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

Hong, Su Z.; Huang, Shiyong; Severín, Daniel; Kirkwood, Alfredo

doi:10.7554/elife.54455

Cited by 10 publications

(11 citation statements)

References 60 publications

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“…In these studies, an elaborated set of possible mechanisms including LTP and LTD (Cooke & Bear, 2014) are invoked to explain the unexpected. A most recent study in mice (Hong, Huang, Severin, & Kirkwood, 2020) suggests that rapid bidirectional changes in OD with monocular stimulation are explained by the differential action of two types of designer receptors exclusively activated by designer drugs (DREADDs): activation of G q ‐DREADDs strongly suppresses the stimulated‐eye responses, resulting in a large decrease in imaging‐based ODI (ocular dominance index),[(Contralateral‐eye response, C − ipsilateral‐eye response, I)/(C + I)], while G s DREADDs enhances the stimulated‐eye responses, leading to a large increase in ODI. They suggest that the push‐pull action of two types of G protein‐coupled receptors, G q which coupled to α1‐adrenorecotors and G s to ß‐adrenoreceptors, underlies the observed changes in ODI.…”

Section: A Conceptual Issue: Tests Of Odp Per Sementioning

confidence: 99%

Ocular dominance plasticity: Molecular mechanisms revisited

Kasamatsu

Imamura

2020

J of Comparative Neurology

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Ocular dominance plasticity (ODP) is a type of cortical plasticity operating in visual cortex of mammals that are endowed with binocular vision based on the competition-driven disparity. Earlier, a molecular mechanism was proposed that catecholamines play an important role in the maintenance of ODP in kittens. Having survived the initial test, the hypothesis was further advanced to identify noradrenaline (NA) as a key factor that regulates ODP in the immature cortex. Later, the ODPpromoting effect of NA is extended to the adult with age-related limitations. Following the enhanced NA availability, the chain events downstream lead to the β-adrenoreceptor-induced cAMP accumulation, which in turn activates the protein kinase A. Eventually, the protein kinase translocates to the cell nucleus to activate cAMP responsive element binding protein (CREB). CREB is a cellular transcription factor that controls the transcription of various genes, underpinning neuronal plasticity and long-term memory. In the advent of molecular genetics in that various types of new tools have become available with relative ease, ODP research has lightly adopted in the rodent model the original concepts and methodologies. Here, after briefly tracing the strategic maturation of our quest, the review moves to the later development of the field, with the emphasis placed around the following issues: (a) Are we testing ODP per se? (b) What does monocular deprivation deprive of the immature cortex? (c) The critical importance of binocular competition, (d) What is the adult plasticity? (e) Excitation-Inhibition balance in local circuits, and (f) Species differences in the animal models.

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Section: A Conceptual Issue: Tests Of Odp Per Sementioning

confidence: 99%

Ocular dominance plasticity: Molecular mechanisms revisited

Kasamatsu

Imamura

2020

J of Comparative Neurology

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“…7a). We used intrinsic signal imaging to evaluate cortical responses in the binocular zone of V1 as described 24, 25 . Cortical responses in mice are normally biased toward the contralateral eye and this bias is reduced by MD, reflected as a shift of the ocular dominance index (ODI, see methods).…”

Section: Resultsmentioning

confidence: 99%

All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

Severín

Hong

Roh³

et al. 2021

Preprint

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Disinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience. Our investigation on disinhibitory mechanisms in the classical model of ocular dominance plasticity uncovered an unexpected novel form of experience-dependent circuit plasticity. In layer 2/3 of mouse visual cortex monocular deprivation triggers a complete, “all-or-none”, elimination of connections from pyramidal cells onto nearby parvalbumin-positive interneurons (Pyr➔PV). This circuit plasticity is unique as it is transient, local and discrete. It lasts only one day, and it does not manifest as widespread changes in synaptic strength, rather, only about half of local connections are lost and the remaining ones are not affected in strength. Mechanistically, the deprivation-induced loss of Pyr➔PV is contingent on a reduction of the protein neuropentraxin2 (NPTX2). Functionally, the loss of Pyr➔PV is absolutely necessary for ODP. We surmise, therefore, that this “all-or-none” loss of local Pyr➔PV circuitry gates experience-dependent cortical plasticity.

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“…Initially neuromodulators were thought as permissive/enabling factors that promote the induction Hebbian synaptic plasticity via the enhanced cellular and network excitability associated with arousal and the awake state. It was later found that besides facilitating it, specific neuromodulators can also act directly at the level of the expression of plasticity to control its magnitude and polarity 45,46 . Aligned with this latter idea, disruptions of the serotonergic system or the noradrenergic system during ODP respectively prevent the closed-eye depression of the non-deprived eye response potentiation 47 .…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine Potentiates and Serotonin Depresses Visual Cortical Responses by Transforming Eligibility Traces

Sz¹,

Mesik²,

Grossman³

et al. 2021

Preprint

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Reinforcement allows organisms to learn which stimuli predict subsequent biological relevance. Hebbian mechanisms of synaptic plasticity are insufficient to account for reinforced learning because neuromodulators signaling biological relevance are delayed with respect to the neural activity associated with the stimulus. A theoretical solution is the concept of eligibility traces (eTraces), silent synaptic processes elicited by activity which upon arrival of a neuromodulator are converted into a lasting change in synaptic strength. Previously we demonstrated in visual cortical slices the Hebbian induction of eTraces and their conversion into LTP and LTD by the retroactive action of norepinephrine and serotonin Here we show in vivo in V1 that the induction of eTraces and their conversion to LTP/D by norepinephrine and serotonin respectively potentiates and depresses visual responses. We also show that the integrity of this process is crucial for ocular dominance plasticity, a canonical model of experience-dependent plasticity.

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

Cited by 10 publications

References 60 publications

Ocular dominance plasticity: Molecular mechanisms revisited

Ocular dominance plasticity: Molecular mechanisms revisited

All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

Norepinephrine Potentiates and Serotonin Depresses Visual Cortical Responses by Transforming Eligibility Traces

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