Ocular dominance plasticity: Molecular mechanisms revisited

Abstract

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.

V1-Origin Bidirectional Plasticity in Visual Thalamo–Ventral Pathway and Its Contribution to Saliency Detection of Dynamic Visual Inputs

“…The ODI of tested Area 17 neurons is 0.15 6 0.06 (Fig. 2E; n = 26), consistent with previous studies (Hubel and Wiesel, 1962;Wiesel and Hubel, 1963;Kara and Boyd, 2009;Kasamatsu and Imamura, 2020) showing a binocular-driven feature. The interocular transferability test consists of several steps.…”

“…Previous literature has shown that the orientation-adaptation effect could transfer interocularly in cat Areas 17 and 18 (Maffei et al, 1986). Considering that neurons in Areas 17 and 18 are mainly binocularly driven (Hubel and Wiesel, 1962;Maffei et al, 1986;Kasamatsu and Imamura, 2020), whereas LGN neurons are monocularly driven (Sanderson, 1971;LeVay and Ferster, 1977;Weyand, 2016;Ghodrati et al, 2017), interocular transferability supports the cortical origin hypothesis of orientation adaptation.…”

“…In this study we found that the potentiation induced by biased adaptation is originated in Area 17, supported by the interocular-transfer experiment, latency-analysis, and Area 17 lesion. Interocular transferability is useful when locating a visual function, especially in cats (Peck et al, 1979;Maffei et al, 1986), because LGN neurons are monocular driven, whereas Area 17 neurons of cats are mainly binocular driven (Hubel and Wiesel, 1962;Kasamatsu and Imamura, 2020). Latency analysis is a classical method for investigating the origin of sensory neuronal response (Angelucci and Bullier, 2003;Patterson et al, 2013;Yao et al, 2015), and our results suggest the intracortical origin of potentiation.…”

Visual stimulation drives retinotopic acetylcholine release in the mouse visual cortex

“…A prominent view that behaviorally salient events evoke diffuse ACh release across the cortex has recently been challenged by imaging experiments that used these indicators to show heterogeneous patterns across cortical regions correlating with behavioral states and locomotion (Lohani et al, 2022). In the visual cortex, cholinergic signaling is involved in ocular dominance plasticity (Kasamatsu & Imamura, 2020) and required to encode spatiotemporal sequences (Gavornik & Bear, 2014) and intervals (Chubykin et al, 2013). While microdialysis has shown that visual stimulation can increase ACh levels in the visual cortex of anesthetized rats (Laplante et al, 2005), the extent to which this occurs during passive viewing in awake animals, and the spatiotemporal granularity of release, are unknown.…”

Neural circuits for binocular vision: Ocular dominance, interocular matching, and disparity selectivity

“…These studies have demonstrated that the maturation of specific inhibitory circuits in the visual cortex is important for both opening and closing the critical period, and they have also revealed a number of “molecular brakes” that restricts plasticity after the critical period and consequently approaches to “reopening” the window of plasticity in adulthood (Stryker and Lowel, 2018 ). It is beyond the scope of this article to provide a comprehensive review of molecular and synaptic mechanisms of OD plasticity and critical period regulation, on which there are plenty in recent publications (Espinosa and Stryker, 2012 ; Hensch and Quinlan, 2018 ; Hooks and Chen, 2020 ; Kasamatsu and Imamura, 2020 ; Xu et al, 2020a ). We will therefore limit our discussion to two issues of OD that are the most relevant to binocular vision.…”