Ongoing learning continuously shapes the distribution of neurons' synaptic weights in a system with plastic synapses. Plasticity may change the weights of synapses that were active during the induction-homosynaptic changes, but also may change synapses not active during the induction-heterosynaptic changes. Here we will argue, that heterosynaptic and homosynaptic plasticity are complementary processes, and that heterosynaptic plasticity might accompany homosynaptic plasticity induced by typical pairing protocols. Synapses are not uniform in their susceptibility for plastic changes, but have predispositions to undergo potentiation or depression, or not to change. Predisposition is one of the factors determining the direction and magnitude of homo- and heterosynaptic changes. Heterosynaptic changes which take place according to predispositions for plasticity may provide a useful mechanism(s) for homeostasis of neurons' synaptic weights and extending the lifetime of memory traces during ongoing learning in neuronal networks.
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http://dx.doi.org/10.1007/s00221-009-1859-5 | DOI Listing |
Mater Horiz
January 2025
School of Chemical Sciences, National Institute of Science Education and Research (NISER), An OCC of HBNI, Bhubaneswar, 752050, Odisha, India.
Neuromorphic and fully analog in-memory computations are promising for handling vast amounts of data with minimal energy consumption. We have synthesized and studied a series of homo-bimetallic silver purine MOFs (1D and 2D) having direct metal-metal bonding. The N7-derivatized purine ligands are designed to form bi-metallic complexes under ambient conditions, extending to a 1D or 2D metal-organic framework.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
October 2024
Center for Neuroscience, University of California, Davis, CA 95616.
Systems consolidation is a common feature of learning and memory systems, in which a long-term memory initially stored in one brain region becomes persistently stored in another region. We studied the dynamics of systems consolidation in simple circuit architectures with two sites of plasticity, one in an early-learning and one in a late-learning brain area. We show that the synaptic dynamics of the circuit during consolidation of an analog memory can be understood as a temporal integration process, by which transient changes in activity driven by plasticity in the early-learning area are accumulated into persistent synaptic changes at the late-learning site.
View Article and Find Full Text PDFBiochem Biophys Res Commun
November 2024
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, 117485, Russia. Electronic address:
Long-term changes of synaptic transmission can be induced by Hebbian-type homosynaptic mechanisms which require activation of both pre- and postsynapse and mediate associative learning, as well as by heterosynaptic mechanisms which do not require activation of the presynapse and are non-associative. The rules for induction of homosynaptic plasticity depend on the distance of the synapse from the soma. Does induction of heterosynaptic plasticity also depend on synaptic location? Here, we investigated heterosynaptic changes in pharmacologically isolated glutamatergic inputs arriving at either the proximal or the distal segments of the apical dendrite of layer 2/3 pyramidal neurons in rat visual cortex.
View Article and Find Full Text PDFSci Rep
September 2024
Department of Biophysics and Neuroscience, Wroclaw Medical University, 3a Chalubinskiego Str., 50-368, Wroclaw, Poland.
Cell Rep
August 2024
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address:
Long-term synaptic plasticity at glutamatergic synapses on striatal spiny projection neurons (SPNs) is central to learning goal-directed behaviors and habits. Our studies reveal that SPNs manifest a heterosynaptic, nitric oxide (NO)-dependent form of long-term postsynaptic depression of glutamatergic SPN synapses (NO-LTD) that is preferentially engaged at quiescent synapses. Plasticity is gated by Ca entry through Ca1.
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