Rats emit 22-kHz or 50-kHz ultrasonic vocalizations (USVs) to signal their emotional state to other conspecifics. The 22-kHz USVs signal a negative emotional state while 50-kHz USVs reflect a positive affective state. The initiation of 22-kHz USVs is dependent on the activity of cholinergic neurons within the laterodorsal tegmental nucleus that release acetylcholine along the medial cholinoceptive vocalization strip. Emission of 50-kHz USVs is dependent upon the activation of dopaminergic neurons located within the ventral tegmental area that release dopamine into the medial shell of the nucleus accumbens. There have been reports that showed an antagonistic interaction between acetylcholine and dopamine during the expression of emotional states, and dopamine agonists decreased carbachol-induced emission of 22-kHz USVs. The current study tests the hypothesis that initial antagonism of dopamine receptors by systemic haloperidol or intraacumbens raclopride should increase the subsequent emission of 22 kHz USVs induced by carbachol from the lateral septum. Our findings showed that antagonism of dopaminergic signaling either via systemic haloperidol or via intracerebral raclopride did not alter the number of emitted 22-kHz USVs. Thus, inhibition of the mesolimbic dopamine system did not increase the magnitude of a negative emotional state. It was found, however, that prolonged emission of 22-kHz USVs initiated by carbachol caused a delayed rebound emission (R) of 50-kHz USVs appearing after 300 s of emission of 22-kHz USVs, i.e., when the response was subsiding. The R-50-kHz USVs were predominantly frequency modulated (FM) USVs and their number was directly proportional to the number of recorded 22-kHz USVs. The emission of R-50-kHz USVs was reversed by systemic pretreatment with haloperidol or intraacumbens injection of raclopride. It is argued that the R-50-kHz USVs represent a rebound emotional state that is opposite in valence and arousal induced by carbachol. Importantly, prolonged emission of amphetamine-induced 50 kHz USVs failed to show any vocalization rebound effect.

大鼠发出22 kHz或50 kHz的超声波发声（USV），以向其他特定对象传达其情绪状态。22 kHz的USV表示负性情绪状态，而50 kHz的USV表示正性情绪状态。22 kHz USV的启动取决于后嗅方被膜核内胆碱能神经元的活动，该神经沿内侧胆碱感受性发声带释放乙酰胆碱。50 kHz USV的发射取决于位于腹侧被盖区的多巴胺能神经元的激活，该神经元将多巴胺释放到伏隔核的内侧壳中。有报道表明，在情绪状态的表达过程中，乙酰胆碱和多巴胺之间存在拮抗作用，多巴胺激动剂降低了卡巴胆碱诱导的22 kHz USV发射。目前的研究检验了以下假说：全身性氟哌啶醇或刺五加内酯雷克必利对多巴胺受体的初始拮抗作用应增加由卡巴胆碱引起的从侧中隔发出的22 kHz USV的后续发射。我们的研究结果表明，通过全身性氟哌啶醇或脑内雷洛必利对多巴胺能信号的拮抗作用不会改变发射22 kHz USV的数量。因此，抑制中脑边缘的多巴胺系统并没有增加负面情绪状态的强度。但是，发现由卡巴胆碱引起的22 kHz USV的长时间发射导致在发射22 kHz USV 300 s后出现了50 kHz USV的延迟回弹发射（R），即当响应减弱时。R-50 kHz USV主要是调频（FM）USV，其数量与记录的22 kHz USV的数量成正比。R-50 kHz USV的发射通过氟哌啶醇或瑞普利特的锐角内注射全身性预处理得以逆转。有人认为，R-50kHz的USV代表一种反弹的情绪状态，这种状态在由卡巴胆碱引起的化合价和唤醒中是相反的。重要的是，苯丙胺诱导的50 kHz USV的长时间发射未能显示任何发声反弹效果。