Breathing impairments, such as an alteration in breathing
pattern, dyspnoea, and sleep apnoea, are common health deficits
recognised in Parkinson’s disease (PD). The mechanism that
underlies these disturbances, however, remains unclear. We
investigated the effect of the unilateral damage to the rat
nigrostriatal pathway on the central ventilatory response to
hypercapnia, evoked by administering 6-hydroxydopamine
(6-OHDA) into the right medial forebrain bundle (MFB). The
respiratory experiments were carried out in conscious animals in
the plethysmography chamber. The ventilatory parameters were
studied in normocapnic and hyperoxic hypercapnia before and
14 days after the neurotoxin injection. Lesion with the 6-OHDA
produced an increased tidal volume during normoxia. The
magnified response of tidal volume and a decrease of breathing
frequency to hypercapnia were observed in comparison to the
pre-lesion and sham controls. Changes in both respiratory
parameters resulted in an increase of minute ventilation of the
response to CO2 by 28 % in comparison to the pre-lesion state
at 60 s. Our results demonstrate that rats with implemented
unilateral PD model presented an altered respiratory pattern
most often during a ventilatory response to hypercapnia.
Preserved noradrenaline and specific changes in dopamine and
serotonin characteristic for this model could be responsible for
the pattern of breathing observed during hypercapnia.
The key role of the vagus nerves in the reflex control of breathing is generally accepted. Cardiopulmonary vagal receptors and their afferent connection with the medullary respiratory centers secures the proper regulatory feedback. Section of the vagi at the midcervical level interrupts primary vagal reflexes and those due to activation of lung afferents by neuroactive substances. In this context the present review focuses on the reflex contribution of the inferior (nodose) vagal ganglia to the respiratory pattern, considering that this structure contains perikarya of vagal afferent neurons which house neurotransmitters, neuropeptides and neurochemical substances. In experimental animals with removed sensory input from the lungs (midcervical vagotomy) the following evidence was reported. Transient respiratory suppression in the form of apnoea, occuring after systemic injection of serotonin, adenosine triphosphate and anandamide (N-arachidonoyl-ethanolamine-endogenous cannabinoid neurotransmitter), which was abrogated by nodose ganglionectomy. Preserved nodose-NTS connection conditioned respiratory depression affecting the timing component of the breathing pattern evoked by N-6-cyclopentyl-adenosine (CPA) and inhibition of both respiratory constituents induced by NPY. Stimulatory effect of NPY13-36 on tidal volume required nodosal connection. The cardiovascular effects of majority of the tested substances occurred beyond the nodose ganglia (with exclusion of serotonin and anandamide)., K. Kaczyńska, M. Szereda-Przestaszewska., and Obsahuje seznam literatury