Long-Term Depression and Depotentiation in the Sensorimotor Cortex of the Freely Moving Rat

Froc, David J.; Chapman, C. Andrew; Trepel, Christopher; Racine, R.

doi:10.1523/jneurosci.20-01-00438.2000

Cited by 111 publications

(62 citation statements)

References 45 publications

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“…The ability to experimentally induce longterm potentiation (LTP) and long-term depression (LTD) in many different regions of the brain lends support to this hypothesis (Tsumoto, 1992;Bear and Malenka, 1994;Linden, 1994). Both LTP and LTD can be induced by relatively brief, specific patterns of afferent activity and can persist for days in vivo (Bliss and Gardner-Medwin, 1973;1992;Mulkey and Malenka, 1992;Froc et al, 2000). Consequently, these phenomena are widely studied as models for information storage by synapses; however, a direct causal link between LTP-and/or LTD-like synaptic strength changes and behavioral learning has yet to be demonstrated.…”

Section: Abstract: Long-term Depression; Visual Cortex; Poisson Stimmentioning

confidence: 95%

“…In addition to the visual cortex, LTD has been induced by regular LFS in other neocortical regions in the adult (Castro-Alamancos et al, 1995;Chen et al, 1996;Hess and Donoghue, 1996;Cho et al, 2000;Froc et al, 2000). Thus, the sustained low-frequency spike activity of a neuron in the adult cortex could be sufficient to depress the synapses that a cell makes with its postsynaptic targets.…”

Section: Functional Implications Of Poisson Patterns Of Stimulationmentioning

confidence: 99%

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LTD Induction in Adult Visual Cortex: Role of Stimulus Timing and Inhibition

et al. 2001

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One Hertz stimulation of afferents for 15 min with constant interstimulus intervals (regular stimulation) can induce longterm depression (LTD) of synaptic strength in the neocortex. However, it is unknown whether natural patterns of lowfrequency afferent spike activity induce LTD. Although neurons in the neocortex can fire at overall rates as low as 1 Hz, the intervals between spikes are irregular. This irregular spike activity (and thus, presumably, irregular activation of the synapses of that neuron onto postsynaptic targets) can be approximated by stimulation with Poisson-distributed interstimulus intervals (Poisson stimulation). Therefore, if low-frequency presynaptic spike activity in the intact neocortex is sufficient to induce a generalized LTD of synaptic transmission, then Poisson stimulation, which mimics this spike activity, should induce LTD in slices. We tested this hypothesis by comparing changes in the strength of synapses onto layer 2/3 pyramidal cells induced by regular and Poisson stimulation in slices from adult visual cortex. We find that regular stimulation induces LTD of excitatory synaptic transmission as assessed by field potentials and intracellular postsynaptic potentials (PSPs) with inhibition absent. However, Poisson stimulation does not induce a net LTD of excitatory synaptic transmission. When the PSP contained an inhibitory component, neither Poisson nor regular stimulation induced LTD. We propose that the short bursts of synaptic activity that occur during a Poisson train have potentiating effects that offset the induction of LTD that is favored with regular stimulation. Thus, natural (i.e., irregular) low-frequency activity in the adult neocortex in vivo should not consistently induce LTD.

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Section: Abstract: Long-term Depression; Visual Cortex; Poisson Stimmentioning

confidence: 95%

Section: Functional Implications Of Poisson Patterns Of Stimulationmentioning

confidence: 99%

LTD Induction in Adult Visual Cortex: Role of Stimulus Timing and Inhibition

et al. 2001

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“…This reversal of synaptic strength from the potentiated state to pre-LTP levels has been called depotentiation and may provide a mechanism of preventing the saturation of synaptic potentiation and increase the efficiency and the capacity of the information storage of the neuronal networks (10). Although depotentiation has been consistently demonstrated in several brain regions including hippocampus (3)(4)(5)(6)(11)(12)(13)(14), visual cortex (15), sensorimotor cortex (16), and prefrontal cortex (17), the exact biochemical processes and molecular mechanisms responsible for this synaptic plasticity are incomplete. We have demonstrated previously that the LFS-induced depotentiation at Schaffer collateral-CA1 synapses may attribute to an increase of extracellular adenosine acting on the A 1 adenosine receptors to interrupt the cAMP-PKA-dependent signaling cascades leading to the development of LTP (7).…”

Section: Long Term Potentiation (Ltp)mentioning

confidence: 99%

Characterization of the Mechanism Underlying the Reversal of Long Term Potentiation by Low Frequency Stimulation at Hippocampal CA1 Synapses

