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To cite this article: Jaak Panksepp Ph.D. (2003) Commentary on Understanding Addictive Vulnerability,
Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 5:1, 21-29, DOI:
10.1080/15294145.2003.10773404
To link to this article: http://dx.doi.org/10.1080/15294145.2003.10773404
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psychobiological vectors that contribute to addiction. Since this topic remains fairly poorly developed experimentally and I have outlined some
relevant approaches previously (i.e., the development of neurochemically based psychoethological
research endeavors, Panksepp, 1999a, 1999b), I will
here largely focus on what basic brain researchers
may need to do to contribute to positive interdisciplinary building efforts. As Khantzian indicates,
explanations are too often presented as competing
with or in isolation from alternative theories, and
this is certainly a common attitude in neuroscience,
where many are acutely aware of the rewards that
attend substantive solutions to this area of great
societal concern.
Since psychoanalytic approaches are less experimental, they are less likely to yield profound new
insights, unless connections to neuroscientific perspectives are cultivated. In the absence of ample
funding, the competitive spirit is also not so fierce,
providing fertile ground for the emergence of more
complementarity than competition among those
who pursue the Holy Grail of deep psychobiological insights to understanding the core sources of
addictions. In general, my view will be complementary with Khantzians in developing the claim that if
we do not better understand emotional/affective
processes, we cannot have a coherent theory of
addiction (see Koob & Le Moal, 2001; Panksepp,
Knutson, & Burgdorf, 2002). In short, I do not
believe addictions exist unless the addictive agents
generate experienced affective states in both humans and other animals. If true, this simple assertion
should be a major call for behavioral neuroscience
to pay better heed to the global emotional issues that
must frame our molecular investigations.
At present, the emerging brainemotion area is
having great difficulty coming to terms with the
affective nature of the mammalian neuromental apparatus (for a contentious coverage of some recent
trends, see Panksepp, 2002a, 2003), and the integrative approach advocated by Khantzian will hinge
very much on how that difficult issue is finally
resolved by the larger community of interested
scholars. Since this point bears emphasis, my own
view is that addictions would never emerge, and
would not be as troublesome as they are, without our
ability to experience life and a large array of endogenous neurochemistries and man-made molecules
with experiential affective intensity (Panksepp,
Burgdorf, Gordon, & Turner, 2002; Panksepp,
Nocjar, Burgdorf, Panksepp, & Huber, 2003). This
has traditionally been an intellectually unattractive
view in basic neuroscience, which is still guided
heavily by twentieth-century behavioristic biases.
Hence emotional issues currently remain a minority
approach in behavioral neuroscience. Even among
Jaak Panksepp
key dopamine target zones of the nucleus accumbens and ventral pallidum, lie at the core of addictive and appetitive urges, and this provides an
umbrella concept for pretty much all subvariants of
psychobiological theories that we consider here,
including the important issue of how plastic neuropsychobiological processes (such as sensitization)
are critical for the transition to addiction. These
thumbnail sketches are simply aimed to provide a
context for discussing neuroscience issues, and I
will not attempt to weigh the pros and cons of each
approach in the limited space available here. For a
more detailed summary and critique, see the recent
review by Robinson and Berridge (2003); an overall
neuropsychiatric view of addictions is available in
Graham and Schultz (1998).
1. The most generic theory in behavioral-neuroscience is that which comes down to us directly
from human studies and the generally accepted role
of rewardreinforcement processes in the guidance of behavior. In everyday parlance, this straightforward view is that people are likely to consume
drug agents that cause pleasurable feelings. In the
past twenty years, Roy Wise (1982, with subtle
transitions to 1998) has been the most prominent
proponent of this perspective in neuroscience, although it has faltered on the ambiguity of the hedonia concept and on the probable need to parse
positive affect in a variety of distinct forms to really
understand the natural order of emotional feelings.
