Sensory memory

Tiitinen, H., P. May, K. Reinikainen, and R. Naatanen. 1994. "Acute Novelty Detection in Humans Is Governed by Preattentive Sensory Memory." Nature 372 90-92. 

Javitt DC, Steinschneider M, Schroeder CE, Arezzo JC. 1996. Role of cortical N-methyl-D-aspartate receptors in auditory sensory memory and mismatch negativity generation Implications for schizophrenia. Proc Natl Acad Sci... 

Catts SV, Shelley AM, Ward PB, Liebert B, McConaghy N, et al. 1995. Brain potential evidence for an auditory sensory memory deficit in schizophrenia. Am J Psychiatry 152 213-219. 

Sensory memory, or sensory register, notes or registers sensory stimuli as they are experienced. It consists of representations of the outside world as experienced through the senses such as touch, sight, or smell. It holds information for approximately one to two seconds. 

If, for instance, you glance at the ocean and turn away, the image of the ocean will be lost in one to two seconds unless the image is quickly transferred into the shortterm memory system. The contents of sensory memory are constantly changing as new stimuli are perceived. Information that does not fade from sensory memory enters short-term memory. 

Sensory memory—Part of the memory system that registers experience through the senses, holding onto information for one to two seconds before it is lost or transferred to short-term memory. 

Furthermore, multi-sensory experience design has also attracted more and more attention since user experience is closely related to how the senses are stimulated and gratified [39 1]. In addition, it should not merely focus on visual aesthetics but should consider all of the senses [42]. Actually, user experience can be enriched to a certain extent if there are more sensory modalities involved [40] and more sensory memories activated [43]. Researchers have studied sensory experience from several facets such as roles of the senses [44], sensory importance [27, 28] and various kinds of interactions between senses [45]. 

The aroma of fmit, the taste of candy, and the texture of bread are examples of flavor perception. In each case, physical and chemical stmctures ia these foods stimulate receptors ia the nose and mouth. Impulses from these receptors are then processed iato perceptions of flavor by the brain. Attention, emotion, memory, cognition, and other brain functions combine with these perceptions to cause behavior, eg, a sense of pleasure, a memory, an idea, a fantasy, a purchase. These are psychological processes and as such have all the complexities of the human mind. Flavor characterization attempts to define what causes flavor and to determine if human response to flavor can be predicted. The ways ia which simple flavor active substances, flavorants, produce perceptions are described both ia terms of the physiology, ie, transduction, and psychophysics, ie, dose-response relationships, of flavor (1,2). Progress has been made ia understanding how perceptions of simple flavorants are processed iato hedonic behavior, ie, degree of liking, or concept formation, eg, crispy or umami (savory) (3,4). However, it is unclear how complex mixtures of flavorants are perceived or what behavior they cause. Flavor characterization involves the chemical measurement of iadividual flavorants and the use of sensory tests to determine their impact on behavior. 

Motion sickness arises in the vestibular apparatus. Stimulation of the semicircular canals or the utricles by unfamiliar accelerating movement may cause a mismatch between the sensory information reaching the brain centres controlling balance and posture, with that anticipated. Motion sickness may be avoided by reducing sensory conflict fixing vision on a stable reference point, such as the horizon may be effective. Cortical centres may also contribute memories of previous travel or the sight, and sounds of others being affected often increases susceptibility. 

The hippocampus, which got its name from the Greek word for seahorse, due to its form, is a nucleus in the depth of the temporal lobe. The hippocampus is important for the integration of sensory information, for spatial orientation and for memory formation. The hippocampal formation contains the CA (cornu ammonis) regions, the dentate gyms and the subiculum. 

Dementia is the loss of function in multiple cognitive domains that occurs over a longer period of time, usually months to years. Diagnostic features include memory impairment and at least one of the following aphasia (deterioration of speech), apraxia (impaired ability to execute motor activities despite intact motor abilities, sensory function, and comprehension of the required task), agnosia (failure to recognize or identify objects despite intact sensory function), or disturbances in executive functioning.1... 

In the vertebrate CNS monoamines have been associated with a number of physiological functions (reviewed in Kandel et al., 1991). Serotonin has functions associated with mood, pain, sleep, learning, and memory. Dopamine has functions associated with schizophrenia, Parkinson s disease, and cocaine addiction. In vertebrates, dopamine is further metabolized into two additional neurotransmitters, norepinephrine and epinephrine. Norepinephrine increases the excitability of cells in response to sudden sensory input such as fear. Epinephrine has been identified in specific neurons of the brain, but the function of these cells is unknown. In addition, AADC has also been found in a class of neurons that do not have any of the four neurotransmitters discussed above (Jaeger et al., 1983). These neurons may use one of the trace amines, tyramine, tryptamine, or phenylethylamine, as a neurotransmitter. 

One study has reported effects on neurobehavioral function in lead-exposed workers at mean PbB levels of 50 pg/dL (Williamson and Teo 1986). Neurobehavioral function was measured using tests that are based on information processing theory in 59 lead workers and 59 controls matched for age, type of job, time on the job, education level, smoking history, and alcohol consumption. Statistically significant decreases in the lead-exposed workers were seen for critical flicker fusion reaction, simple reaction time, tracking speeds, hand steadiness tests, and sensory store memory. Sensory store memory speed showed a low but statistically significant correlation with PbB concentrations. Measurements of neurobehavioral function seemed well chosen, and repeated measures with associated appropriate statistics were used. 

Cannabinoid receptors are expressed throughout the cerebral cortex and the hippocampus, and a subpopulation of these cells appear to show an unusually high level of activity. It is possible that cells in these areas modulate the sensory effects of cannabis, particularly the effects on perception, task performance and memory. In addition, the anticonvulsant properties of cannabis are believed to be mediated here. Parts of the hypothalamus show high levels of receptor sites for cannabinoids this may be related to hypothermia effects. High levels in the cerebellum may be related to mediating the property of cannabinoids that produces the reduction in ataxic (muscle co-ordination) symptoms in certain disorders (Herkenham et al., 1991). 

Studies reveal that a homozygous GlyT-1 (-/-) knockout in mice is neonatally lethal. However heterozygous GlyT-1 (+/-) mice survive to adulthood and display enhanced NMDA receptor function in the hippocampus, better memory retention, and no disruption in sensory gating when dosed with amphetamine [15]. 

Partial (focal) seizures begin in one hemisphere of the brain and, unless they become secondarily generalized, result in an asymmetric seizure. Partial seizures manifest as alterations in motor functions, sensory or somatosensory symptoms, or automatisms. If there is no loss of consciousness, the seizures are called simple partial. If there is loss of consciousness, they are termed complex partial, and the patients may have automatisms, memory loss, or aberrations of behavior. 

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