Name: EDUARDO AKIRA FUJIWARA
Type: MSc dissertation
Publication date: 14/10/2016
Examining board:
Name |
Role |
|---|---|
| KARLA NÍVEA SAMPAIO | External Examiner * |
| LUIZ CARLOS SCHENBERG | Internal Alternate * |
| RITA DE CÁSSIA RIBEIRO GONÇALVES | External Alternate * |
| VANESSA BEIJAMINI HARRES | Internal Examiner * |
Summary: Chemoreflex is an important neural mechanism involved in cardiovascular and
respiratory control under hypoxic or hypercapneic situation. In experimental
studies, activation of this reflex promotes not only cardiorespiratory but also
behavioural changes. Previous studies from our research group have
demonstrated that the dorsal hippocampus (DH) can modulate cardiovascular
responses evoked by aversive stimuli such as contextual fear conditioning and
restraint stress. Evidences also show that modulation of the cholinergic
transmission within the DH produces marked changes in mean arterial pressure (MAP) and heart rate (HR) (Hori et al. 1995). However, whether the cholinergic neurotransmission within the DH participate in the cardiorespiratory responses of the chemoreflex remained unexplored. The goal of the present study was to evaluate the involvement of the DH cholinergic neurotransmission in the modulation of cardiovascular and respiratory responses evoked by the
peripheral chemoreflex activation. Male Wistar rats (280-340g) were anesthetized (Tribromethanol, 250 mg/kg) and stainless steel guide cannulae were implanted bilaterally into the DH using a stereotaxic apparatus. Three
days after the stereotaxic surgery, also under tribromethanol anesthesia, the
femoral artery and vein was catheterized to allow pulsatile arterial pressure
(PAP) recordings and drugs injection, respectively. The MAP and HR were
derived from the PAP recordings. Whole body plethysmograph was used to
assess the respiratory frequency (fR), the minute ventilation (VE) and the tidal
volume (VT). The chemoreflex was activated using KCN (40 µg/0.05 mL, iv) and the evoked MAP, HR, fR, VE and VT responses were evaluated before, 10 and 60 minutes after the bilateral microinjections of cholinergic agents within the DH. The drugs tested were: hemicholinium (1 nmol/500 nL), a choline reuptake inhibitor, atropine (0.6; 6; 18 and 30nmol/500 nL), non-selective muscarinic receptor antagonist, J104129 fumarate (6 nmol/500 nL) M1/M3 muscarinic receptor antagonist and pirenzepine (6 nmol/500 nL) a M1 selective antagonist. Data were analyzed by two way ANOVA for repeated measures, followed by Bonferroni post hoc test (P<0.05). Bilateral microinjections of the cholinergic modulatory agents within the DH did not alter the cardiorespiratory basal levels, as well as did not change any of the cardiorespiratory responses induced by the chemoreflex activation with KCN (P > 0.05). The present data shows that cholinergic neurotransmission within the DH neither seems to be involved in the control of cardiorespiratory basal levels nor in the processing of the cardiorespiratory responses induced by the peripheral chemoreflex activation.