2. A more sophisticated variant of this theory is
the opponent-process theory of addiction, originally enunciated by Richard Solomon (1977) and
colleagues, which posits that one key component of
addictionsthe initial positively experienced state
of drugsis followed by accruing negative affective consequences (opponent processes), which set
the stage for a vicious addictive cycle. These unpleasant feelings, and the capacity of drugs to alleviate them, sustain addictive behavior. This, of course,
is a formalization of the classic view that abstention
from addictive agents can generate negative withdrawal symptoms that are critical for sustaining
addictions. Neural versions of this theory (Koob &
Le Moal, 1997) also focus on the fact that the
positive hedonic effects of drugs sensitize the underlying neural substrates, which can magnify not only
the positive hedonic effects of certain drugs, but also
the affectively aversive after-effect. Of course, the
neuro-adaptations that can emerge during these
stages of addiction can also be conceptualized in
learning terms.
3. Among the learning-theory approaches, investigators focus on addiction reflecting natural, albeit
intense, learning processes that are known to be
controlled to some extent by the ML/MC DAp. The
specific types of learning that may be affected are
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Jaak Panksepp
clusion that opiates do not have to produce conscious euphoria to sustain addictive behavior. By
generalization, this is seen as a piece of research
that strongly implicates unconscious reinforcement
processes in the governance of addictive behavior
in humans (e.g., Berridge & Robinson, 1998). That,
unfortunately, is a conclusion that is not justified
by the experiment that Lamb et al. actually conducted.
To set the record straight on that seminal and oftmisinterpreted study, let me describe it in some
detail and indicate why it should not be used to
argue against the role of conscious processes in
drug-seeking behavior patterns. Although this classic experiment was highly creative from various
methodological perspectives, it said nothing important about the role of consciousness in the mediation
of addictive behaviors. Lamb and colleagues studied five heroin addicts who were allowed to work
for one of five doses of morphine (vehicle placebo,
3.75, 7.5, 15, or 30 mg per dose). Their task was a
cognitively mediated fixed-ratio schedule during a
daily, one-hour access session freely provided for
five continuous days each week, under each of the
five dose conditions. Subjects were permitted to
work on a strenuous Fixed-Ratio 3000 schedule for
slowly absorbed intramuscular injections administered by the nursing staff, which typically allowed a
maximum of 46 infusions per session if the subjects worked at maximal rates. Not only was their
operant response rate monitored (they typically responded at a rapid average rate of about 45 lever
presses per second), but several affective and autonomic responses were also monitored about an hour
and a half after the end of each session.
The major finding of the study was that the
subjects would continue working vigorously for
pretty much all of the doses of morphine, but subjects only exhibited significant levels of drug-induced liking at the highest 30-mg dose (in fact, only
three of the five subjects experienced substantial
levels of drug liking, even at that dose). It should be
noted that even for the placebo injections, responding was sustained at a very high level on the first
placebo (or extinction) day (and rapidly declined
on succeeding days), suggesting that cognitive mediation sustained asymptotic behavior for at least
one full session. Thus, the role of reinforcement
in drug-seeking behavior (at least in the Thorndikian sense of short-term law of effect processes
that presumably help shape behavior) was probably
not even evaluated by this experimental design.
The widely touted mystery emerged at the three
intermediate dose conditions, with the lowest dose
being the most perplexing. Four of the five subjects
continued to work quite hard for the morphine, but
they did not exhibit any subjective drug-liking when
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asked about such matters 90 minutes after the session. Thus behavior was clearly dissociated from
conscious experiences of euphoric reward.
Fair enough? Well, not quite. After all, this was
more of a cognitively mediated operant task rather
than a reinforced self-administration task (after
all, the subjects were explicitly told about the contingencies, but not the dose being administered;
under such conditions it seems unlikely the subjects
would ever have picked up the behavior on their
own with those outrageous reinforcement contingencies). Perhaps the subjects knew that they were
getting some drug and were aspiring to go even
faster to get more. (Data that may have helped
resolve this issue, on the daily response rates for the
two lowest doses, were not provided.) Also, the
subjects were heroin addicts, and it is known that
during a stable level of opiate addiction, the euphoric subjective effects of agents have almost completely diminished. However, when unable to obtain
the mega-doses needed to re-establish euphoric
states, an addict may still be satisfied to take the
lower doses that simply help him/her feel a bit more
normal.
