Sensory Deprivation and Sensory Reinforcement with Shock

1966 ◽  
Vol 18 (3) ◽  
pp. 803-808 ◽  
Author(s):  
Gordon M. Harrington ◽  
Glenn R. Kohler

Groups of rats were raised from weaning under normal animal colony conditions and conditions of reduced sensory stimulation. In a shuttle box groups of 5, 2, and 2 showed acquisition for mild shock proportional to degree of deprivation ( P < .02). In a second experiment 16 deprived animals preferred shock more than did 14 nondeprived animals ( P < .01). Nondeprived rats preferred shock to no shock ( P < .01). The results are interpreted as effects of arousal and satiation.

1959 ◽  
Vol 105 (438) ◽  
pp. 235-237 ◽  
Author(s):  
A. Harris

Much interest has been displayed in the past few years in the effect on human subjects of reduction, or as far as possible, abolition of sensory stimulation, so that virtual isolation from the environment is produced. Recent comprehensive reviews have appeared, dealing with experimental work (Solomon et al. 1957) and conditions arising incidentally in the course of various therapeutic procedures (Grünthal 1957), and it is therefore unnecessary to deal with the topic at length here.


1973 ◽  
Vol 67 (3) ◽  
pp. 119-126

To develop properly, it is necessary for the infant, and particularly the infant who is blind, to be provided with a rich environment of sensory stimulation. When such stimulation is absent, as evidenced by the findings of researchers in sensory deprivation, a variety of undesirable behaviors can result. Parents can be helped in a variety of ways to provide their child with adequate stimulation. The concept of an infant curriculum, as developed by Barsch, is suggested as a particularly useful means of insuring that appropriate kinds and amounts of sensory stimulation are provided at each developmental stage.


2021 ◽  
Author(s):  
Zhe Zhang ◽  
Jeffrey Rumschlag ◽  
Carrie R Jonak ◽  
Devin K Binder ◽  
Khaleel A Razak ◽  
...  

Reduced structural and functional interhemispheric connectivity correlates with the severity Autism Spectrum Disorder (ASD) behaviors in humans. Little is known of how ASD-risk genes regulate callosal connectivity. Here we show that Fmr1, whose loss-of-function leads to Fragile X Syndrome (FXS), cell autonomously promotes maturation of callosal excitatory synapses between somatosensory barrel cortices. Postnatal, cell-autonomous deletion of Fmr1 in postsynaptic Layer (L) 2/3 or L5 neurons results in a selective weakening of AMPA receptor- (R), but not NMDA receptor-, mediated synaptic function, indicative of increased 'silent', or immature, callosal synapses. Sensory deprivation by contralateral whisker trimming normalizes callosal input strength, suggesting that experience-driven activity of postsynaptic Fmr1 KO L2/3 neurons weakens callosal synapses. In contrast to callosal inputs, synapses originating from local L4 and L2/3 circuits are normal, revealing an input-specific role for postsynaptic Fmr1 in promoting callosal synaptic connectivity. Multielectrode EEG recordings in awake Fmr1 KO mice find reduced coherence of bilateral neural oscillations in beta and gamma frequencies during rest and sensory stimulation, reflecting reduced interhemispheric integration. Our findings reveal the cellular and synaptic mechanisms by which loss of Fmr1 leads to reduced interhemispheric connectivity and suggests a novel biomarker of brain dysfunction in FXS.


2020 ◽  
Vol 54 (6) ◽  
pp. 50-57
Author(s):  
L.N. Kornilova ◽  

The paper reports results of the author's sensorimotor physiology studies made under the guidance of I.B.Kozlovskaya. The vestibular function and ocular tracking tests were performed by more than 100 cosmonauts prior to and after long-term missions to the Mir and International space station. Fifty two of them implemented these tests between mission days 129 to 215. We studies orientation illusions, spontaneous eye movements, static vestibulo-ocular response to head turns (static otolith-cervical reflex), dynamic vestibulo-ocular reactions to the head roll about the body axis, precision of fixational eye movements, and smooth tracking. Results of testing in the real changed gravity were compared with the data from 7 to 21-day simulation studies in horizontal dry immersion. The tests revealed 4 forms of vestibular disorders characterized by disturbances of spatial perception, orientation illusions, inversions of vection illusions, weakening of static and strengthening of dynamic vestibulo-ocular reactions, a new visual tracking strategy termed a saccadic approximation, that is the gaze approaches or tracks a target using a series of saccadic movements. In addition, the tests made it possible to specify the impact of afferentation deficit (sensory deprivation) on accuracy of ocular and ocular-manual tracking and validate additional sensory stimulation as a method to counteract the effects of sensory deprivation in real and simulated microgravity.


