Narcolepsy patients show more activation of the NAc than healthy controls when reading humorous cartoon 22. The NAc has also been considered a critical nucleus related to cataplexy with positive emotion. In contrast, activity in the caudal NAc increases with negative emotions such as defensive treading in rats 21. Activity in the rostral NAc increases when mice engage in behaviors associated with positive emotion, such as feeding. ![]() Furthermore, a previous study revealed the rostrocaudal segregation of emotional behavior in the NAc 21. Activation of projections from the basolateral amygdala to the NAc code positive valence in mice 20. The dorsal NAc shell activation of dynorphinergic neurons drives reward behavior and the ventral NAc shell drive aversion in mice 19. Blockade of dopamine receptors in the NAc reduces 50-kHz USVs as a marker of positive emotion induced by tactile stimulation of the skin 17, 18. The NAc plays roles in positive emotional behavior such as motivation, drug abuse, alcohol, and rewards 15, 16. The nucleus accumbens (NAc) is commonly known as the ventral striatum and a part of the mesolimbic structure called the reward pathway 13, 14. Thus, cataplexy is believed to be triggered by positive emotion in narcoleptic mice and can be used as a behavioral index of positive emotion. In addition, we previously showed that female encounters increased the number of cataplexy-like behaviors in male ORX-AB mice, and 85% of cataplexy-like behavior preceded ultrasonic vocalization (USVs) that is thought to reflect sexual excitation 11. These narcoleptic mice show cataplexy behavior caused by positive emotion with running wheel 7, 8, sweetened cereal 9, and chocolate 8, 10, 11, 12. The muscle atonia is observed in animal models with orexin receptor-2 gene mutant dog 3, deficiency of orexin (also known as hypocretin) ( prepro-orexin knockout mice) 4, and orexin neuron-ablated (ORX-AB) mice 5, 6. The symptom is a sudden transient loss of muscle tone without impairment of consciousness 1 triggered by strong emotions such as laughter, joke, or surprise in human 2. We propose that the initiation of cataplexy-like behavior is facilitated by activation of the NAc, while NAc-independent mechanisms determine the termination of the behavior.Ĭataplexy is the main symptom of type 1 narcolepsy, a sleep disorder. On the other hand, our study's result from optogenetic inhibition of the NAc (no effect) was different from chemogenetic inhibition (reduction of cataplexy-like behavior) in our previous study. Thus, activation of the NAc, whether transient (light stimulation) or longer-lasting (chemical stimulation in our previous study), facilitates cataplexy-like behaviors and contributes to the induction but not maintenance in them. Immunohistochemical analysis revealed that photo-illumination activated channel rhodopsin-expressing NAc shell neurons. The episode duration of cataplexy-like behavior was not affected by activation or inactivation. Meanwhile, inactivation with archaerhodopsin did not affect incidence. Photo-illumination to the NAc in the channel rhodopsin-expressing mice showed a higher incidence (34.9 ± 5.1%) of cataplexy-like behavior than the control mice (17.8 ± 3.1%, P = 0.0056). ![]() In this study, we investigated whether a short-lasting stimulation/inhibition of the NAc by optogenetics led to a similar result. In our previous study using chemogenetic techniques in narcoleptic mice (orexin neuron-ablated mice), we found that the rostral nucleus accumbens (NAc) shell is needed for chocolate-induced cataplexy. It can be seen as a behavioral index of salience, predominantly positive emotion, since it is triggered by laughter in humans and palatable foods in mice. Cataplexy is one of the symptoms of type 1 narcolepsy, characterized by a sudden loss of muscle tone.
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