We tested the hypothesis that homosynaptic long-term depression (LTD) can be induced at the CA3-CA3 synapses in the adult, in vivo hippocampus while the CA3-CA1 synapses remain unchanged. Low-frequency conditioning stimulation of the contralateral fimbria significantly depressed the CA3 population response but did not change the simultaneously recorded CA3 response to angular bundle test stimulation. Similarly, in another group of animals, low-frequency conditioning stimulation of the contralateral fimbria depressed the CA3 synaptic response and left the collateral CA1 synaptic response unchanged. Among the possible explanations for this differential induction of homosynaptic LTD at the CA3-CA3 and CA3-CA1 synapses are differential control of intracellular calcium, differing levels of inhibition in these two regions, and the recency of 'natural' long-term potentiation in the two regions.
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http://dx.doi.org/10.1016/s0006-8993(98)00100-0 | DOI Listing |
Biochem 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 PDFPhilos Trans R Soc Lond B Biol Sci
July 2024
Department of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.
Nitric oxide (NO) is a key diffusible messenger in the mammalian brain. It has been proposed that NO may diffuse retrogradely into presynaptic terminals, contributing to the induction of hippocampal long-term potentiation (LTP). Here, we present novel evidence that NO is required for kainate receptor (KAR)-dependent presynaptic form of LTP (pre-LTP) in the adult insular cortex (IC).
View Article and Find Full Text PDFCurr Issues Mol Biol
April 2024
Institute of Higher Nervous Activity and Neurophysiology of RAS, Moscow 117485, Russia.
Heterosynaptic plasticity, along with Hebbian homosynaptic plasticity, is an important mechanism ensuring the stable operation of learning neuronal networks. However, whether heterosynaptic plasticity occurs in the whole brain in vivo, and what role(s) in brain function in vivo it could play, remains unclear. Here, we used an optogenetics approach to apply a model of intracellular tetanization, which was established and employed to study heterosynaptic plasticity in brain slices, to study the plasticity of response properties of neurons in the mouse visual cortex in vivo.
View Article and Find Full Text PDFMol Cell Neurosci
June 2024
Cellular and Systems Neurobiology, NOVA Medical Research, NOVA Medical School, Universidade NOVA de Lisboa, Portugal. Electronic address:
Synapses change their weights in response to neuronal activity and in turn, neuronal networks alter their response properties and ultimately allow the brain to store information as memories. As for memories, not all events are maintained over time. Maintenance of synaptic plasticity depends on the interplay between functional changes at synapses and the synthesis of plasticity-related proteins that are involved in stabilizing the initial functional changes.
View Article and Find Full Text PDFJ Neurophysiol
April 2023
Division of Basic Biomedical Sciences, Center for Brain and Behavior Research, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, United States.
Noxious stimuli or injury can trigger long-lasting sensitization to non-nociceptive stimuli (referred to as allodynia in mammals). Long-term potentiation (LTP) of nociceptive synapses has been shown to contribute to nociceptive sensitization (hyperalgesia) and there is even evidence of heterosynaptic spread of LTP contributing to this type of sensitization. This study will focus on how activation of nociceptors elicits heterosynaptic LTP (hetLTP) in non-nociceptive synapses.
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