Sleep disturbances are common in chronic stress, depression, and neurodegenerative disorders, yet the underlying neural mechanisms remain poorly understood. This research study demonstrated that chronic social defeat stress increases the excitability and burst firing of ventral tegmental area (VTA) dopamine neurons, leading to excessive dopamine release in the medial prefrontal cortex (mPFC). This hyperdopaminergic signaling disrupted sleep spindle generation and continuity, resulting in fragmented non-rapid eye movement (NREM) sleep characterized by frequent sleep-wake transitions, reduced spindle density and duration, impaired spindle–slow wave coupling, and poor sleep quality despite increased total NREM sleep. The authors further showed that activation of the VTA–mPFC dopaminergic pathway reproduced these sleep abnormalities, whereas inhibition of the pathway, blockade of dopamine D1/D2 receptors, or suppression of stress-induced HCN channel activity in VTA dopamine neurons improved sleep architecture and spindle properties. A particularly innovative aspect of the study was the use of fast high-resolution miniature two-photon microscopy (FHIRM-TPM) in freely moving mice, which enabled simultaneous monitoring of dopamine dynamics in the mPFC alongside EEG/EMG recordings during natural sleep. This approach provided direct evidence that elevated dopamine transients in the mPFC interrupt sleep spindle continuity, establishing a mechanistic link between chronic stress, dopaminergic circuit dysfunction, and sleep fragmentation.