From: gts (gts@optexinc.com)
Date: Tue Oct 01 2002 - 13:36:53 MDT
We can learn a great deal about human motivation from the field of
addiction science. This is a field with which I am well acquainted for
professional reasons. This message is supported by several research
abstracts, contained below.
An addiction is essentially a "hijacking" of the brain's reward system.
The addicted individual loses motivation to seek reward and pleasure
from normal healthy experiences and instead seeks the more intense
rewards available from his addiction. This "substitution" of normal
rewards for drug-rewards is very strong empirical evidence that normal
rewards are mediated by the same neural processes as drug-rewards. Other
evidence for the same is found in the lab through epidemiological
research involving genetic testing, brain scans, and via microdialysis
and reverse microdialysis techniques in live subjects (the latter only
in lab animals, since humans are not inclined to undergo such invasive
procedures).
In an earlier message here I quoted from an article by Desmond Morris.
In that article Morris states that every animal species can be
categorized into one of two groups: the "specialists" and the
"opportunists." The human animal is an opportunist, meaning that
nature/evolution has provided us with no specialized survival skills.
We've survived largely by staying busy as hunters and novelty seekers
(this is in contrast to, for example, venomous snakes which have a very
specialized skill: the snake can lie quietly in wait for its prey and
thereby survive with relatively little physical activity relative to
humans and other opportunistic animals, e.g., wolves).
In neurological terms, the motivation to experience novelty is closely
related to the motivations to eat, to use addictive drugs, to find
comfort and shelter, to take risks, to seek sexual experiences, and yes
even to engage in the socially constructive acts that we call
"altruistic". Essentially all human motivations are, at least in my
view, manifestations of the basic biological incentive to experience
reward and satisfaction.
The biological underpinnings of the human motivation to seek novelty
seems to be located (like other forms of reward, including drug reward)
in the mesolimbic dopaminergic system. Studies show increased activity
especially in the nucleus accumbens when the organism is confronted by
novelty. Neurons in the ventral tegmental area release dopamine into the
nucleus accumbens (NAC), which seems to be the source of the pleasurable
and reinforcing effects of rewarding experiences.
As Rafal likes to say, the cortex is also implicated in the reward
experience, specifically the pre-frontal cortex. I certainly agree that
the cortex is involved in the conscious recognition of pleasure and
reward, and that in some sense this recognition cannot be removed from
the experience of reward itself. Also the conscious or preconscious
*recognition* of reward is no doubt very important in establishing
learned behaviors and habits and conscious preferences. But as this
first abstract below suggests, the actual "pleasure" property of the
reward experience seems to be mediated by activity in the nucleus
accumbens rather than the cortex. (Injections of the cocaine-like drug
nomifensine into the frontal cortex did not result in reinforcement of
the behavior, while injections into the NAC did. This suggests the
primacy of the NAC in the pleasurable reward experience itself, at least
with respect to rewards that are mediated by the neurotransmitter
dopamine [and I know of none that are not].)
The mechanisms underlying the reward from novelty is described in the
second abstract.
The human motivation to seek novelty is investigated in more detail in
the third abstract below. Researchers have learned that in humans,
certain polymorphisms of the dopamine receptor are associated with
greater motivation to seek novelty. Some people get a bigger "kick" out
of new experiences than do others, and it is possible to predict these
personality differences between individuals through genetic testing.
People with these alleles of the dopamine receptor genes are more
motivated than average to "boldly go where no one has gone before" :).
This third abstract also underscores the importance of the information
contained in our genes with respect to the preservation of our
personalities. We may someday be able to dispense with the *form* of our
genes (currently in the form of protein molecules) but I see no way to
dispense with the *information* they contain. We may not need their form
but we do need their substance if we hope to keep our personalities
intact in some transhuman existence.
ABSTRACT 1
Habit-forming actions of nomifensine in nucleus accumbens.
Psychopharmacology (Berl) 1995 Nov;122(2):194-7 (ISSN: 0033-3158)
Carlezon WA; Devine DP; Wise RA
Department of Psychology, Concordia University, Montreal, Quebec,
Canada.
