Pathophysiology of Irritable bowel syndrome:The role of brain-gut axis and serotoninergic receptors
(EN)
D.G. Karamanolis, I. Kyrlagkitsis,
SUMMARY
The last decade has been marked by substantial progress
in the understanding of the pathophysiology of Irritable
Bowel Syndrome (IBS). Considerable advances contributing
to this progress include the decryption of the secrets of
the enteric nervous system (ENS) and the neuronal pathways
involved in the transmission of visceral nociception
as well as the localisation of potential processing centres
in the central nervous system (CNS). Serotonin is sequestered
in the neterochromaffin cells and is an essential mediator
in the ENS. It manifests its actions mainly by 5-HT3
and 5-HT4 receptors and plays a key role in intestinal motility
and secretion. The central processing unit of serotoninergic
actions in the ENS is the AH/Dogiel morphologic
type II neuron which was formerly considered to be the
primary afferent neuron. It remains unknown whether the
neurologic disorder in IBS consists of an exaggerated response
to noxious stimuli in the gut, or misinterpretation
by the CNS of otherwise accurate information. The exact
locus of projection of visceral information in the brain is
not known, but there is increasing evidence for areas such
as the thalamus, the prefrontal cortex and the amygdaloid
nucleous in the limbic system. Anxiogenic colonic response
is probably mediated by CRF-1 receptors. Autonomic pathways
from the brain stem may also play a role by regulating
the intensity of perception during visceral stimulation.
More accurate localisation of the neurologic derangement
along the brain-gut axis is required, thus permitting a more
targeted therapeutic intervention.
Gastroenterology department, Tzaneion Hospital, Pireus, Greece Key words: Serotonin, visceral nociception, affered neuron
presynaptic inhibition
(EN)
