Mechanisms underlying rapid experience-dependent plasticity in the human visual cortex

Abstract

Visual deprivation induces a rapid increase in visual cortex excitability that may result in better consolidation of spatial memory in animals and in lower visual recognition thresholds in humans. ␥-Aminobutyric acid (GABA)ergic, N-methyl-D-aspartate (NMDA), and cholinergic receptors are thought to be involved in visual cortex plasticity in animal studies. Here, we used a pharmacological approach and found that lorazepam (which enhances GABAA receptor function by acting as a positive allosteric modulator), dextrometorphan (NMDA receptor antagonist), and scopolamine (muscarinic receptor antagonist) blocked rapid plastic changes associated with light deprivation. These findings suggest the involvement of GABA, NMDA, and cholinergic receptors in rapid experience-dependent plasticity in the human visual cortex.

Short-term plasticity of the human adult visual cortex measured with 7T BOLD

“…This is also in line with the decrease of inhibition after full visual deprivation (blindfolding), measured by TMS, pharmacological manipulations and BOLD (38)(39)(40)(41). A decrease of GABA should affect not only overall neuronal excitability, but also neuronal selectivity, as both orientation and spatial frequency selectivity are mediated by GABAergic intra-cortical inhibitory circuitry (reviewed in42).…”

GABAA Agonist Reduces Visual Awareness: A Masking–EEG Experiment

“…For example, a study that recorded the activity of single V1 neurons in macaque monkeys demonstrated that SCO suppressed top-down attentional modulation of the primary visual cortex (Herrero et al, 2008). Furthermore, research by Boroojerdi and colleagues showed that experience-dependent plasticity in the human visual cortex was blocked with all the three agents (LZP, SCO, and DM; Boroojerdi et al, 2001). A combination of task and measurement differences between the reports and our experiments may have contributed to the conflicting results.…”

“…In each test session, a different drug was administered at a dosage selected to have mild psychogenic and sedating effects (Boroojerdi, Battaglia, Muellbacher, & Cohen, 2001). The following agents were used (within subjects): (i) DM (120 mg, 40 ml of Dampo syrup), a potent noncompetitive NMDA receptor antagonist (Wong, Coulter, Choi, & Prince, 1988); (ii) LZP (1.5 mg, pill), a short-acting benzodiazepine that at this dose produces functional potentiation in specifically the GABA A receptors (Sybirska et al, 1993); and (iii) SCO (1.5-mg dermal patch behind the ear), a muscarinic receptor antagonist (Frey et al, 1992).…”

“…Immediately after drug intake, participants practiced a block of 216 trials. The task and EEG recording commenced ∼120 min after ingestion of the medication to maximize the levels of drug during the task (Boroojerdi et al, 2001). During the task, participants performed 2160 trials (with a short break after each block of 216 trials) with a breakdown of 480 no-mask trials, 480 full-mask trials, 480 subjective mask trials, and an additional 80 trials for the intermediate masking strengths.…”

Visual–Procedural Memory Consolidation during Sleep Blocked by Glutamatergic Receptor Antagonists

“…It has been strongly implicated in synaptic plasticity and learning (Artola and Singer, 1987;Miller et al, 1989;Kirkwood et al, 1996). Both AMPA and NMDA glutamate receptors can be found in the visual cortex (Kumar et al, 1994;Rivadulla et al, 2001) and both play roles in synaptic potentiation (Bear, 1996;Rumpel et al, 1998;Quinlan et al, 1999;Boroojerdi et al, 2001;Watt et al, 2004). AMPA receptors are thought to contribute to information transmission between neurons, whereas NMDA receptors are mainly considered to be coincidence detectors that activate after multiple previous depolarizations (Malenka and Nicoll, 1999).…”