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Multiple neural clocks These 1 #109448Modern neurology has failed to identify any single neural clock in the human brain. Current evidence suggests the brain has multiple time-keeping mechanisms, specialized to different durations. One proposed mechanism based on the rate of decay of memories may have some relation to entropy. | |
+Verweise (1) - VerweiseHinzufügenList by: CiterankMapLink[1] The Inner Experience of Time
Zitieren: Marc Whittmann - Department of Psychiatry, University of California, San Diego Zitiert von: Peter Baldwin 5:10 AM 23 May 2011 GMT Citerank: (3) 109447Psychologically, we inhabit a 'specious present'Psychological and neurological studies suggest that we do not perceive events moment-by-moment but rather integrate them into perceptual units of approximately 2 to 3 seconds duration. This results in successive events forming a perceptual unity that can be apprehended without recourse to memory.959C6EF, 114533Some weak evidence for entropy clocksSince Eddington's time extensive neurological and psychological studies have sought to identify time-keeping mechanisms in the brain. Some hypothesized mechanisms are based on the rate of decay of memories, which would be aligned with the direction of increasing entropy (see citation).1198CE71, 114551Brain doesn't work with instantsNeurological studies show that the brain does not work with instants. It works with an 'extended present' (aka specious present) generally thought to be 2 to 3 seconds duration. Given this, it is feasible for the brains working memory to apprehend memory accretion. See also Julian Barbour citation.13EF597B URL:
| Auszug - "It is intuitively most unlikely that one mechanism or one neural system would be responsible for all possible durations that an organism has to process. Different temporal processing mechanisms must be involved on different time scales (Trevarthen 1999; Wittmann 1999; Mauk & Buonomano 2004; Buhusi & Meck 2005). Experimental interventions have repeatedly shown duration-specific effects of psychopharmacological agents on interval timing. For example, the dopamine receptor antagonist haloperidol as well as the benzodiazepine midazolam impair duration discrimination of intervals ranging approximately 1 s, whereas processing of 50 ms intervals is affected by haloperidol only (Rammsayer 1999). According to these results, any pharmacological treatment that affects working memory capacity (e.g. midazolam) would interfere with temporal processing of intervals above 1 s. However, intervals with a length of up to a few hundred milliseconds (such as the 50 ms interval) are supposed to be processed based on brain mechanisms outside of motor and cognitive control and reflect pure timing processes (thus, not being influenced by midazolam). According to this view, additional processes such as attention and working memory, not related to time per se, come into play with intervals exceeding several hundred milliseconds in length and complementing dopamine-driven processes, which are involved both in shorter and longer time intervals (Rammsayer et al. 2001). A similar theoretical proposal, derived from a meta-analysis on neuroimaging data, suggests two distinct neural timing systems: (i) an automatic timing system for shorter intervals up to approximately 1 s, which recruits motor systems of the brain (SMA, basal ganglia and cerebellum) and (ii) a cognitively controlled timing system for supra-second intervals connected mainly to right prefrontal and parietal cortical areas (Lewis & Miall 2003b). This separation of time perception systems is to some extent mirrored by findings n motor-timing studies, where qualitative changes in tapping performance occur with inter-tap intervals of approximately 1 and 1.5 s duration (Madison 2001). Time ranges between 0.45 and 1.5 s seem to be automatically processed, i.e. not strongly affected by attentional demands, whereas attention and working memory processes (stimulated by secondary tasks) affect intervals in the range between 1.8 and 3.6 s (Miyake et al. 2004)." |
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