Recent evidence indicates that inhibition within the visual cortex is greater in older than young adults. Increased inhibition has been associated with reduced visual cortex plasticity in animal models. We investigated whether age-related increases in human visual cortex inhibition occur in conjunction with reduced visual cortex plasticity. Visual cortex inhibition was measured psychophysically using binocular rivalry alternation rates (AR) for dichoptic gratings. Slower ARs are associated with a greater concentration of the inhibitory neurotransmitter GABA within the human visual cortex. Visual cortex plasticity was measured using an established paradigm for induction of long-term potentiation (LTP) -like increases in visually evoked potential (VEP) amplitude. Following rapid visual stimulation, greater increases in VEP amplitude indicate greater visual cortex plasticity. The study involved two groups; young (18–40 years, n = 29) and older adults (60–80 years, n = 18). VEPs were recorded for a 1 Hz onset/offset checkerboard stimulus before and after 9 Hz visual stimulation with the same stimulus. ARs were slower in older than young adults. In contrast to most previous studies, VEP amplitudes were significantly reduced following the rapid visual stimulation for young adults; older adult VEP amplitudes were unaffected. Our AR results replicate previous observations of increased visual cortex inhibition in the older adults. Rapid visual stimulation significantly altered VEP amplitude in young adults, albeit in the opposite direction than predicted. VEP amplitudes did not change in older adults suggesting an association between increased inhibition and reduced plasticity within the human visual cortex.

Neuromodulation of the primary visual cortex using anodal transcranial direct current stimulation (a-tDCS) can alter visual perception and enhance neuroplasticity. However, the mechanisms that underpin these effects are currently unknown. When applied to the motor cortex, a-tDCS reduces the concentration of the inhibitory neurotransmitter gamma aminobutyric acid (GABA), an effect that has been linked to increased neuroplasticity. The aim of this study was to assess whether a-tDCS also reduces GABA-mediated inhibition when applied to the human visual cortex. Changes in visual cortex inhibition were measured using the mixed percept duration in binocular rivalry. Binocular rivalry mixed percept duration has recently been advocated as a direct and sensitive measure of visual cortex inhibition whereby GABA agonists decrease mixed percept durations and agonists of the excitatory neurotransmitter acetylcholine (ACH) increase them. Our hypothesis was that visual cortex a-tDCS would increase mixed percept duration by reducing GABA-mediated inhibition and increasing cortical excitation. In addition, we measured the effect of continuous theta-burst transcranial magnetic stimulation (cTBS) of the visual cortex on binocular rivalry dynamics. When applied to the motor or visual cortex, cTBS increases GABA concentration and we therefore hypothesized that visual cortex cTBS would decrease the mixed percept duration. Binocular rivalry dynamics were recorded before and after active and sham a-tDCS (N = 15) or cTBS (N = 15). Contrary to our hypotheses, a-tDCS had no effect, whereas cTBS increased mixed percepts during rivalry. These results suggest that the neurochemical mechanisms of a-tDCS may differ between the motor and visual cortices.

Neuromodulation of the primary visual cortex using anodal transcranial direct current stimulation (a-tDCS) can alter visual perception and enhance neuroplasticity. However, the mechanisms that underpin these effects are currently unknown. When applied to the motor cortex, a-tDCS reduces the concentration of the inhibitory neurotransmitter gamma aminobutyric acid (GABA), an effect that has been linked to increased neuroplasticity. The aim of this study was to assess whether a-tDCS also reduces GABA-mediated inhibition when applied to the human visual cortex. Changes in visual cortex inhibition were measured using the mixed percept duration in binocular rivalry. Binocular rivalry mixed percept duration has recently been advocated as a direct and sensitive measure of visual cortex inhibition whereby GABA agonists decrease mixed percept durations and agonists of the excitatory neurotransmitter acetylcholine increase them. Our hypothesis was that visual cortex a-tDCS would increase mixed percept duration by reducing GABA-mediated inhibition and increasing cortical excitation. In addition, we measured the effect of continuous theta-burst transcranial magnetic stimulation (cTBS) of the visual cortex on binocular rivalry dynamics. When applied to the motor or visual cortex, cTBS increases GABA concentration and we therefore hypothesized that visual cortex cTBS would decrease the mixed percept duration. Binocular rivalry dynamics were recorded before and after active and sham a-tDCS (N=15) or cTBS (N=15). Contrary to our hypotheses, a-tDCS had no effect, whereas cTBS significantly increased mixed percepts during rivalry. These results suggest that the neurochemical mechanisms of a-tDCS may differ between the motor and visual cortices.

Long-term potentiation (LTP) is the process of strengthening synaptic efficacy through repeated activation. This fundamental mechanism of neuroplasticity involves a cascade of cellular and molecular changes and underpins the processes of learning and memory formation (Bliss & Collingridge, 1993; Bliss & Lomo, 1973). Early research revealed that the rapid electrical stimulation of presynaptic cells within the rabbit hippocampus induced a lasting increase in the response amplitude of postsynaptic cells (Bliss & Lomo, 1973). Subsequent studies demonstrated similar effects (Bröcher et al., 1992) and characterized the neurochemical changes that occurred as a result of the stimulation (Hayashi et al., 2000; Teyler & DiScenna, 1987). These changes included a rise in postsynaptic calcium, the release of glutamate, and the activation of N-methyld-aspartate (NMDA) receptors (Malenka & Nicoll, 1999). While LTP is typically induced using electrical stimulation in vitro, similar effects (a strengthening of neural responses following stimulation) have been reported in the visual

There is compelling evidence from animal models that physical exercise can enhance visual cortex neuroplasticity. In this narrative review, we explored whether exercise has the same effect in humans. We found that while some studies report evidence consistent with exercise-induced enhancement of human visual cortex neuroplasticity, others report no effect or even reduced neuroplasticity following exercise. Differences in study methodology may partially explain these varying results. Because the prospect of exercise increasing human visual cortex neuroplasticity has important implications for vision rehabilitation, additional research is required to resolve this discrepancy in the literature.