 receptors on
vagal afferent nerve fibers. This depolarization of vagal afferents
may result in a 5-HT increase in the brainstem and, thus, lead to
emesis.


Chyba więcej nie trzeba przynajmniej na razie.

[dala.tata]

zadna nowoscia jest to, ze serotonina jest produkowana w jelicie. moze jednak te
nowe badania cos nnowego poweidzialy. cholera wie.

[neuroleptyk]

dala.tata napisał:

> zadna nowoscia jest to, ze serotonina jest produkowana w jelicie.
moze jednak t
> e
> nowe badania cos nnowego poweidzialy. cholera wie.
>

To temat dla specjalistów, literatura dotycząca serotoniny jest
ogromna.

Biol Psychiatry. 2007 May 1;61(9):1081-9. Epub 2006 Sep 18.

Reduced serotonin-1A receptor binding in social anxiety disorder.


Lanzenberger RR, Mitterhauser M, Spindelegger C, Wadsak W, Klein N,
Mien LK, Holik A, Attarbaschi T, Mossaheb N, Sacher J, Geiss-
Granadia T, Kletter K, Kasper S, Tauscher J.

Department of General Psychiatry, Medical University of Vienna,
Vienna, Austria. [e-mail]

BACKGROUND: Results from studies in serotonin-1A (5-HT1A) knockout
mice and previous positron emission tomography (PET) studies in
humans imply a role for 5-HT1A receptors in normal state anxiety as
well as in certain anxiety disorders. The objective of this study
was to investigate 5-HT1A receptor binding potential (BP) in social
anxiety disorder (SAD). METHODS: Using PET and [carbonyl-11C]WAY-
100635, we compared a homogeneous group of 12 unmedicated, male SAD
patients with 18 healthy control subjects (HC). A multivariate ANOVA
with all regional BP values as dependent variables, age and four
radiochemical variables as covariates was performed. RESULTS: We
found a significantly lower 5-HT1A BP in several limbic and
paralimbic areas but not in the hippocampus (p = .234) of SAD
patients. The difference in 5-HT1A binding was most significant in
the amygdala (-21.4%; p = .003). There was also a more than 20%
lower 5-HT(1A) BP of SAD patients in the anterior cingulate cortex
(p = .004), insula (p = .003), and dorsal raphe nuclei (p = .030).
CONCLUSIONS: The lower 5-HT1A binding in the amygdala and
mesiofrontal areas of SAD patients is consistent with 1) preclinical
findings of elevated anxiety in 5-HT1A knockout mice, 2) a previous
PET study in healthy volunteers showing an inverse correlation
between 5-HT1A BP and state anxiety, and 3) another human PET study
in patients with panic disorder showing reduced 5-HT1A binding, thus
corroborating the potential validity of 5-HT1A receptors as targets
in the treatment of human anxiety disorders.

Mol Psychiatry. 2004 Apr;9(4):386-92.

Persistent reduction in brain serotonin1A receptor binding in
recovered depressed men measured by positron emission tomography
with [11C]WAY-100635.

Bhagwagar Z, Rabiner EA, Sargent PA, Grasby PM, Cowen PJ.

University Department of Psychiatry, Warneford Hospital, Oxford, UK.

Positron emission tomography (PET) studies with the selective 5-HT
(1A) receptor ligand, [(11)C]WAY-100635, have indicated that the
binding potential (BP) of brain 5-HT(1A) receptors is lowered in
unmedicated subjects with acute major depression. However, it is
unclear if these changes persist after recovery from depression. To
resolve this issue, we used [(11)C]WAY-100635 in conjunction with
PET imaging to compare 5-HT(1A) BP in 18 healthy controls and 14
male subjects with recurrent major depression who were clinically
recovered and free of antidepressant medication. BP values, derived
from a reference tissue model, were analysed by region of interest
and statistical parametric mapping. Both analyses showed a
widespread and substantial (17%) decrease in 5-HT(1A) receptor BP in
cortical areas in the recovered depressed subjects. In contrast, 5-HT
(1A) BP in the raphe nuclei did not distinguish depressed subjects
from controls. Our results suggest a persistent dysfunction in
cortical 5-HT(1A) BP as measured by [(11)C]WAY-100635 in recovered
depressed men. Lowered 5-HT(1A) receptor binding availability could
represent a trait abnormality that confers vulnerability to
recurrent major depression.

