There is now compelling evidence that the allocation of memory to specific neurons (neuronal allocation) and synapses (synaptic allocation) in a neurocircuit is not random and that instead specific mechanisms, such as increases in neuronal excitability and synaptic tagging and capture, determine the exact sites where memories are stored. We propose an integrated view of these processes, such that neuronal allocation, synaptic tagging and capture, spine clustering and metaplasticity reflect related aspects of memory allocation mechanisms. Importantly, the properties of these mechanisms suggest a set of rules that profoundly affect how memories are stored and recalled.
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http://dx.doi.org/10.1038/nrn3667 | DOI Listing |
Elife
January 2025
Graduate School of Life Sciences, Tohoku University, Sendai, Japan.
Dopamine can play opposing physiological roles depending on the receptor subtype. In the fruit fly , and encode the D- and D-like receptors, respectively, and are reported to oppositely regulate intracellular cAMP levels. Here, we profiled the expression and subcellular localization of endogenous Dop1R1 and Dop2R in specific cell types in the mushroom body circuit.
View Article and Find Full Text PDFBiol Psychiatry
January 2025
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:
Background: Long-term fear memory storage involves gradual reorganization of supporting brain regions over time, a process termed systems consolidation. Memories initially rely on the hippocampus but gradually shift dependence to the neocortex. Although hippocampal activity drives this transfer, the molecular basis of systems consolidation is largely unknown.
View Article and Find Full Text PDFDiverse sources of inhibition serve to modulate circuits and control cell assembly spiking across various timescales. For example, in hippocampus area CA1 the competition between inhibition and excitation organizes spike timing of pyramidal cells (PYR) in network events, including sharp wave-ripples (SPW-R). Specific cellular-synaptic sources of inhibition in SPW-R remain unclear, as there are >20 types of GABAergic interneurons in CA1.
View Article and Find Full Text PDFNeurosci Res
January 2025
Department of Cell Physiology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan. Electronic address:
Sensorineural hearing loss causes cell death in central auditory neurons, but molecular mechanisms of triggering this process are not fully understood. We report here that loss of afferent activity promotes cell death by facilitating proBDNF-p75NTR signals in cochlear nucleus of chicks around hatch. RNA-seq analyses revealed up-regulation of genes related to proBDNF-p75NTR-JNK signals as well as apoptosis at the nucleus within 24 h after unilateral cochlea deprivation.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Translational Neurobiology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, 187-8502, Japan.
Caspases are known to mediate neuronal apoptosis during brain development. However, here we show that nonapoptotic activation of caspase-3 at presynapses drives microglial synaptic phagocytosis. Real-time observation and spatiotemporal manipulation of synaptic caspase-3 in the newly established, mouse-derived culture system demonstrate that increased neuronal activity triggers localized presynaptic caspase-3 activation, facilitating synaptic tagging by complements.
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