Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ga...Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ganglial plexus between aorta and pulmonary artery (A-PGP) in 33 anesthetized open-chest dog, electrocardiogram, atrial force and ventricular intramyocardial pressures (IMP) were recorded. The responses were also recorded following administration of atropine or propranolol and after heart acute decentralization. Results Ventricular arrhythmia (VA) was induced by injections of nicotine into A-PGP, but not by injections of nicotine into RAGP in 13 dogs. Atrioventricilar (A-V) block was induced by nicotine activating RAGP in 10 dogs, but not by nicotine activating A-PGP. Propranolol could reduce the frequency of VA elicited by stimulating A-PGP, atropine could reduce the frequency of A-V block elicited by stimulating RAGP. After acute decentralization, VA was still induced by activation of A-PGP in 9 dogs, but A-V block elicited by stimulating RAGP was decreased. Conclusion VA is induced by stimulating N receptor in cardiac nicotine-sensitive efferent sympathetic neurons of ventricular ganglial plexus (A-PGP), and then modifying β receptor of ventricles. A-V block is elicited by stimulating N receptor in atrial ganglial plexus (RAGP), then modifying M receptor of A-V node not only via efferent parasympathetic neurons, but also via afferent pathway.展开更多
The accessory olfactory bulb(AOB), located at the posterior dorsal aspect of the main olfactory bulb(MOB), is the first brain relay of the accessory olfactory system(AOS), which can parallelly detect and process volat...The accessory olfactory bulb(AOB), located at the posterior dorsal aspect of the main olfactory bulb(MOB), is the first brain relay of the accessory olfactory system(AOS), which can parallelly detect and process volatile and nonvolatile social chemosignals and mediate different sexual and social behaviors with the main olfactory system(MOS). However, due to its anatomical location and absence of specific markers, there is a lack of research on the internal and external neural circuits of the AOB. This issue was addressed by singlecolor labeling and fluorescent double labeling using retrograde rAAVs injected into the bed nucleus of the stria terminalis(BST), anterior cortical amygdalar area(ACo), medial amygdaloid nucleus(MeA), and posteromedial cortical amygdaloid area(PMCo) in mice. We demonstrated the effectiveness of this AOB projection neuron labeling method and showed that the mitral cells of the AOB exhibited efferent projection dispersion characteristics similar to those of the MOB. Moreover, there were significant differences in the number of neurons projected to different brain regions, which indicated that each mitral cell in the AOB could project to a different number of neurons in different cortices. These results provide a circuitry basis to help understand the mechanism by which pheromone information is encoded and decoded in the AOS.展开更多
文摘Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ganglial plexus between aorta and pulmonary artery (A-PGP) in 33 anesthetized open-chest dog, electrocardiogram, atrial force and ventricular intramyocardial pressures (IMP) were recorded. The responses were also recorded following administration of atropine or propranolol and after heart acute decentralization. Results Ventricular arrhythmia (VA) was induced by injections of nicotine into A-PGP, but not by injections of nicotine into RAGP in 13 dogs. Atrioventricilar (A-V) block was induced by nicotine activating RAGP in 10 dogs, but not by nicotine activating A-PGP. Propranolol could reduce the frequency of VA elicited by stimulating A-PGP, atropine could reduce the frequency of A-V block elicited by stimulating RAGP. After acute decentralization, VA was still induced by activation of A-PGP in 9 dogs, but A-V block elicited by stimulating RAGP was decreased. Conclusion VA is induced by stimulating N receptor in cardiac nicotine-sensitive efferent sympathetic neurons of ventricular ganglial plexus (A-PGP), and then modifying β receptor of ventricles. A-V block is elicited by stimulating N receptor in atrial ganglial plexus (RAGP), then modifying M receptor of A-V node not only via efferent parasympathetic neurons, but also via afferent pathway.
基金supported by the National Natural Science Foundation of China(31400946,31771156,91632303/H09,91732304 and 31830035)Strategic Priority Research Program of the Chinese Academy of Sciences(XDB32030200)。
文摘The accessory olfactory bulb(AOB), located at the posterior dorsal aspect of the main olfactory bulb(MOB), is the first brain relay of the accessory olfactory system(AOS), which can parallelly detect and process volatile and nonvolatile social chemosignals and mediate different sexual and social behaviors with the main olfactory system(MOS). However, due to its anatomical location and absence of specific markers, there is a lack of research on the internal and external neural circuits of the AOB. This issue was addressed by singlecolor labeling and fluorescent double labeling using retrograde rAAVs injected into the bed nucleus of the stria terminalis(BST), anterior cortical amygdalar area(ACo), medial amygdaloid nucleus(MeA), and posteromedial cortical amygdaloid area(PMCo) in mice. We demonstrated the effectiveness of this AOB projection neuron labeling method and showed that the mitral cells of the AOB exhibited efferent projection dispersion characteristics similar to those of the MOB. Moreover, there were significant differences in the number of neurons projected to different brain regions, which indicated that each mitral cell in the AOB could project to a different number of neurons in different cortices. These results provide a circuitry basis to help understand the mechanism by which pheromone information is encoded and decoded in the AOS.