Rats learned to lever-press when reinforced with response-contingent
microinfusions of the dopamine uptake inhibitor nomifensine (1.7 nmol
per injection) into the ventro-medial (shell) region of nucleus
accumbens septi (NAS). The drug was not effective when similar
injections were given either in random relation to lever-pressing, into
the more dorso-lateral (core) region of NAS, or into the frontal cortex.
Cocaine was also effective in NAS, but considerably less so. These data
suggest that response-contingent dopamine uptake blockade within the NAS
is sufficient to establish and maintain instrumental response habits.
ABSRACT 2
Novelty-evoked elevations of nucleus accumbens dopamine: dependence on
impulse flow from the ventral subiculum and glutamatergic
neurotransmission in the ventral tegmental area.
Eur J Neurosci 2001 Feb;13(4):819-28 (ISSN: 0953-816X)
Legault M; Wise RA
Center for Studies in Behavioural Neurobiology, Department of
Psychology, Concordia University, Montreal, Quebec, Canada, H3G 1M8.
Mark.Legault@CRFS.Umontreal.ca.
In vivo microdialysis in freely moving rats was used to monitor
novelty-evoked elevations in extracellular dopamine in the nucleus
accumbens septi (NAS) and to examine the role of the ventral subiculum
of the hippocampus and glutamatergic transmission in the ventral
tegmental area (VTA) on these elevations. Exposure to novel stimuli
evoked investigatory activity and increased nucleus accumbens dopamine.
Unilateral injections of the sodium channel blocker tetrodotoxin (0.16
ng/0.5 microL) into the ventral subiculum ipsilateral to the dialysed
NAS abolished novelty-evoked elevations in dopamine. Injections of
tetrodotoxin into the contralateral VS did not prevent novelty-evoked
elevations in nucleus accumbens dopamine. Unilateral perfusion (via
microdialysis) of the ionotropic glutamate receptor antagonists
kynurenic acid (1 mM) into the ipsilateral but not the contralateral VTA
blocked novelty-evoked elevations in nucleus accumbens dopamine. Neither
unilateral injections of tetrodotoxin nor unilateral perfusion of
kynurenic acid disrupted investigatory behaviour. These data indicate
that phasic elevations in nucleus accumbens dopamine evoked by exposure
to unconditioned novel stimuli are dependent on impulse flow from the
hippocampus and glutamatergic transmission in the VTA.
ABSTRACT 3
D2 and D4 dopamine receptor polymorphisms and personality.
Am J Med Genet 1998 May 8;81(3):257-67 (ISSN: 0148-7299)
Noble EP; Ozkaragoz TZ; Ritchie TL; Zhang X; Belin TR; Sparkes RS
Department of Psychiatry and Biobehavioral Sciences, University of
California, Los Angeles 90024-1759, USA. epnoble@ucla.edu.
The relationship of various dimensions of temperament, measured by the
Tridimensional Personality Questionnaire (TPQ), to polymorphisms of the
D2 dopamine receptor (DRD2) and D4 dopamine receptor (DRD4) genes was
determined in 119 healthy Caucasian boys who had not yet begun to
consume alcohol and other drugs of abuse. Total Novelty Seeking score of
the TPQ was significantly higher in boys having, in common, all three
minor (A1, B1, and Intron 6 1) alleles of the DRD2 compared to boys
without any of these alleles. Boys with the DRD4 7 repeat (7R) allele
also had a significantly higher Novelty Seeking score than those without
this allele. However, the greatest difference in Novelty Seeking score
was found when boys having all three minor DRD2 alleles and the DRD4 7R
allele were contrasted to those without any of these alleles. Neither
the DRD2 nor the DRD4 polymorphisms differentiated total Harm Avoidance
score. Whereas subjects having all three minor DRD2 alleles had a
significantly higher Reward Dependence 2 (Persistence) score than
subjects without any of these alleles, no significant difference in this
personality score was found between subjects with and without the DRD4
7R allele. In conclusion, DRD2 and DRD4 polymorphisms individually
associate with Novelty Seeking behavior. However, the combined DRD2 and
DRD4 polymorphisms contribute more markedly to this behavior than when
these two gene polymorphisms are individually considered.
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