Sensory cortices are inherently dynamic and exhibit plasticity in response to a variety of stimuli. Few studies have revealed that depending upon the nature of stimuli, excitation of the corresponding sensory region also evokes a response from other neighboring connected areas. It is even more striking, when somatosensory areas undergo reorganization as a result of an intentional disturbance and further explored as a paradigm to understand neuroplasticity. In addition, it has also been proved that drugs too can be used as a model to explore potential plasticity in sensory systems. To this aim, through electrophysiology in cats, we explored that visual neurons, throughout the cortical column, have a tendency to alter their inherent properties even when presented a non-visual stimulus. Furthermore, it was explored in mice, how the application of drugs (serotonin and ketamine) modulates potential plasticity within the visual system. Indeed, we found a shift in orientation tuning of neurons indicated by Gaussian tuning fits in both scenarios. These results together suggest that sensory cortices are capable of adapting to intense experiences by going through a recalibration of corresponding or neighboring sensory area(s) to redirect the sensory function and exhibit remarkable extent of neuroplasticity within the brain.
Part of the book: Sensory Nervous System
Sensory systems need to process signals in a highly dynamic way to efficiently respond to variations in the animal’s environment. For instance, several studies showed that the visual system is subject to neuroplasticity since the neurons’ firing changes according to stimulus properties. This dynamic information processing might be supported by a network reorganization. Since antidepressants influence neurotransmission, they can be used to explore synaptic plasticity sustaining cortical map reorganization. To this goal, we investigated in the primary visual cortex (V1 of mouse and cat), the impact of ketamine on neuroplasticity through changes in neuronal orientation selectivity and the functional connectivity between V1 cells, using cross correlation analyses. We found that ketamine affects cortical orientation selectivity and alters the functional connectivity within an assembly. These data clearly highlight the role of the antidepressant drugs in inducing or modeling short-term plasticity in V1 which suggests that cortical processing is optimized and adapted to the properties of the stimulus.
Part of the book: Ketamine Revisited