Depression, a widespread psychiatric disorder, is characterized by a diverse array of symptoms such as melancholic mood and anhedonia, imposing a significant burden on both society and individuals. Despite extensive research into the neurobiological foundations of depression, a complete understanding of its complex mechanisms is yet to be attained, and targeted therapeutic interventions remain under development. Synaptic homeostasis, a compensatory feedback mechanism, involves neurons adjusting synaptic strength by regulating pre- or postsynaptic processes. Recent advancements in depression research reveal a crucial association between the disorder and disruptions in synaptic homeostasis within neural regions and circuits pivotal for emotional and cognitive functions. This paper explores the mechanisms governing synaptic homeostasis in depression, focusing on the role of ion channels, the regulation of presynaptic neurotransmitter release, synaptic scaling processes, and essential signaling molecules. By mapping new pathways in the study of synaptic homeostasis as it pertains to depression, this research aims to provide valuable insights for identifying novel therapeutic targets for more effective antidepressant treatments.
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http://dx.doi.org/10.1186/s13578-025-01369-y | DOI Listing |
Vision Res
March 2025
Department of Psychology & Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada.
Monocular deprivation obstructs the development of visual neural circuits and can impair vision for a lifetime. Effective treatment of this visual disorder, amblyopia, with patching therapy is limited by a short and early critical period, as well as by poor compliance with prescribed treatment. Temporary pharmacological inactivation of the dominant eye has emerged as a means to rapidly correct the effects of monocular deprivation in animal models.
View Article and Find Full Text PDFAnnu Rev Neurosci
March 2025
Center for Cognition and Sociality, Institute for Basic Science (IBS), Daejeon, South Korea; email:
Astrocytes, traditionally viewed as supportive cells within the central nervous system (CNS), are now recognized as dynamic regulators of neural signaling and homeostasis. They actively engage in synaptic transmission and brain health by releasing gliotransmitters such as glutamate, GABA, ATP, adenosine, lactate, and d-serine. Astrocytes also play a critical role in ion homeostasis and immune response through cytokine modulation and reactive oxygen species regulation.
View Article and Find Full Text PDFJ Neurochem
March 2025
Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Synaptic homeostasis of the principal neurotransmitters glutamate and GABA is tightly regulated by an intricate metabolic coupling between neurons and astrocytes known as the glutamate/GABA-glutamine cycle. In this cycle, astrocytes take up glutamate and GABA from the synapse and convert these neurotransmitters into glutamine. Astrocytic glutamine is subsequently transferred to neurons, serving as the principal precursor for neuronal glutamate and GABA synthesis.
View Article and Find Full Text PDFFront Genet
February 2025
Department of Reparative and Reconstructive Surgery, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Introduction: Melanoma, a highly aggressive form of skin cancer, and Parkinson's disease (PD), a progressive neurodegenerative disorder, have been epidemiologically linked, showing a positive association that suggests a shared etiology. This association implies that individuals with one condition may have an increased risk of developing the other. However, the specific molecular mechanisms underlying this relationship remain unclear.
View Article and Find Full Text PDFBrain Commun
February 2025
Program for Genetics and Genome Biology, Hospital for Sick Children, Toronto, ON M5G 0A4, Canada.
Biallelic loss of expression/function variants in cause the inherited peripheral neuropathy Charcot-Marie-Tooth type 4B3. There is an incomplete understanding of the disease pathomechanism(s) underlying Charcot-Marie-Tooth type 4B3, and despite its severe clinical presentation, currently no disease-modifying therapies. A key barrier to the study of Charcot-Marie-Tooth type 4B3 is the lack of pre-clinical models that recapitulate the clinical and pathologic features of the disease.
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