Huang

Liang

Hsu

2001

Journal of Biological Chemistry

142

119

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Reversal of long term potentiation (LTP) may function to increase the flexibility and storage capacity of neuronal circuits; however, the underlying mechanisms remain incompletely understood. We show that depotentiation induced by low frequency stimulation (LFS) (2 Hz, 10 min, 1200 pulses) was input-specific and dependent on Nmethyl-D-aspartate (NMDA) receptor activation. The ability of LFS to reverse LTP was mimicked by a brief application of NMDA. This NMDA-induced depotentiation was blocked by adenosine A 1 receptor antagonist. However, the reversal of LTP by LFS was unaffected by metabotropic glutamate receptor antagonism. This LFS-induced depotentiation was specifically prevented by protein phosphatase (PP)1 inhibitors, okadaic acid, and calyculin A but not by the PP2A or PP2B inhibitors. Furthermore, by using phosphorylation site-specific antibodies, we found that LFS-induced depotentiation is associated with a persistent dephosphorylation of the GluR1 subunit of amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor at serine 831, a protein kinase C and calcium/ calmodulin-dependent protein kinase II (CaMKII) substrate, but not at serine 845, a substrate of cAMPdependent protein kinase. This effect was mimicked by bath-applied adenosine or NMDA and was specifically prevented by okadaic acid. Also, the increased phosphorylation of CaMKII at threonine 286 and the decreased PP activity seen with LTP were overcome by LFS, adenosine, or NMDA application. These results suggest that LFS erases LTP through an NMDA receptor-mediated activation of PP1 to dephosphorylate amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors and CaMKII in the CA1 region of the hippocampus. Long term potentiation (LTP)1 is a long lasting form of synaptic plasticity that is thought to play important roles in learning and memory in the brain (1). Although LTP is very persistent, current work has provided evidence that various manipulations or pharmacological treatment when applied shortly after LTP induction can reverse it. For example, it has been shown that transient anoxia occurring 1-2 min after LTP induction prevented the stable expression of LTP (2). Such time-dependent reversal of LTP was also effectively induced by low frequency afferent stimulation (1-5 Hz) when delivered within 10 min of LTP induction, both in vivo (3, 4) and in vitro (5-7). In addition, antagonists that prevent cell-cell and cellmatrix interactions were also observed to reverse effectively LTP in a time-dependent manner (8, 9). This reversal of synaptic strength from the potentiated state to pre-LTP levels has been called depotentiation and may provide a mechanism of preventing the saturation of synaptic potentiation and increase the efficiency and the capacity of the information storage of the neuronal networks (10). Although depotentiation has been consistently demonstrated in several brain regions including hippocampus (3-6, 11-14), visual cortex (15), sensorimotor cortex (16), and prefrontal cortex (17), the exact biochemical processes and mol...

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“…Synaptic plasticity and long-term potentiation (LTP)-and long-term depression (LTD)-like changes within the neocortex depend on modulation mediated by both glutamatergic and GABAergic neurons Racine, 1998, 2000;Froc et al, 2000). Both the anodal facilitation and cathodal inhibition of motor-evoked potentials (MEPs) are blocked by the NMDA-receptor antagonist dextromethorphan (Liebetanz et al, 2002;Nitsche et al, 2003b).…”

Section: Introductionmentioning

confidence: 99%

Polarity-Sensitive Modulation of Cortical Neurotransmitters by Transcranial Stimulation

Stagg¹,

Best²,

Stephenson³

et al. 2009

J. Neurosci.

812

744

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Transcranial direct current stimulation (tDCS) modulates cortical excitability and is being used for human studies more frequently. Here we probe the underlying neuronal mechanisms by measuring polarity-specific changes in neurotransmitter concentrations using magnetic resonance spectroscopy (MRS). MRS provides evidence that excitatory (anodal) tDCS causes locally reduced GABA while inhibitory (cathodal) stimulation causes reduced glutamatergic neuronal activity with a highly correlated reduction in GABA, presumably due to the close biochemical relationship between the two neurotransmitters.

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Long-Term Depression and Depotentiation in the Sensorimotor Cortex of the Freely Moving Rat

Cited by 111 publications

References 45 publications

LTD Induction in Adult Visual Cortex: Role of Stimulus Timing and Inhibition

LTD Induction in Adult Visual Cortex: Role of Stimulus Timing and Inhibition

Characterization of the Mechanism Underlying the Reversal of Long Term Potentiation by Low Frequency Stimulation at Hippocampal CA1 Synapses

Polarity-Sensitive Modulation of Cortical Neurotransmitters by Transcranial Stimulation

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