scholarly journals Pull-push neuromodulation of cortical plasticity enables rapid bi-directional shifts in ocular dominance

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Su Z Hong ◽  
Shiyong Huang ◽  
Daniel Severin ◽  
Alfredo Kirkwood
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation

Neuromodulatory systems are essential for remodeling glutamatergic connectivity during experience-dependent cortical plasticity. This permissive/enabling function of neuromodulators has been associated with their capacity to facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability. In vitro studies indicate that neuromodulators also affect the expression of Hebbian plasticity in a pull-push manner: receptors coupled to the G-protein Gs promote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense of LTP. Here we show that pull-push mechanisms can be recruited in vivo by pairing brief monocular stimulation with pharmacological or chemogenetical activation of Gs- or Gq-coupled receptors to respectively enhance or reduce neuronal responses in primary visual cortex. These changes were stable, inducible in adults after the termination of the critical period for ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

scholarly journals Pull-Push Neuromodulation of Cortical Plasticity Enables Rapid Bi-Directional Shifts in Ocular Dominance

2019 ◽  
Author(s):  
Su Z. Hong ◽  
Shiyong Huang ◽  
Daniel Severin ◽  
Alfredo Kirkwood
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation ◽  
Visual Cortical

SUMMARYNeuromodulatory systems are essential for remodeling glutamatergic connectivity during experience-dependent cortical plasticity. This permissive/enabling function of neuromodulators has been associated with their capacity to facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability. In vitro studies indicate that neuromodulators can also affect the expression of Hebbian plasticity in a pull-push manner: receptors coupled to the G-protein Gs promote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense of LTD. Here we show that the pull-push mechanism can be recruited in vivo by pairing brief monocular stimulation with pharmacological or chemogenetical activation of Gs- or Gq-coupled receptors to respectively enhance or reduce visual cortical responses. These changes were stable, can be induced in adults after the termination of the critical period for juvenile ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

scholarly journals Bidirectional synaptic mechanisms of ocular dominance plasticity in visual cortex

2008 ◽  
Vol 364 (1515) ◽  
pp. 357-367 ◽  
Author(s):  
Gordon B Smith ◽  
Arnold J Heynen ◽  
Mark F Bear
Keyword(s):  
Research Evidence ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Ocular Dominance Plasticity ◽  
Nmda Receptor Subunit ◽  
Term Potentiation ◽  
Alternative Hypotheses ◽  
Synaptic Mechanisms

As in other mammals with binocular vision, monocular lid suture in mice induces bidirectional plasticity: rapid weakening of responses evoked through the deprived eye followed by delayed strengthening of responses through the open eye. It has been proposed that these bidirectional changes occur through three distinct processes: first, deprived-eye responses rapidly weaken through homosynaptic long-term depression (LTD); second, as the period of deprivation progresses, the modification threshold determining the boundary between synaptic depression and synaptic potentiation becomes lower, favouring potentiation; and third, facilitated by the decreased modification threshold, open-eye responses are strengthened via homosynaptic long-term potentiation (LTP). Of these processes, deprived-eye depression has received the greatest attention, and although several alternative hypotheses are also supported by current research, evidence suggests that α-amino-3- hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor endocytosis through LTD is a key mechanism. The change in modification threshold appears to occur partly through changes in N -methyl- d -aspartate (NMDA) receptor subunit composition, with decreases in the ratio of NR2A to NR2B facilitating potentiation. Although limited research has directly addressed the question of open-eye potentiation, several studies suggest that LTP could account for observed changes in vivo . This review will discuss evidence supporting this three-stage model, along with outstanding issues in the field.

P4-378: REVERSAL OF AB-INDUCED DEFICITS IN LONG-TERM POTENTIATION (LTP) IN VITRO AND IN VIVO BY MRZ-99030

2014 ◽  
Vol 10 ◽  
pp. P926-P926
Author(s):  
Christopher G. Parsons ◽  
Ross David Jeggo ◽  
Lydia Staniaszek ◽  
David Spanswick ◽  
Gerhard Rammes
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex

2015 ◽  
Vol 112 (41) ◽  
pp. 12852-12857 ◽  
Author(s):  
Michael S. Sidorov ◽  
Eitan S. Kaplan ◽  
Emily K. Osterweil ◽  
Lothar Lindemann ◽  
Mark F. Bear
Keyword(s):  
Visual Cortex ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Excitatory Synapses ◽  
Ocular Dominance Plasticity ◽  
Metabotropic Glutamate

A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.

scholarly journals In vivo and in vitro exposure to PCB 153 reduces long-term potentiation.

2000 ◽  
Vol 108 (9) ◽  
pp. 827-831 ◽  
Author(s):  
R J Hussain ◽  
J Gyori ◽  
A P DeCaprio ◽  
D O Carpenter
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation ◽  
In Vitro Exposure

Blockade of long-term potentiation by phencyclidine and σ opiates in the hippocampus in vivo and in vitro

1983 ◽  
Vol 280 (1) ◽  
pp. 127-138 ◽  
Author(s):  
Janet L. Stringer ◽  
L. John Greenfield ◽  
John T. Hackett ◽  
Patrice G. Guyenet
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation

Aβ25–35-Induced Depression of Long-Term Potentiation in Area CA1 In Vivo and In Vitro Is Attenuated by Verapamil

2003 ◽  
Vol 89 (6) ◽  
pp. 3061-3069 ◽  
Author(s):  
D. B. Freir ◽  
D. A. Costello ◽  
C. E. Herron
Keyword(s):  
Long Term Potentiation ◽  
Slice Preparation ◽  
Ca1 Region ◽  
Combined Application ◽  
Significant Reversal ◽  
Term Potentiation ◽  
Prior Application

The effect of intracerebroventricular (icv) injection of Aβ25–35 and/or intraperitoneal (ip) application of the L-type calcium channel (VDCC) blockers verapamil or diltiazem were examined in vivo. To by-pass possible systemic actions of these agents, their effects on long-term potentiation (LTP) in the CA1 region of the in vitro hippocampal slice preparation were also examined. Application of Aβ25–35 (10 nmol in 5 μl, icv) significantly impaired LTP in vivo, as did IP injection of verapamil (1 or 10 mg/kg) or diltiazem (1 or 10 mg/kg). In the in vitro slice preparation, LTP was also depressed by prior application of Aβ25–35 (500 nmol), verapamil (20 μM), or diltiazem (50 μM). Combined application of Aβ25–35 and verapamil in either the in vivo or in vitro preparation resulted in a significant reversal of the LTP depression observed in the presence of either agent alone. However, co-application of diltiazem and Aβ25–35 failed to attenuate the depression of LTP observed in the presence of either agent alone in vivo or in vitro. Since LTP is a cellular correlate of memory and Aβ is known to be involved in Alzheimer's disease (AD), these results indicate that verapamil, a phenylalkylamine, may be useful in the treatment of cognitive deficits associated with AD.

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