“Sensory gating”的意思、由来-开放百科全书

The cocktail party effect illustrates how the brain inhibits input from environmental stimuli, while still processing sensory input from the attended stimulus.^[5] The cocktail party effect demonstrates sensory gating in hearing, but the other senses also go through the same process protecting primary cortical areas from being overwhelmed.

Neural regions involved

Information from sensory receptors make their way to the brain through neurons and synapse at the thalamus. The pulvinar nuclei in the thalamus function as the gatekeeper, deciding which information should be inhibited, and which should be sent to further cortical areas. Sensory gating is mediated by a network in the brain which involves the auditory cortex (AC), prefrontal cortex and hippocampus.^[6] Other areas of the brain associated with sensory gating include the amygdala, striatum, medial prefrontal cortex, and midbrain dopamine cell region (GABAergic neurons only).^[5]

Research of sensory gating primarily occurs in cortical areas where the stimulus is consciously identified because it is a less invasive means of studying sensory gating.^[1] Studies on rats show the brain stem, thalamus, and primary auditory cortex play a role in sensory gating for auditory stimuli.

Techniques for measurement

Paired-click paradigm

The paired-click paradigm is a common non-invasive technique used to measure sensory gating, a type of event-related potential. For normal sensory gating, if a person hears a pair of clicks within 500 ms of one another, the person will gate out the second click because it is perceived as being redundant. Evidence of the gating can be seen in the P50 wave, occurring in the brain 50 ms after the click. Low values of the P50 wave indicate that sensory gating has occurred. High values of the P50 wave indicate a lack of sensory gating.^[2] Individuals with schizophrenia only reduce the amplitude of S2 by 10–20%, whereas individuals without schizophrenia reduce the amplitude of S2 by 80–90%.^[7]

Other techniques

Electroencephalography (EEG) and magnetoencephalographies (MEG) are used to measure brain responses and are common techniques for studying sensory gating. One type of EEG measure used for sensory gating research is the event-related potential (ERP). EEG research on sensory gating shows that gating starts almost immediately after receiving a stimulus.^[3] Positron emission tomography (PET) studies have shown that an increased need to gate information is accompanied by increased engagement of the thalamus.^[3] P50 wave testing is one of many auditory event-related potential studies.

Sensory gating deficits and mental illness

Schizophrenia

A large interest in sensory gating research is directed at improving deficits among people diagnosed with Schizophrenia. People with schizophrenia often have deficits in gating the neuronal response of the P50 wave.^[2] Since people with schizophrenia can often have an overload of attended stimuli, the P50 wave may serve a critical role in illuminating sensory gating at a neurological level.

The P50 Auditory Gating deficit is one of the best established biological traits associated with schizophrenia.^[1]

Autism disorders

Individuals diagnosed with autism spectrum disorders (ASD) show patterns of restrictive and repetitive behaviors, reflecting a difficulty to inhibit excess sensory information in the brain. This information suggests sensory gating may be affecting some of the visible symptoms of ASD.^[8]

Drug influences

Nicotine

One reason people report they like smoking cigarettes is nicotine's ability to aid their selective attention.^[3] In order to alleviate the stress of not being able to gate sensory input, nicotine can correct sensory gating deficits for individuals with schizophrenia, but the effects only last about thirty minutes after nicotine intake.^[9] The same self-medication is present among those with attention-deficit/hyperactivity disorder and even those on the autism spectrum as well.

See also

References

1. ^¹²Cromwell, H.C. (2008). Sensory gating: A translational effort from basic to clinical science. Clinical EEG and Neuroscience.
2. ^¹²Freedman, R., Adler, L.W., Gerhardt, G.A., Baker, N., Rose, G.M, Dreging, C., Nagamoto, H.,…Franks, R. (1987). Neurobiological studies of sensory gating in schizophrenia. Schizophrenia Bulletin, 13(4), 669-676.
3. ^¹²³Banich, M.T. (2004). Cognitive neuroscience and neuropsychology (2nd Edition). Houghton Mifflin Company: pp. 49-50, 258-259.
4. ^Brenner, C.A., Edwards, C.R., Carroll, C.A., Kieffaber, P.D., Hetrick, W.P. (2004). P50 and acoustic startle gating are not related in healthy participants. Psychophysiology, 41, 1-7.
5. ^¹Eysenck, M, Keane, M. (2000). Cognitive Psychology: A Student’s Handbook (4th Edition). Psychology Print.
6. ^Mayer, A. R., Hanlon, F. M., Franco, A. R., Teshiba, T. M., Thoma, R. J., Clark, V. P., & Canive, J. M. (2009). The neural networks underlying auditory sensory gating. NeuroImage, 44, 182-189.
7. ^Wan, L., Friedman, B. H., Boutrous, N. N., Crawford, H. J. (2008). P50 Sensory Gating and Attentional Performance. International Journal of Psychophysiology, 67: 91-100.
8. ^Perry, W., Minassian, A., Lopex, B., Lincoln, A. (2007). Sensorimotor Gating Deficits in Adults with Autism. Society of Biological Psychiatry, 61: 482-496.
9. ^Adler, L. E., Oliency, A., Waldo, M., Harris, j. G., Griffith, J., Stevens, K., Flach, K., Nagamoto, H., Bickford, P., Leonard, S., Freedman, R. (1998). Schizophrenia, Sensory Gating, and Nicotinic Receptors. Schizophrenia Bulletin, 24(2):189-202.