social perception discussion

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Monicarodr

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Mar 5, 2010, 4:38:41 AM3/5/10
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Some notes, comments:

Kross et al hypothesized that increased levels of distress in Hi RS
individuals could be due to:

a) increased activity in neural systems involved in affective
appraisals (bottom up processing) or alternatively b) failure to
recruit the neural regions involved in the cognitive control of
emotions, namely, prefrontal regions.

b) Their study showed that when Hi RS individuals viewed rejection
stimuli it was accompanied by a decreased activity in the left lateral
PFC and the SFG, in accord with the self-regulation theory. That is,
rather than an increase in activity in regions involved emotional
appraisal (dACC), there was a decrease in those regions involved in
the cognitive control of emotions or emotion regulation.

c) When comparing rejection vs acceptance, activation was present in
the following regions: Posterior Cingulate Cortex , parahypoccampal
regions, Mid-Dorsal ACC activity.

I agree with Beka that they present a very clean study which is
discussed in the context of other relevant studies. However, I was
surprised by the fact that Burklund and Eisenberger, Gable et al were
not cited.


In Eisenberger et al, individuals who showed greater activation of
amygdale, dACC and preiaquedactal gray during scanner session while
exposed to a social exclusion situation also reported higher levels of
momentary social distress in everyday social interactions. In
contrast, those participants who showed greater activation of the
hypoccampus and medial PFC (involvd in episodic memory and self-
referential encoding) showed greater correpsondence between momentary
social distress and overall distress at the end of the day
(retrospective affective reports). However, these participants did not
show amygdale or dACC activation, which maybe critical only in
momentary distress.

Does dACC play a unique role when responding specifically to social
threats involving rejection? Burklund et al, activation in the
presence of emotion expressions of disapproval, anger, disgust. All
result in activation of amygdale. But: when Hi RS were exposed to
disapproval emotional expressions, higher activity of dACC, but not
when exposed to other emotions. Dissaproval may convey a different,
purely “social” threat. However, because distress levels were not
measured, it is unclear whether greater dACC activity in Hi RS is due
to higher distress experience or heightened detection of cues related
to rejection.

In Schaefer et al, hot or schematic (automatic) processing was
associated with increased activity in ventromedial PFC; cold,
propositional (controlled) processing was associated with anterior
lateral PFC.

Authors converge that cingulate cortex may be comprised of multiple
regions that carry out related but different computations.

dACC : related to violation of expectations, attention to feelings,
neural alarm system
posterior ACC : experience of distress
ventral ACC and medial PFC: related to acceptance, positive
experiences, rewarding feedback, generation of emotional responses.
Lateral PFC: reappraisal of emotion “cooling”, executive tasks,
volitional control of emotion

Vmpfc: convergence/divergence zone with multiple areas of
connectivity

Thus, related to Camille’s point, it is not clear whether the presence
or absence of interpersonal feedback, the levels of experienced
distress, or the violation of expectations recruit similar neural
mechanisms.

Do physical and social pain share similar patterns of activation? Yes
according to Eisenberger et al. Patterns of activation linked to
physical pain (increased dACC activity) was also associated with
increased distress after social exclusion. Furthermore, increased
activity in RVPFC associated with the regulation of pain distress, was
associated with less reported distress after social exclusion. Opiates
alleviate physical pain as well as social pain. Why? ACC is involved
with the distress to pain (felt unpleasantness), which is different
from sensory processing, which may inform of the source of pain. Yes,
as Stuart says, Tylenol (which is opioid based) helps with both social
and physical pain (recently demonstrated by deWall and Baumeister) and
this is not different than the evidence that social support alleviates
social as well as physical pain. Shared areas of neural underpinnings
of experiences of unpleasantness and distress, however, is not
contradictory with the fact that there may be unique areas related to
each (alarm system activates different responses). Also, the release
of opioids in response to physical pain may reduce the distress from
other sources of pain such as isolation and viceversa (e.g., self-
injury example).

Following Decety and Batson, when exposed to disapproval faces are we
examining the experience of how the other feels or how we feel in
relation to the picture as interactant? What would happen if people
were asked to produce an emotional expression in response to the
picture or social exclusion? (For instance, congruent vs.
incongruent/) Would this tell us anything about the possibility for
modifying emotional experience, as Jenny suggests?

beka strock

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Mar 5, 2010, 4:00:09 PM3/5/10
to socialn...@googlegroups.com
Just following up on some of our discussion today, i got really interested in the glucose rgulation mechanisms...this site was helpful in general:

http://www.fi.edu/learn/brain/carbs.html

 
Matt, in your 2008 article you noted the effects of singular episodes of physical exercise (intense v moderate) on self-regulation.  I was thinking about our conversation today, and the long-term effects of physical fitness training on blood sugar levels.  I found some references that indicate that although depleting over the short term, over the long term, physical fitness seems to increase the regulatory ability of the blodd-glucose system (e.g. ability to react to too much or too little glucose, in both healthy and diabetic subjects;

Lindgärde, Malmquist and Balke (1982); Annuzzi, Vaccaro, Caprio , Di Bonito, Caso, Riccardi, Rivellese (1984); Kriska , Hanley , Harris , Zinman (2001)).  If executive control and self-regulation particularly are indeed dependent on glucose availability to function, physical exercise could improve homeostasis of glucose regulation.  And if homeostatis is improved despite extreme exposure, maybe this could be one mechanism by which self-control is improved, i.e., via better resource availability for self-control to function over the long term.  It is still possible that self-control practice, separately and addatively, increases the efficiency of use of those resources although I didnt see any evidence of that thus far.  Sounds like Matt's come the closest to testing that idea.

 
Also, Matt referenced we were talking about literally running out of glucose aka "central fatigue" of the central executive system.  Ultramarathon runners seem to experience this commonly based on extreme glucose depletion when they dont compensate properly for loss and the demands overtake the bodys ability to replenish (here a link if your interested:

http://www.ultrarunning.com/ultra/features/health/nutrition-and-your-mental.shtml).  This is a real-world example, although not from the scientific literature.

 

Another interesting idea i ran across is the "Selfish Brain Theory" (WIKI LINK: http://en.wikipedia.org/wiki/Selfish_Brain_Theory) which basically implies that the brain can order the body to fail (i.e. external functions shut down, or limit severely during low nutrient intake periods) in order to supply itself adequately.  Although the whole body is supplied by the level of glucose in the blood, there seems to be a mechanism for selectively supplying the brain because "the brain is separated from the rest of the body’s circulation by the blood-brain-barrier. The blood glucose has to be brought there via a special, insulin-independent transporter." 

 

I interpreted these to mean that the central exective/selfish brain would "command" the end of physical exercise before the brain could completely shut down and that mental impairments would occur during events of extreme glucose depletion, and would thereby prevent true failure due solely to muscular fatigue.  Not sure if this is correct, but seemed like the logical conclusion. So maybe muscular fatigue is impossible, because we can only push ourselves as far as our brains let us?

 

Just some thoughts that were running around my head...

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