Mitochondria located within neuronal presynaptic terminals have been shown to play important roles in the release of chemical neurotransmitters. In the present study, a genetic screen for synaptic transmission mutants of Drosophila has identified the first mutation in a Drosophila homolog of the mitochondrial protein P32. Although P32 is highly conserved and has been studied extensively, its physiological role in mitochondria remains unknown and it has not previously been implicated in neural function. The Drosophila P32 mutant, referred to as dp32(EC1), exhibited a temperature-sensitive (TS) paralytic behavioral phenotype. Moreover, electrophysiological analysis at adult neuromuscular synapses revealed a TS reduction in the amplitude of excitatory postsynaptic currents (EPSC) and indicated that dP32 functions in neurotransmitter release. These studies are the first to address P32 function in Drosophila and expand our knowledge of mitochondrial proteins contributing to synaptic transmission.
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http://dx.doi.org/10.1534/g3.111.001586 | DOI Listing |
J Gen Physiol
March 2025
Department of Physiology, University of Maryland School of Medicine, Baltimore, MD, USA.
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View Article and Find Full Text PDFJ Neurosci
January 2025
Carney Institute for Brain Science, Brown University, Providence, RI 02912
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View Article and Find Full Text PDFPsychiatr Clin North Am
March 2025
Department of Neurology, Johns Hopkins University School of Medicine, Kennedy Krieger Institute, Baltimore, MD, USA.
The pathophysiology of tic disorders involves an alteration in the transmission of messages through the cortico-basal ganglia-thalamo-cortical circuit. A major requirement for the passage of a message through this circuit is an intact chemically mediated synaptic neurotransmitter system (ie, neurotransmitters and second messengers). This article reviews the scientific evidence supporting the involvement of a variety of neurotransmitters (ie, dopamine, glutamate, gamma-aminobutyric acid, serotonin, acetylcholine, and the opioid system).
View Article and Find Full Text PDFThe effect of Constraint-induced movement therapy (CIMT) or Intermittent theta-burst stimulation (iTBS) alone is limited in improving motor function after a stroke. In this study, we explored the efficacy and possible mechanisms in combination of CIMT and iTBS through behavioral evaluation, RNA sequencing, Golgi staining, transmission electronic microscope (TEM), high-performance liquid chromatography (HPLC), western blotting (WB) and immunofluorescence. Firstly, we observed that combination therapy is safe and effective, and it can significantly reduce the number of immature dendritic spines and increase the number of functional dendritic spines, the amount of glutamate (Glu) and the expression of Glu1 receptor (Glu1R).
View Article and Find Full Text PDFBiol Psychiatry
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Department of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Heidelberg University, 69120 Heidelberg, Germany; Department of Molecular and Cellular Cognition Research, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, 68159 Mannheim, Germany. Electronic address:
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