Tesis
Função colinérgica cardiorrespiratória no núcleo do trato solitário
Date
2013-08-26Registration in:
Author
Furuya, Werner Issao
Institutions
Abstract
The nucleus of the solitary tract (NTS) is the primary synaptic site of the
peripheral baroreceptors and chemoreceptors. It has been shown that acetylcholine
(ACh) microinjected into the NTS of rats induces hypotension and bradycardia.
However, the contribution of cholinergic mechanisms at different NTS subnuclei
(intermediate and commissural) as well as the cholinergic receptors blockade on the
control of sympathetic (SNA) and phrenic (PNA) nerve activities have not been
studied yet. In this study we assessed the role of ACh and its cholinergic receptors at
the intermediate NTS (iNTS) and commissural NTS (cNTS) on the control of SNA,
PNA and electrophysiological properties of these subnuclei neurons, as well as on
baro and chemoreflex responses. Decorticated arterially-perfused in situ preparations
of male juvenile rats were used to record SNA and PNA. Microinjections of ACh and
cholinergic antagonists were performed into the iNTS or cNTS. Coronal slices of the
brainstem containing either cNTS or iNTS subnuclei were obtained from male
juvenile rats and used in whole cell patch clamp – current clamp recordings. It was
observed that ACh microinjected into the iNTS inhibited both SNA and PNA. These
effects were reduced by the pre-treatment with atropine (muscarinic antagonist) or
mecamylamine (nicotinic antagonist). The cholinergic antagonists into the iNTS did
not change the effects on SNA and PNA induced by baro and chemoreflex activation.
In contrast, microinjections of ACh into the cNTS did not induce changes in SNA, but
increased PNA. Despite the absence of changes in SNA, ACh into the cNTS
changed the pattern of respiratory-sympathetic coupling. Both atropine and
mecamylamine into the cNTS inhibited the ACh-induced tachypnea, but only
mecamylamine inhibited the chemoreflex-induced tachypnea and the ACh-induced
change in respiratory-sympathetic coupling. In vitro studies demonstrated that ACh
promotes depolarization in both iNTS and cNTS neurons. Both muscarinic and
nicotinic antagonism in the iNTS inhibited the ACh-induced depolarization. However,
only nicotinic antagonist was effective in diminishing this response in the cNTS. The
results suggest that ACh plays an important role in the control of cardiovascular and
respiratory activities, with distinct functions between iNTS and cNTS. This cholinergic
control involves activation of both muscarinic and nicotinic receptors within NTS, but
only nicotinic receptors are involved in the chemoreflex tachypneic response.