time perception
This question goes back thousands of years, and is a lot more complex than it first appears
In short science doesn’t know how the passage of time, in the seconds to hour area, is perceived. There are some tantalising clues and parts of the picture but so far no one has put all the pieces together. I have often thought about this question but I haven’t looked at the literature for years, (it feels like just yesterday
). I used to think the ultimate smart drug would be one that slowed time perception. This unfortunately is an illusion, the number of ideas and thoughts would still be the same but they would stay longer and be less fleeting. It could also be the ultimate hell, imagine being stuck in traffic or at a dull meeting and time perception slowing so every second seemed to take hours to pass.
I’m going to avoid the earlier philosophical debate not because it’s not of value more because it is complex metaphysics: I think therefore I am etc and I don’t think I could understand it enough to summarize it succinctly. It is relevant because it explores the ideas of external event time and internal perceived time or brain time which is important for a scientific understanding of time perception…. …
The important unknown area is how we perceive time, from about 1 second intervals to a few hours.
In the early scientific work it was assumed that the brain had an internal clock, neuronal circuitry which provided a reference signal, which the rest of the brain could use. This stemmed from the finding that in patients with fevers, and thyroid disorders, which increase the metabolic rate appeared to over estimate the passage of external time. Time for them appeared to slow down. The theory being that the internal clock would be speeded up and then the reference signals, ticks of the clock, would be created more often. If the brain then used these ticks as a reference it would then overestimate the duration of external events. This idea of an internal clock was developed further with the discovery that there was a correlation between dopamine levels and the perception of time; it then seemed obvious that dopamine was the key. This fitted with most of the known facts drugs like haloperidol and the major tranquilizers that reduce dopamine levels appear to speed up the perception of time, those that increase dopamine levels like methamphetamine appear to slow brain time. The areas of the brain that were associated with time perception at the time were also known to be rich in dopamine. Eureka problem solved. There does seem to be a case for a clock type oscillator in the brain, some papers have even estimated its frequency as 40 -49 Hz which does stretch the available evidence somewhat.
FMRI has identified areas of the brain associated with time perception, maybe there is a clock although how it works and whether the brain uses something else as well who knows? It would appear that the clock is more of a subconscious device; if it was consciously accessible and accurate then why do people count seconds using 1 Mississippi 2 Mississippi or 1 banana 2 banana?
Research has appeared and has kept appearing that undermined this hypothesis or confused things.
For example administration of general dopamine ‘antagonist’ alpha methyl tyrosine reduced the dopamine concentrations but didn’t effect time perception in human subjects.
Neuropsychobiology. 1992;26(1-2):71-80. So possibly dopamine isn’t the key after all?
More recent work has concentrated on D2 agonists and antagonists. Which do appear to effect time perception, in the expected way, other drugs such as scopolamine effect time perception and these drugs do not directly effect dopaminergic systems.
How psychedelics effect time perception is also not known. They don’t alter dopamine directly. There is also good evidence that 5ht2a receptor stimulation (and therefore indirectly dopamine release) in the clock area (basal ganglia) of the brain is not the mechanism. So they probably act on the clock watching level rather than changing the speed of the clock.
5-HT2 receptor stimulation alters temporal differentiation in free-operant timing schedules. The anatomical location of the receptor population responsible for this effect is unknown. We examined the effect of a 5-HT2 receptor agonist and antagonists, injected systemically and into the dorsal striatum, a region that is believed to play a major role in interval timing. Rats were trained under the free-operant psychophysical procedure to press levers A and B in 50s trials in which reinforcement was provided intermittently for responding on A in the first half, and B in the second half of the trial. Percent responding on B (%B) was recorded in successive 5s epochs of the trials; logistic functions were fitted to the data from each rat to derive timing indices (T50: time corresponding to %B = 50; Weber fraction: [T75-T25]/2T50, where T75 and T25 are the times corresponding to %B = 75 and %B = 25). Systemic treatment with the 5-HT(2A/2C) receptor agonist 2,5,-dimethoxy-4-iodo-amphetamine (DOI) (0.25 mg/kg, s.c.) reduced T50; the 5-HT2A receptor antagonist MDL-100907 (0.5 mg/kg, i.p.) did not affect performance, but completely blocked the effect of DOI. DOI (1 and 3 microg) injected bilaterally into the dorsal striatum did not alter T50. The effect of systemic treatment with DOI (0.25 mg/kg, s.c.) was not altered by intra-striatal injection of MDL-100907 (0.3 microg) or the 5-HT2C receptor antagonist RS-102221 (0.15 microg). The ability of systemically administered MDL-100907 to reverse DOI's effect on T50 confirms the sensitivity of temporal differentiation to 5-HT2A receptor stimulation. The failure of intra-striatal MDL-100907 to antagonize the effects of DOI suggests that 5-HT2A receptors in the dorsal striatum are unlikely to be primarily responsible for DOI's effects on timing. Furthermore, the results provide no evidence for a role of striatal 5-HT2C receptors in DOI's effect on timing.
Behav Processes. 2006 Feb 28;71(2-3):258-67
So if they don’t alter the clock speed how do they do it? My instinct is that it is a consequence of they way they change the novelty detection systems in the brain. Under the influence of psychedelics many more things are recognized as novel, everyday things that would be normally be ignored and forgotten catch the attention. Therefore a lot more novel events occur per hour on psychedelics. These novel events are used as markers by the brain, they are stored in the memory and when the brain wants to estimate the duration of an external event it looks at how many novel or interesting events occurred.
This wouldn’t require an internal clock as a reference, but it might use it as well.
This novelty marker idea fits with the idea of time speeding up as one ages, there are less and less novel things as time goes on, so there are less novel markers left in the memory.
Its quite interesting to estimate time whilst under the influence of a low dose, set an alarm for 10 seconds and whilst under the influence train yourself to estimate guess when the alarm will go off, the first 5 times or so you’re early then after 5 times or so you are spot on. I have tried this with various hairless test monkeys and it seems to be a real effect. So you can retrain to take account of the time perception effects, which would imply it is at the conscious level.
There is loads of ongoing research in this area. The trouble is the more we know the less we understand.
its great not having anything on at work I've been looking into time perception all day and getting paid
still don't have the answer unfortunately