Biol Psychiatry. 2006 Jan 15;59(2):106-13. Epub 2005 Sep 9.

Altered serotonin 1A binding in major depression: a [carbonyl-C-
11]WAY100635 positron emission tomography study.

Parsey RV, Oquendo MA, Ogden RT, Olvet DM, Simpson N, Huang YY, Van
Heertum RL, Arango V, Mann JJ.

Department of Psychiatry, Columbia University College of Physicians
and Surgeons, New York, New York, USA.
[e-mail]

BACKGROUND: Serotonin 1A receptors (5-HT(1A)) are implicated in the
pathophysiology of major depressive disorder (MDD) and in the action
of selective serotonin reuptake inhibitors (SSRI). SSRI desensitize
5-HT(1A) and down-regulate 5-HT transporters (5-HTT) with the latter
persisting for weeks after discontinuation of SSRI. MDD subjects are
more likely to be homozygous for the functional 5-HT(1A) G(-1019)
allele of the promoter polymorphism and are postulated to have
higher 5-HT(1A) than healthy volunteers (controls). We measure 5-HT
(1A) in MDD, assess the effects of antidepressant exposure (AE), and
examine the role of the C(-1019)G polymorphism. METHODS: Genotyped
and determined 5-HT(1A) binding potential (BP) by positron emission
tomography (PET) using [carbonyl-C-11]-WAY-100635 in 28 medication-
free MDD subjects during a current major depressive episode and 43
controls. RESULTS: No difference in BP between controls and MDD
subjects (p = .235). There was a difference in BP comparing the
controls, antidepressant naive (AN) MDD subjects, and subjects with
AE across all regions (p = .013). Post hoc testing reveals higher BP
in AN compared to controls (p = .008) and to AE (p = .007). The GG
genotype is overrepresented in MDD subjects (p = .059), and BP
appears higher with the G allele. CONCLUSIONS: AN have higher 5-HT
(1A) than controls and AE suggesting a model of depression
characterized by an over expression of autoinhibitory
somatodendritic 5-HT(1A) receptors, perhaps due to the higher
expressing G allele, that may result in reduced terminal field 5-HT
release. AE appears to have long-term effects on 5-HT(1A).

Zagadnienie jest skomplikowane, i nie ma sensu tego tu wszystkiego
cytować. Jeśli chodzi o SSRI i transporter serotoniny to poniżej
link do ciekawej pracy na łamach The American Journal Of Psychiatry:

ajp.psychiatryonline.org/cgi/content/full/161/5/826

lub PDF

ajp.psychiatryonline.org/cgi/reprint/161/5/826

[neuroleptyk]

Jeszcze dla ciekawskich, negatywna korelacja nasłonecznienia, pory
roku z BP transportera serotoniny.

archpsyc.ama-assn.org/cgi/content/full/65/9/1072PDF
archpsyc.ama-assn.org/cgi/reprint/65/9/1072

[awanturka]

Litości !!!!

czy dziennikarze myślą, że wystarczy wynaleść gdziekolwiek (a najlepiej - w wikipedii) pierwszą lepszą informację i podać ją jako sensacyjne, wielkie, najnowsze odkrycie??

A może rzeczywiście wystarczy??? Jak myślicie, ilu ludzi przyjmuje za dobrą monetę takie "pseudosensacje".

[iso1]

ciekawi mnie to
jakieś artykuły po polsku są ?