Alexei Volkov
Ocular dominance plasticity (ODP) is a type of cortical plasticity that operates in the visual cortex of mammals with binocular vision. It is based on competition-driven disparity, with catecholamines playing a significant role in its maintenance. Noradrenaline (NA), in particular, has been identified as a key regulator of ODP in the immature cortex, and its ODP-promoting effect extends into adulthood with certain limitations. While short-term ocular dominance plasticity is not significantly influenced by visual cortex tDCS, the length of monocular deprivation can impact its effectiveness. Furthermore, the thalamus has been found to play a crucial role in experience-dependent plasticity in adulthood, challenging the traditional view of cortical processes.
| Characteristics | Values |
|---|---|
| Type | Cortical plasticity |
| Location | Visual cortex of mammals with binocular vision |
| Mechanism | Competition-driven disparity |
| Molecular Mechanism | Catecholamines, Noradrenaline (NA), β-adrenoreceptor-induced cAMP accumulation, protein kinase A, cAMP responsive element binding protein (CREB) |
| Models | Chemotaxis, Hebbian activity-dependent mechanism |
| Role | Important in early studies of cortical plasticity, believed to be crucial for binocular vision |
| Modulation Techniques | Transcranial direct current stimulation (tDCS), Transcranial random noise stimulation (tRNS) |
| Thalamic Regulation | Inhibitory innervation in the dorsolateral geniculate nucleus, plasticity in the adult dorsal lateral geniculate nucleus (dLGN) |
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What You'll Learn
Noradrenaline and functional plasticity in kitten visual cortex
Noradrenaline, also known as norepinephrine, is a key factor in regulating ocular dominance plasticity (ODP) in the immature cortex. The presence of noradrenaline-containing terminals and NA-related receptors within the visual cortex is necessary to maintain the high level of neuronal plasticity in the immature visual cortex of kittens. This was demonstrated in a study where the local perfusion of noradrenaline maintained visual cortical plasticity.
The role of noradrenaline in functional plasticity in kitten visual cortex has been examined in various studies. One study investigated the cortical effects of monocular deprivation starting from the age of 5 weeks in both lesioned and intact kittens. It was found that the disappearance of noradrenaline in area 17 did not prevent the loss of binocularity in cortical cells. However, another study found that the presence of noradrenaline is not required for functional plasticity to occur in kitten area 17.
The effects of noradrenaline on kitten visual cortex plasticity have also been studied in combination with other treatments. For example, one study found that the plastic response to monocular deprivation persisted in kitten visual cortex after chronic depletion of norepinephrine. Another study examined the effects of intraventricular injection of 6-hydroxydopamine in the developing kitten, finding noradrenaline hyperinnervation in the pons.
Overall, noradrenaline plays a crucial role in modulating ocular dominance plasticity in the kitten visual cortex, particularly during the critical period of postnatal development. Its presence is necessary to maintain high levels of neuronal plasticity, and it can also protect or promote recovery from neural damage.
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Role of the thalamus in adult ocular dominance plasticity
Ocular dominance plasticity (ODP) is a type of cortical plasticity that operates in the visual cortex of mammals with binocular vision. ODP is maintained by catecholamines, with noradrenaline (NA) identified as a key regulator in the immature cortex.
Several recent studies have shown that perceptual learning or monocular deprivation can induce plasticity in the adult dorsolateral geniculate nucleus (dLGN) of the thalamus. This challenges the traditional view that experience-dependent plasticity in the adult visual system is primarily a cortical process.
Inhibitory innervation in the dLGN is crucial for adult thalamic and cortical ODP, indicating a potential thalamic contribution to conditions like amblyopia and learning disabilities. Using multielectrode recordings, researchers found that ODP in the primary visual cortex (V1) requires thalamic synaptic inhibition. In adult mice, the absence of thalamic inhibition and plasticity resulted in the absence of OD plasticity in V1.
Further research silenced V1 to study its influence on thalamic plasticity. Results showed that during the critical period, the OD shift in dLGN was partially caused by feedback from V1, but this effect was not observed in adulthood. Thus, the thalamus assumes a dominant role in experience-dependent plasticity during adulthood, contrary to previous understandings.
In conclusion, the thalamus plays a significant role in modulating adult ocular dominance plasticity, particularly through the dLGN and its interaction with V1. However, the exact mechanisms of thalamic and cortical plasticity interaction remain to be fully elucidated.
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Transcranial direct current stimulation (tDCS) and its effects
Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique that involves delivering a weak direct electrical current to targeted cortical sites via electrodes placed on the scalp. The current delivered by tDCS is not strong enough to trigger an action potential in a neuron. Instead, it changes the pattern of already active neurons. tDCS modulates neural excitability in the stimulated brain area in a polarity-dependent manner. Anodal tDCS (a-tDCS) elevates motor evoked potential (MEP) amplitude, indicating increased cortical excitability, whereas cathodal tDCS (c-tDCS) has the opposite effect. tDCS may alter neural membrane potentials and increase or decrease the activity of sodium and calcium channels, thereby altering the probability of action potentials.