If the investigators were taking the conscious
mediation of behavior into account more seriously,
they might have been tempted to study the changing
feelings associated with returns to psychological
normalcy, which is affectively positive, especially if one is experiencing a mild background
discomfort of protracted withdrawal (but which may
not leach into measures of drug liking, especially
if the individuals have had experiences with many
highs). During withdrawal symptoms, might there
not even be a reasonable psychological concept
such as craving for normalcy, at least in humans
who can have desires about desires?
The investigators could also have harvested other
relevant subjective feelings, such as the urge to
respond or the desire for drug reward. In other
words, since the range of relevant subjective feelings was not adequately assessed, especially those
psychological states related to response urgency or
desire, the Lamb et al. (1991) study was, at best,
measuring only a few of the relevant subjective
issues that may have been contributing to the mediation of behavior. Indeed, they apparently did not
even ask the most important question: Why were
the subjects continuing to respond on this cognitively mediated task? If the answer had been a
consistent dunno or there was nothing else to
do, then perhaps their data might be justifiably
used to conclude that the subjects were really behaving unconsciously.
Were the investigators biased? We doubt it, but
we would note a bias against detecting positive
affective responses in the sequence of morphine
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Jaak Panksepp
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Conclusion
If one is willing to provisionally accept these admittedly radical points of view (at least for many neuroscientists and pure animal behaviorists), then we
might also conclude that biology-alone approaches,
even when linked to rigorous behavioral analyses,
will not suffice to completely understand changes in
brain functions that can lead to addiction. Psychological perspectives are essential for an adequate
confrontation with the problem, and to do that cogently requires us to link certain brain-system functions to psychological issues. Since the details of the
relevant brain circuitries can only be worked out in
animal models, we must also try to fathom the types
of psychological experiences that these circuits may
generate. A blending of basic behavioral neuroscience in other animals and relevant neuropsychological studies in humans is essential for progress.
Addiction, I would submit, operates largely
through the modulation of the organic-affective
state-control rather than the sensory-perceptual
channel-control functions of the brain. In short,
neither we nor other animals are unconscious zombies, but inheritors of an emotionally guided neuromental apparatus that has psychologically relevant
organizational aspects. Such approaches may facilitate translation of substantial parts of the animal
neuroscience data to new predictions in the human
realm (such as specifying neurochemical modulators of human feelings). This liberalization could
broaden the types of experiments and interpretive
structures that we might be more likely to conduct
and consider in animal brain research laboratories
(e.g., Panksepp & Burgdorf, 1999, 2000). Again, the
big payoff might be more rapid translations between
the basic neuroscience data and advances in neuropsychiatric practice.
It is unreasonable to think that affective states do
not govern human behaviors, and we think it equally
unreasonable to believe that they do not in related
mammals. In my estimation, the most reasonable,
data-based position is that emotional states simply
could not exist without a variety of instinctual
subcortically concentrated, emotional operating
systems that natural selection constructed into the
neural matrix a long time ago (Panksepp, 1998a). In
other words, our cognition-mediating neocortex
simply could not have any emotional feelings without the ancestral neural heritage we share with many
other animals. This does not imply that the various
neuroscientific nuts and bolts needed to construct
emotional operating systems are conscious in and of
themselves, only that experiential properties do
emerge when certain global state-control systems of
the brain come to interact in a hierarchical fashion
with each other as well as with the many sensorimo-
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tor channel-control functions that exhibit such enormous variability across species.
REFERENCES
Jaak Panksepp
Panksepp, J. (1982). Toward a general psychobiological
theory of emotions. Behavioral and Brain Sciences, 5:
407467.
