Presynaptic Ca appears to play multiple roles in synaptic development and physiology. We examined the effect of buffering presynaptic Ca by expressing parvalbumin (PV) in Drosophila neurons, which do not normally express PV. The studies were performed on the identified Ib terminal that innervates muscle fiber 5. The volume-averaged, residual Ca resulting from single action potentials (APs) and AP trains was measured using the fluorescent Ca indicator, OGB-1. PV reduced the amplitude and decay time constant (τ) for single-AP Ca transients. For AP trains, there was a reduction in the rate of rise and decay of [Ca] but the plateau [Ca] was not affected. Electrophysiological recordings from muscle fiber 5 showed a reduction in paired-pulse facilitation, particularly the F component; this was likely due to the reduction in residual Ca. These synapses also showed reduced synaptic enhancement during AP trains, presumably due to less buildup of synaptic facilitation. The transmitter release for single APs was increased for the PV-expressing terminals and this may have been a homeostatic response to the decrease in facilitation. Confocal microscopy was used to examine the structure of the motor terminals and PV expression resulted in smaller motor terminals with fewer synaptic boutons and active zones. This result supports earlier proposals that increased AP activity promotes motor terminal growth through increases in presynaptic [Ca].
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1080/01677063.2018.1498496 | DOI Listing |
Nat Commun
January 2025
Unit on the Development of Neurodegeneration, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Traumatic brain injury (TBI) is a risk factor for neurodegeneration, however little is known about how this kind of injury alters neuron subtypes. In this study, we follow neuronal populations over time after a single mild TBI (mTBI) to assess long ranging consequences of injury at the level of single, transcriptionally defined neuronal classes. We find that the stress-responsive Activating Transcription Factor 3 (ATF3) defines a population of cortical neurons after mTBI.
View Article and Find Full Text PDFJ Comp Neurol
January 2025
Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai, Tamil Nadu, India.
Direction selectivity is a fundamental feature in the visual system. In the retina, direction selectivity is independently computed by ON and OFF circuits. However, the advantages of extracting directional information from these two independent circuits are unclear.
View Article and Find Full Text PDFWhile CNS microglia have well-established roles in synapse pruning during neurodevelopment, only a few studies have identified roles for microglia in synapse formation. These studies focused on the cortex and primary sensory circuits during restricted developmental time periods, leaving substantial gaps in our understanding of the early developmental functions of microglia. Here we investigated how the absence of microglia impacts synaptic development in the nucleus accumbens (NAc), a region critical for emotional regulation and motivated behaviors and where dysfunction is implicated in psychiatric disorders that arise early in life.
View Article and Find Full Text PDFOrganisms continually tune their perceptual systems to the features they encounter in their environment . We have studied how ongoing experience reorganizes the synaptic connectivity of neurons in the olfactory (piriform) cortex of the mouse. We developed an approach to measure synaptic connectivity , training a deep convolutional network to reliably identify monosynaptic connections from the spike-time cross-correlograms of 4.
View Article and Find Full Text PDFiScience
January 2025
Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
Mutations in the human genes encoding the endothelin ligand-receptor pair and cause Waardenburg-Shah syndrome (WS4), which includes congenital hearing impairment. The current explanation for auditory dysfunction is defective migration of neural crest-derived melanocytes to the inner ear. We explored the role of endothelin signaling in auditory development in mice using neural crest-specific and placode-specific mutation plus related genetic resources.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!