Deprivation Of Sensory Input Research Articles

Altered Regional and Circuit Resting-State Activity Associated with Unilateral Hearing Loss

The deprivation of sensory input after hearing damage results in functional reorganization of the brain including cross-modal plasticity in the sensory cortex and changes in cognitive processing. However, it remains unclear whether partial deprivation from unilateral auditory loss (UHL) would similarly affect the neural circuitry of cognitive processes in addition to the functional organization of sensory cortex. Here, we used resting-state functional magnetic resonance imaging to investigate intrinsic activity in 34 participants with UHL from acoustic neuroma in comparison with 22 matched normal controls. In sensory regions, we found decreased regional homogeneity (ReHo) in the bilateral calcarine cortices in UHL. However, there was an increase of ReHo in the right anterior insular cortex (rAI), the key node of cognitive control network (CCN) and multimodal sensory integration, as well as in the left parahippocampal cortex (lPHC), a key node in the default mode network (DMN). Moreover, seed-based resting–state functional connectivity analysis showed an enhanced relationship between rAI and several key regions of the DMN. Meanwhile, lPHC showed more negative relationship with components in the CCN and greater positive relationship in the DMN. Such reorganizations of functional connectivity within the DMN and between the DMN and CCN were confirmed by a graph theory analysis. These results suggest that unilateral sensory input damage not only alters the activity of the sensory areas but also reshapes the regional and circuit functional organization of the cognitive control network.

Plasticity at the axon initial segment

Experience dependent alterations in neural activity are mediated by diverse forms of plasticity, which are conventionally thought to occur at either synaptic terminals and/or postsynaptic membrane, such as dendrites and cell soma. However, our recent study has revealed that plasticity is not limited to synaptic sites, but it also takes place at the site where neural activity arises, the axon initial segment (AIS), which is a highly specialized region in the axon concentrated with voltage-gated Na+ channels. We observed in an avian brainstem auditory neuron that the AIS reorganized itself to elongate after deprivation of sensory inputs, which augmented the excitability of the neuron. Notably, this elongation of AIS caused spontaneous firing in some neurons, suggesting its compensatory role to restore neural activity in the circuit. Given that the AIS is the source of neural activity, this plasticity should be a most efficient mechanism for neurons to control their activity. This finding will provide a new insight into development, maintenance and refinement of neural circuits.

Internally Mediated Developmental Desynchronization of Neocortical Network Activity

During neocortical development, neurons exhibit highly synchronized patterns of spontaneous activity, with correlated bursts of action potential firing dominating network activity. This early activity is eventually replaced by more sparse and decorrelated firing of cortical neurons, which modeling studies predict is a network state that is better suited for efficient neural coding. The precise time course and mechanisms of this crucial transition in cortical network activity have not been characterized in vivo. We used in vivo two-photon calcium imaging in combination with whole-cell recordings in both unanesthetized and anesthetized mice to monitor how spontaneous activity patterns in ensembles of layer 2/3 neurons of barrel cortex mature during postnatal development. We find that, as early as postnatal day 4, activity is highly synchronous within local clusters of neurons. At the end of the second postnatal week, neocortical networks undergo a transition to a much more desynchronized state that lacks a clear spatial structure. Strikingly, deprivation of sensory input from the periphery had no effect on the time course of this transition. Therefore, developmental desynchronization of spontaneous neuronal activity is a fundamental network transition in the neocortex that appears to be intrinsically generated.

Early vibrissae removal facilitates cortical spreading depression propagation in the brain of well-nourished and malnourished developing rats

Reduced sensory input activity during brain development can induce morphological and physiological changes in the cerebral cortex, altering their response properties. Malnutrition delays the formation of somatosensory pathways. Here we used cortical spreading depression as a neurophysiological parameter to investigate electrophysiological changes after vibrissae removal in well-nourished and malnourished rats. Male Wistar rat pups had the right mystacial vibrissae-removed at postnatal days 2–3, and were submitted to spreading depression recording at 30–40 days of life. In both nutritional conditions, spreading depression velocities were increased in the hemisphere contralateral to the vibrissae removal, as compared to age- and nutrition-matched non-lesioned controls, in which no inter-hemispheric differences were found. In contrast to the well-nourished rats, in the vibrissae-removed malnourished animals the spreading depression propagation in the ipsilateral hemisphere decreased as compared to the corresponding hemisphere of the non-lesioned malnourished rats. It is concluded that deprivation of sensory input from whiskers during brain development facilitates spreading depression propagation, and early malnutrition seems to influence this effect. Since the effect persisted until 40 days, it is tempting to suggest that it is permanent, or at least long-lasting. Data might contribute to the understanding of sensory input deprivation-induced plasticity mechanisms underlying cerebral electrophysiological changes in the developing brain.

