From: gts (gts@optexinc.com)
Date: Mon Sep 02 2002 - 21:57:22 MDT
To Rafal, Lee, and others...
The abstract below is from another study in which researchers discovered
evidence supporting the hypothesis that the experience of reward is
mediated by activity in the mesolimbic system (including and especially
the nucleus accumbens). The lack of any reference to the cortex seems to
cast doubt on Rafal's contention that the reward experience is dependant
upon or mediated by activity in the cortex.
Note that "anhedonia" is a condition characterized by diminished
experience of reward and pleasure. Studies that investigate the etiology
and pathology of this condition are very relevant to this discussion of
how and where the experience of reward arises in the human brain.
In the study I posted previously, the researchers stated flatly and
unequivocally that anhedonia has its biological underpinnings in the
mesolimbic dopamine system (as opposed to the cortex). However they
noted this fact only as part of an introductory statement, by way of
informing the reader of what they considered to be a pre-established
scientific finding. This additional research below confirms and helps to
explain their statement.
The following from this abstract deserves special attention: "The
behavioral changes [i.e., the diminished capacity to experience reward
and pleasure], induced by exposure to chronic mild stress, were shown to
be associated with a number of changes in dopaminergic neurotransmission
in the mesolimbic system, especially in the nucleus accumbens."
In other words, chronic stress causes changes in the mesolimbic system
especially the NAC which negatively affect the ability to experience
reward and pleasure. This suggests very strongly that the experience of
reward arises in the mesolimbic system, as I contend.
I think it is incorrect to state, as does Rafal, that "we know too
little" to be able to identify the mesolimbic system as the location of
the fundamental reward experience. There is a tremendous amount of
research in this area, most of it very new (dated in the last 5 years).
I've only barely scratched the surface here. When I find time I post
additional research abstracts on this subject.
Perhaps we knew too little five or ten years ago, but not so I think in
2002.
Rafal: as a student/instructor of Neurology I sincerely hope you will
investigate this subject in more detail and offer us a more informed
opinion.
In greater terms, this subject is critical when considering the
extropian dream of encoding oneself in an inorganic substrate for a
trans-human existence. If the rewards and pleasures of life arise
biological correlates in primitive brain systems, as I (and these
researchers) contend, then it will not be sufficient simply to encode
one's conscious "cerebral" personality. We'll need to find a way to
encode the primitive mesolimbic and reptilian brains that lay at the
foundation of our personalities.
I believe this means we'll need to encode the information contained in
our genetic material. And this requirement is very fitting, I think,
because our personalities per se are not designed by nature and
evolution to be immortal. It is nature's design only that our genes
should be immortal.
In my view it is appropriate to state that extropianism is in harmony
with the theory of biological evolution. Darwin himself might have
predicted an extropian future had he been privy to modern technology.
It's all about the survival of genes.
ABSTRACT:
Neuroscience 1997 Sep;80(1):17-20
Social interaction increases the extracellular levels of [Met]enkephalin
in the nucleus accumbens of control but not of chronic mild stressed
rats.
Bertrand E, Smadja C, Mauborgne A, Roques BP, Dauge V.
Departement de Pharmacochimie Moleculaire et Structurale, U266 INSERM,
URA D1500 CNRS, UER des Sciences Pharmaceutiques et Biologiques, Paris,
France.
Chronic application of various mild stress has been shown to decrease
the responsiveness to reward in rats. This effect, which was suggested
to mimic anhedonia, one of the main symptoms observed in depressive
patients, can be measured by various tests. Thus chronic mild stress was
shown to reduce the consumption of a palatable sucrose solution, and to
decrease the acquisition of preferences for a distinct environment
paired with a variety of reinforcing substances. These negative
responses could be prevented by chronic treatment with tricyclic or
atypical antidepressants. The behavioural changes, induced by exposure
to chronic mild stress, were shown to be associated with a number of
changes in dopaminergic neurotransmission in the mesolimbic system,
especially in the nucleus accumbens. The nucleus accumbens contains a
large number of enkephalinergic cell bodies giving rise to local
collaterals and axons projecting to the globus pallidus-ventral pallidum
region (for review see Ref. 9). Furthermore, there is evidence that this
structure is instrumental in mediating the reward effects of exogenous
and endogenous opioids (for reviews see Refs 5,7,17). This study was
carried out to analyse the possible contribution of the enkephalinergic
system in the anhedonic-like state induced by chronic mild stress.
Microdialysis was used to study the extracellular levels of
[Met]enkephalin-like material in the rostral part of the nucleus
accumbens of freely moving rats exposed or not to chronically mild
stress. In both groups, the basal levels of [Met]enkephalin-like
material were found to be similar. Exposure of the two groups to a
congener, increased the extracellular levels of [Met]enkephalin in the
controls but not in chronic mild stressed rats. This suggests that the
reactivity of the endogenous opioid system could be reduced in stress
induced model of anhedonia.
PMID: 9252217 [PubMed - indexed for MEDLINE]
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