2020 ◽  
Author(s):  
Marta Zaforas ◽  
Juliana M Rosa ◽  
Elena Alonso-Calviño ◽  
Elena Fernández-López ◽  
Claudia Miguel-Quesada ◽  
...  

SummaryCortical areas have the capacity of large-scale reorganization following sensory deprivation. However, it remains unclear whether this is a unique process that homogenously affects the entire deprived region or it is suitable to changes depending on local circuitries across layers. By using in vivo electrophysiology to record neuronal activity simultaneously across cortical depth, we showed that sensory deprivation due to spinal cord injury induces layer-specific changes in both spontaneous and evoked-activity. While supragranular layers specifically increased gamma oscillations and the ability to initiate up-states during spontaneous activity, infragranular layers displayed increased, faster and delayed evoked-responses to sensory stimulation. Therefore, sensory deprivation immediately modifies local circuitries allowing supragranular layers to better integrate spontaneous corticocortical information to maintain column excitability, and infragranular layers to better integrate evoked-sensory inputs to preserve subcortical outputs. These layer-specific changes may guide long-term alterations in excitability and plasticity associated to network rearrangements and the appearance of sensory pathologies associated with spinal cord injury.


1965 ◽  
Vol 20 (3) ◽  
pp. 757-762 ◽  
Author(s):  
Kenneth M. Goldstein

The study explores the need for sensory stimulation during sensory deprivation (S.D.). Confined and nonconfined Ss were compared on time spent button-pressing for visual, auditory, visual and auditory, or no stimulation. Thus, there were 8 treatment groups of 10 human Ss each. Ss in confinement spent more time button-pressing than did nonconfined Ss. Ss receiving pleasant visual stimulation spent more time button-pressing than did Ss not receiving such stimulation. No significant relationships were found between button-pressing behavior and performance on a variety of tests.


1968 ◽  
Vol 27 (1) ◽  
pp. 319-334 ◽  
Author(s):  
Marvin Zuckerman ◽  
Harold Persky ◽  
Kathryn E. Link ◽  
Gopal K. Basu

An attempt was made to investigate the interactive roles of social isolation, movement restriction, and prior information in the sensory deprivation experiment. 20 Ss were put into an 8-hr. sensory deprivation condition and 20 other Ss into an 8-hr. social isolation (with sensory stimulation) condition. All Ss were also seen on a non-confined control day in the laboratory. The order of the control and experimental days was counterbalanced within each group. These groups were compared with other groups with less movement restriction. The results indicated that the interaction between confinement and familiarity-uncertainty set produced psychological stress effects. Sensory deprivation and uncertainty produced “primary-process” effects; movement restriction enhanced these effects and produced additional discomfort and more autonomic arousal.


SLEEP ◽  
2020 ◽  
Author(s):  
Cynthia T Hsu ◽  
Juliana Tsz Yan Choi ◽  
Amita Sehgal

Abstract Study Objectives While wake duration is a major sleep driver, an important question is if wake quality also contributes to controlling sleep. In particular, we sought to determine whether changes in sensory stimulation affect sleep in Drosophila. As Drosophila rely heavily on their sense of smell, we focused on manipulating olfactory input and the olfactory sensory pathway. Methods Sensory deprivation was first performed by removing antennae or applying glue to antennae. We then measured sleep in response to neural activation, via TRPA1, or inhibition, via KIR2.1, of subpopulations of neurons in the olfactory pathway. Genetically restricting manipulations to adult animals prevented developmental effects. Results We find that olfactory deprivation reduces sleep, largely independently of mushroom bodies that integrate olfactory signals for memory consolidation and have previously been implicated in sleep. However, specific neurons in the lateral horn, the other third order target of olfactory input, affect sleep. Also, activation of inhibitory second order projection neurons increases sleep. No single neuronal population in the olfactory processing pathway was found to bidirectionally regulate sleep, and reduced sleep in response to olfactory deprivation may be masked by temperature changes. Conclusions These findings demonstrate that Drosophila sleep is sensitive to sensory stimulation, and identify novel sleep-regulating neurons in the olfactory circuit. Scaling of signals across the circuit may explain the lack of bidirectional effects when neuronal activity is manipulated. We propose that olfactory inputs act through specific circuit components to modulate sleep in flies.


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