A Comparison of Experience-Dependent Plasticity in the Visual and Somatosensory Systems

In the visual and somatosensory systems, maturation of neuronal circuits continues for days to weeks after sensory stimulation occurs. Deprivation of sensory input at various stages of development can induce physiological, and often structural, changes that modify the circuitry of these sensory systems. Recent studies also reveal a surprising degree of plasticity in the mature visual and somatosensory pathways. Here, we compare and contrast the effects of sensory experience on the connectivity and function of these pathways and discuss what is known to date concerning the structural, physiological, and molecular mechanisms underlying their plasticity.

Non-verbal development of children with deafness with and without cochlear implants.

Deprivation of sensory input affects neurological development. Our objective was to explore clinically the role of hearing in development of sensorimotor integration and non-verbal cognition. The study involved 54 children (15 males, 839 females; 5 to 9 years old) with severe or profound bilateral prelocutive deafness but without neurological or cognitive impairment. Of these, 25 had received an early cochlear implant (CIm). Patients were compared with 40 children with normal hearing. All were given a battery of non-verbal neuropsychological tests and a balance test, and were timed for simple and complex movement of limbs. Deafness, whether treated by CIm or not, resulted in a delay in development of complex motor sequences and balance. Lack of auditory input was also associated with lower, but non-pathological, scores in visual gnoso-praxic tasks and sustained attention. Such differences were not observed in children with CIm. Hearing contributes to clinical development of spatial integration, motor control, and attention. An early CIm enables good verbal development and might also improve non-verbal capacities.

Histochemical changes in cytochrome oxidase of cortical barrels after vibrissal removal in neonatal and adult mice.

The posteromedial barrel subfield of the somatosensory cortex of mice was examined histochemically for cytochrome oxidase activity (cytochrome c oxidase; ferrocytochrome c:oxygen oxidoreductase, EC 1.9.3.1). In normal mice a high enzymatic activity was found within the barrel hollows, rather than in the sides and septa. Electron microscopic examination indicated that within the hollows reactive mitochondria reside in many dendrites, in some axonal terminals, and in a few neuronal perikarya. After neonatal cauterization of selected row(s) of vibrissae, the corresponding row(s) of barrels appeared as narrowed fused band(s) and their cytochrome oxidase activity was much reduced. Removal of vibrissae in the adult, by either cauterization or repeated plucking, did not cause size changes of cortical barrels. However, there was a significant decrease in the oxidative enzymatic activity within these barrels. Thus, the deprivation of sensory input through damage to, or removal of, the peripheral sensory organ induces an enzymatic response in neurons that are at least two to three synapses away from the periphery.

The effect of sensory deprivation on the behaviour of the polychaete Nereis in T-mazes

Decerebration of Nereis diversicolor that have previously been trained in a T-maze results in a return to random choice at the junction of the maze. The experiments were designed to test whether this is due to the disruption of sensory discrimination at the junction, or to interference with a memory storage or retrieval process. So long as some anterior sense organs are retained, worms can be trained or, if previously trained, continue to perform normally. Deprivation of sensory input from all the major anterior sense organs results in a loss of previously learned behaviour and a return to random choices, but naïve, deafferentiated worms are able to learn the maze in even fewer trials than intact control worms. Disconnection of the supraoesphageal ganglion and its sensory input (from eyes, palps and antennae) from the rest of the nervous system, leaving nervous connection between the tentacular cirri and the ventral nerve cord intact, has no effect on learned behaviour in 5 out of 10 worms. It is concluded that sensory deprivation, preventing discrimination at the junction of the T-maze, is an important factor leading to the apparent loss of learned behaviour when the supra-oesophageal ganglion is removed.