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The full mechanism of action of propofol, a commonly administered intravenous anesthetic drug in clinical practice, remains elusive. The focus of this study was the role of GABAergic neurons which are the main neuron group in the ventral pallidum (VP) closely associated with anesthetic effects in propofol anesthesia. The activity of VP GABAergic neurons following propofol anesthesia in Vgat-Cre mice was observed via detecting c-Fos immunoreactivity by immunofluorescence and western blotting. Subsequently, chemogenetic techniques were employed in Vgat-Cre mice to regulate the activity of VP GABAergic neurons. The role of VP GABAergic neurons in generating the effects of general anesthesia induced by intravenous propofol was further explored through behavioral tests of the righting reflex. The results revealed that c-Fos expression in VP GABAergic neurons in Vgat-Cre mice dramatically decreased after propofol injection. Further studies demonstrated that chemogenetic activation of VP GABAergic neurons during propofol anesthesia shortened the duration of anesthesia and promoted wakefulness. Conversely, the inhibition of VP GABAergic neurons extended the duration of anesthesia and facilitated the effects of anesthesia. The results obtained in this study suggested that regulating the activity of GABAergic neurons in the ventral pallidum altered the effect of propofol on general anesthesia.
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http://dx.doi.org/10.1016/j.neuropharm.2024.110032 | DOI Listing |
J Neurophysiol
September 2025
Department of Neurosurgery, University of Utah School of Medicine, Salt Lake City, UT, USA.
Although glutamatergic and GABAergic synapses are important in seizure generation, the contribution of non-synaptic ionic and electrical mechanisms to synchronization of seizure-prone hippocampal neurons remains unclear. Here, we developed a physiologically relevant model to study these mechanisms by inducing prolonged seizure-like discharges (SLDs) in hippocampal slices from male rats through modest, sustained ionic manipulations. Specifically, we reduced extracellular calcium to 0.
View Article and Find Full Text PDFNeuropsychopharmacology
September 2025
Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
Chronic treatment with fluoxetine, a widely prescribed selective serotonin reuptake inhibitor (SSRI), is known to promote neural plasticity. The role of fluoxetine in plasticity has been particularly tied to parvalbumin-positive interneurons, a key population of GABAergic neurons that regulate inhibitory tone and network stability. While our previous studies have highlighted fluoxetine-induced plasticity in the visual cortex and hippocampus, its cell-type-specific effects in the prefrontal cortex (PFC) remain unclear.
View Article and Find Full Text PDFBrain
September 2025
Okinawa Institute of Science and Technology Graduate University, Okinawa, 904-0495, Japan.
Animal models of the pathology of Parkinson's disease (PD) have provided most of the treatments to date, but the disease is restricted to human patients. In vitro models using human pluripotent stem cells (hPSCs)-derived neural organoids have provided improved access to study PD etiology. This study established a method to generate human striatal-midbrain assembloids (hSMAs) from hPSCs for modeling alpha-synuclein (α-syn) propagation and recapitulating basal ganglia circuits, including nigrostriatal and striatonigral pathways.
View Article and Find Full Text PDFFront Behav Neurosci
August 2025
Department of Sensory and Cognitive Physiology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Sound influences motor functions and sound perception is conversely modulated by locomotion. Accumulating evidence supports an interconnection between the auditory system and the basal ganglia (BG), which has functional implications on the interaction between the two systems. Substantial evidence now supports auditory cortex and auditory thalamus inputs to the tri-laminar region of the tail of the striatum (tTS) in rodents.
View Article and Find Full Text PDFBrain Res
September 2025
Department of Geriatric Rehabilitation, Clinical Research Center for Geriatric Disorders of Guangxi Zhuang Autonomous Region, Guangxi, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, No 85 Hedi Road, Nanning, 530021, Guangxi Zhuang Autonomous Region, China. Electronic address: 13657813091@163
Levofloxacin (LVFX)-associated seizures are thought to arise from disrupted excitatory-inhibitory balance, but the underlying synaptic mechanisms remain unclear. This study investigated how LVFX alters both glutamatergic and GABAergic transmission to promote neuronal hyperexcitability. We combined in vitro and in vivo approaches using primary cortical neurons treated with LVFX and adult rats administered LVFX.
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