Dopamine D2 Receptor Modulated Rhythmic Respiratory Discharge Activity And Discharge Activities Of Inspiratory Neurons In MNRF Of Neonatal Rats In Vitro

Background Breathing is the process of gas exchange between human body and the external environment, is one of the basic signs of life, is a necessary condition of survival of the body. The medullary respiratory center was the most important, it is the origin of the mammalian respiratory rhythm, is the fundamental respiratory motion. To further in-depth analysis of the impact of D2 receptor to basic respiratory rhythm discharge and respiratory neuron, we design and perform this study.Objective To study the roles of D2 receptor to basic respiratory rhythm discharge and action potential of mNRF respiratory neurons, in order to further in-depth analysis of cerebral hypoxia, inflammation and other pathological process of adenosine concentration on medullary respiratory function, influence, provide theoretical guidance and experimental basis for treatment and prevention.Methods1. Using glass microelectrode and adsorption electrode recorded basic respiratory rhythm discharge and action potential of mNRF respiratory neurons of neonatal rat. The dopamine D2 receptor agonist Quinpirole and dopamine D2 receptor antagonist Raclopride were perfused to slice to analysis the effect of D2 receptor on RRDA and action potential of mNRF respiratory neurons of neonatal rat.The slices were divided into 4 groups:Control group:those slices were perfused by ACSF on the brain slices of 70 min, in 15 min,30 min,45 min and 60 min to measure RRDA inspiratory time and integral discharge amplitude, respiratory cycle, respectively; Different concentration of Quinpirole groups:record RRDA 10 min, after using ACSF, different concentrations (2,4,6,8 μmol/L) Quinpirole were used to slices, each concentration 12 min, observe the change of RRDA; Different concentration of Raclopride groups:different concentrations (0.2,0.4,0.6,0.8 μmol/L) of Raclopride on the brain slices were perfused, each concentration 12 min, observe the change of RRDA; Quinpirole and Quinpirole+Raclopride group:after recorded 10 min by ACSF, perfused by 4 mol/L Quinpirole 12 min, then perfused by 4 mol/L Quinpirole+0.4 mol/L Raclopride 12 min after was out.2. Recording action potential of mNRF respiratory neurons, perfused 4 μmol/L Quinpirole 12 min, then perfused 0.4 μmol/L Raclopride 12 min after was out.Results1. Quinpirole has inhibitory effect on RRDA,4 μmol/L was the optimal concentration; Raclopride has exciting effect to RRDA,0.4 mol/L was the optimal concentration. Quinpirole+Raclopride can block the exciting effect of Quinpirole to RRDA.2. Quinpirole decreased the excitability of inspiratory neurons in mNRF, Raclopride increased the excitability of inspiratory neurons in mNRF. Quinpirole short bursting last, decrease bursting amplitude, decrease bursting frequency, lengthen bursting interval; Raclopride increase bursting last, increase bursting amplitude, increase bursting frequency, short bursting interval.ConclusionsThere are dopamine D2 receptor on respiratory neuron membrane in mNRF take part in the modulated effects on RRDA and action potential of mNRF respiratory neurons, after be active, dopamine D2 receptor has negative effects on medullary respiratory center.