TDCS has been found to have beneficial effects in a range of neurological disorders, including stroke, Alzheimer's disease, movement disorders, depression, schizophrenia, and addiction. It has also been shown to enhance cognitive and motor skills. tDCS may potentiate learning by affecting the intracellular Ca2+ concentration. A rise in intracellular Ca2+ concentration drives short and long-term plasticity (LTP). tDCS may also modulate skill learning by altering brain-derived neurotrophic factor (BDNF)-dependent cortical plasticity. BDNF binds to TrkB receptors that regulate the growth and synaptic activity of neurons and are thought to be involved in the formation of LTP. Anodal tDCS has been found to induce synaptic plasticity in vitro, which is dependent on enhanced BDNF-secretion and TrkB-activations.
While tDCS has shown promising results in various applications, there are still questions about its best use. The outcomes of tDCS are highly sensitive to stimulation parameters, making it difficult to maximize its effectiveness. Furthermore, the reproducibility of tDCS effects has been weak in some behaviors. Understanding how tDCS interacts with concurrent brain activity is necessary for its advancement.
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Ocular dominance columns and their development
Ocular dominance columns (ODCs) are stripe-shaped regions of the primary visual cortex that are believed to be important in binocular vision. They were discovered in the 1960s by Hubel and Wiesel as part of their Nobel Prize-winning work on the structure of the visual cortex in cats. ODCs have since been found in many animals, including ferrets, macaques, and humans. However, their absence in some animals with binocular vision, such as rats and squirrel monkeys, has led to questions about their purpose and significance.
The functional significance of ODCs was initially thought to be associated with stereoscopic three-dimensional (3-D) vision. This assumption was based on the segregation of pathways from the two eyes in the early stages of the visual pathway, which was believed to facilitate binocular disparity coding necessary for stereoscopic vision. However, this theory was challenged by the observation that some primate species, such as squirrel monkeys and marmosets, lack ODCs.
Recent discoveries have revealed the presence of ODCs in pigmented rats, prompting a reevaluation of their role and significance. It is now known that ODCs develop before birth, and there is a period after birth, formerly called the "critical period" and now referred to as the “sensitive period," during which ODCs may be modified by activity-dependent plasticity. This plasticity is so strong that blocking signals from both eyes can cause the ODCs to completely desegregate. Similarly, if one eye is closed, removed, or silenced during the sensitive period, the size of the columns corresponding to the affected eye will shrink dramatically.
There is not yet a consensus on how ODCs are initially developed. One possibility is that they develop through Hebbian learning triggered by spontaneous activity from retinal waves in the eyes of the developing fetus or the LGN. Another possibility is that axonal guidance cues guide their formation, or a combination of mechanisms may be at work. Models explaining the development of ODCs can generally be categorized into those that posit formation via chemotaxis and those that posit a Hebbian activity-dependent mechanism. Chemotactic models suggest the existence of axon guidance molecules that direct the initial formation of ODCs, while Hebbian models propose that if two neurons connected to a neuron fire together, they increase the strength of the synapses, "moving" the axon terminals closer together.
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Monocular deprivation and its impact on ocular dominance
Ocular dominance plasticity (ODP) is a type of cortical plasticity that occurs in the visual cortex of mammals with binocular vision. Monocular deprivation (MD) is a key factor in understanding ODP, as it induces changes in the visual cortex that lead to an ocular dominance shift.
Monocular deprivation involves depriving one eye of visual information for a certain period. In young animals, this can lead to a shift in ocular dominance, with the non-deprived eye becoming dominant. For example, in monkeys with long-term lid sutures in one eye, the ocular dominance columns strongly favour the non-deprived eye, with only small islands of input from the deprived eye. This shift is due to the expansion of the non-deprived eye's representation in the brain at the expense of the deprived eye.
The impact of monocular deprivation on ocular dominance has been studied in various animal models, including mice, monkeys, and adult rats. In one study, temporary lid closure in young mice induced two separate modifications: rapid, deprivation-induced response depression and delayed, deprivation-enabled, experience-dependent response potentiation. This suggests that altering retinal activity triggers these cortical responses, providing insight into the critical period of visual development.
Interestingly, the duration of monocular deprivation does not seem to impact the shift in ocular dominance. Even short-term monocular deprivation of 120 minutes in adults can strengthen the deprived eye's contribution to binocular vision. This finding is surprising because it demonstrates residual neural plasticity in the adult visual cortex, contrary to previous beliefs.
In summary, monocular deprivation can induce shifts in ocular dominance, with the non-deprived eye gaining dominance over the deprived eye. These shifts are not dependent on the duration of deprivation and can occur even in adults, challenging previous understandings of neural plasticity. Understanding the impact of monocular deprivation on ocular dominance has important implications for treating visual disorders and enhancing our knowledge of brain plasticity.
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Frequently asked questions
ODP is a type of cortical plasticity that operates in the visual cortex of mammals with binocular vision.
Inhibitory innervation in the dorsolateral geniculate nucleus, thalamic regulation, and the role of the thalamus in experience-dependent plasticity are key mechanisms. Noradrenaline (NA) is also a key factor in regulating ODP, leading to β-adrenoreceptor-induced cAMP accumulation and the activation of protein kinase A.
Monocular deprivation causes a shift in ocular dominance towards the non-deprived eye, with the non-deprived eye assuming control of more cortical cells.
While tDCS can enhance visual cortex neuroplasticity and improve contrast sensitivity, it does not appear to modulate the homeostatic mechanisms driving ODP in individuals with normal binocular vision.