Panksepp, J. (1998a). Affective Neuroscience, The Foundations of Human and Animal Emotion. New York: Oxford
University Press.
Panksepp, J. (1998b). Attention deficit hyperactivity disorders, psychostimulants and intolerance of childhood
playfulness: A tragedy in the making? Current Directions in Psychological Science, 7: 9198.
Panksepp, J. (1999a). Emotions as viewed by psychoanalysis and neuroscience: An exercise in consilience. NeuroPsychoanalysis, 1: 1538.
Panksepp, J. (1999b). Drives, affects, id energies and the
neuroscience of emotions. Neuro-Psychoanalysis, 1: 69
89.
Panksepp, J. (2000a). The neuro-evolutionary cusp between
emotions and cognitions: Implications for understanding
consciousness and the emergence of a unified mind
science. Consciousness & Emotion, 1: 1756.
Panksepp, J. (2000b). Affective consciousness and the instinctual motor system: The neural sources of sadness
and joy. In: The Caldron of Consciousness, Motivation,
Affect and Self-organization. Advances in Consciousness
Research, Vol. 16, ed. R. Ellis & N. Newton. Amsterdam: John Benjamins, pp. 2754.
Panksepp, J. (2001). The long-term psychobiological consequences of infant emotions: Prescriptions for the
twenty-first century. Infant Mental Health Journal, 22:
132173.
Panksepp, J. (2002a). The MacLean legacy and some modern trends in emotion research. In: The Evolutionary
Neuroethology of Paul MacLean, ed. G. A. Cory & R.
Gardner. Westport, CT: Greenwood, pp. ix-xviii.
Panksepp, J. (2002b). ADHD and the neural consequences
of play and joy. Consciousness & Emotion, 3: 16.
Panksepp, J. (2003). At the interface of affective, behavioral
and cognitive neurosciences: Decoding the emotional
feelings of the brain. Brain and Cognition, 52: 414.
Panksepp, J., & Burgdorf, J. (1999). Laughing rats? Playful
tickling arouses high frequency ultrasonic chirping in
young rodents. In: Toward a Science of Consciousness,
Vol. 3, ed. S. Hameroff, D. Chalmers, & A. Kazniak.
Cambridge, MA: MIT Press, pp. 231244.
Panksepp, J., & Burgdorf, J. (2000). 50-kHz chirping
(laughter?) in response to conditioned and unconditioned
tickle-induced reward in rats: Effects of social housing
and genetic variables. Behavioural Brain Research, 115:
2538.
Panksepp, J., Burgdorf, J., Gordon, N., & Turner, C. (2002).
Treatment of ADHD with methylphenidate may sensitize
brain substrates for desire. Consciousness & Emotion, 3:
719.
Panksepp, J., Knuston, B., & Burgdorf, J. (2002). The role
of emotional brain systems in addictions: A neuro-evolutionary perspective. Addiction, 97: 459469.
Panksepp, J., Nocjar, C., Burgdorf, J., Panksepp, J. B., &
Huber, R. (2003). The role of emotional systems in
addiction: A neuroethological perspective. Nebraska
Symposium on Motivation. Motivational Factors in the
Etiology of Drug Abuse, 52: 97105.
Robinson, T. E., & Berridge, K. C. (2000). The psychology
29
reinitiation of drug seeking after abstinence. In: Nebraska Symposium on Motivation. Motivational Factors
in the Etiology of Drug Abuse, ed. R. Bevins & M. Bardo.
Lincoln, NB: University of Nebraska Press.
Vanderschuren, L. J., & Kalivas, P. W. (2000). Alterations
in dopaminergic and glutamatergic transmission in the
induction and expression of behavioral sensitization: a
critical review of preclinical studies. Psychopharmacology, 151: 99120.
Wise, R. A. (1982). Neuroleptics and operant behavior: The
anhedonia hypothesis. Behavioral and Brain Sciences, 5:
3987.
Wise, R. A. (1998). Drug-activation of brain reward pathways. Drug and Alcohol Dependence, 51: 1322.