Experience Dependent Cross-modal Regulation of Cortical Circuitry

Plasticity;Cross-modal;not listed

Petrus, EmilyShuler, Marshall ;

Johns Hopkins University

关键词: Plasticity;    Cross-modal;    not listed;   

Others  :  https://jscholarship.library.jhu.edu/bitstream/handle/1774.2/60290/PETRUS-DISSERTATION-2014.pdf?sequence=1&isAllowed=y

瑞士|英语

来源: JOHNS HOPKINS DSpace Repository

【 摘 要 】

Sensory experience is essential not only for the formation and maintenance of cortical circuits during development but also throughout life.Neural networks within the brain regulate activity based on experience, using both synapse specific (Hebbian) and global (homeostatic) mechanisms to achieve optimal signal processing without compromising their overall excitability.The loss of one sense can trigger compensation of spared sensory modalities, which is called cross-modal plasticity.These behavioral enhancements are realized through both Hebbian and homeostatic mechanisms to compensate for the loss of one sense, processing spared senses with heightened sensitivity via alterations in cortical circuit strengths.Specifically, spared cortex enhances the feed-forward signal arriving from the thalamus while deprived cortex remains unchanged, regardless of sensory modality.Loss of vision induces enhanced feed-forward signal propagation throughout layer 4 of auditory cortex and up to layer 2/3.In layer 2/3, Hebbian strengthening of feed-forward signals combine with homeostatic scaling down of spontaneous events and weakened lateral inputs to enhance the signal to noise ratio in auditory cortex after loss of sight.These changes in excitation are complemented by alterations in inhibitory transmission, with an increase in spontaneous event frequency in superficial layers, and an increase in parvalbumin mediated evoked inhibition in layer 4.An increase in spontaneous inhibitory synaptic transmission in layer 2/3 may dampen excitable inputs, allowing only the strong and salient signals to impact the network, while stronger evoked inhibition in layer 4 may serve to sharpen tuning as the signal arrives to auditory cortex.Both cross-modal and uni-modal (within the modality) plasticity require similar molecular mechanisms, as the scaling down of spontaneous events in superficial auditory cortex is abolished without the presence of Arc, an activity regulated protein which is known to regulate synaptic AMPA receptor localization.Arc’s involvement with activity regulated production of amyloid beta (Aβ) indicates that Aβ may play a role in normal physiological maintenance of homeostasis in the network.Here we observed an inability of visual cortex layer 2/3 neurons to homeostatically adapt to loss of vision in mice lacking the main enzyme necessary to produce Aβ.Together these results indicate that cross-modal and uni-modal plasticity may use similar molecular mechanisms to homeostatically adapt to changes in sensory environment.The brain’s ability to undergo cross-modal regulation of synaptic strength in response to loss of a sensory modality extends well beyond the classical critical period, and in some cases may be more readily recruited after uni-modal sensory perturbations.The critical period may reflect an optimal balance of excitation and inhibition, which may be reopened throughout life to enable an organism to adapt to their surroundings.