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REWARD SYSTEMS OF THE BRAIN?

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Title: PowerPoint Presentation Author: Psychology Dept Last modified by: hakanr Created Date: 1/4/2005 5:27:52 PM Document presentation format: On-screen Show (4:3) – PowerPoint PPT presentation

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Title: REWARD SYSTEMS OF THE BRAIN?


1
REWARD SYSTEMS OF THE BRAIN?
2
ICSS and brain reward centers? A series of
misinterpretations.
  • The lateral hypothalamus (LH)/
  • The reward center?

3
Animal Models of reward
  • James Olds and Intra-cranial Self-stimulationInti
    al studies of learning and RAS stimulation..serend
    ipity!
  • Place preference
  • 2 lever choice

4
BUT! The medial Forebrain Bundle (MFB) runs
through the LH
The MFB is a large tract that arises from many
different nuclei and projects to many forebrain
regions
5
The Ventral tegmental Area (VTA) Dopaminergic
pathways
A component of MFB axons arise from the VTA-DA
projection paths.
VTA
6
mesolimbic and Mesocortical Dopaminergic pathways
The VTA projects to the nucleus accumbens and to
the medial prefrontal cortex
7
DA agonist and antagonist effectson ICSS
  • DA Antagonist (drugs that block the effects of
    DA ) reduce ICSS potency ( actually increase
    rates of responding suggesting the reward value
    has diminished)
  • DA Agonist (drugs that enhance the effects of
    DA ) Increase ICSS potency ( actually decrease
    rates of responding suggesting the reward value
    has increased)

8
Microdialysis Studies support the role of DA in
Reward
Microdialysis probe
9
Microdialysis probe an ultra small cellular
fluid collection system
10
When Implanted in targeted brain regions
11
Extracellular fluids can be collected and
analyzed for neurochemical content. Different
chemicals produced different Chemical
signaturesincluding DA.
12
ICCS increases DA release in Nucleus Accumbens
13
Drugs increase DA release in accumbens
14
Brain reward and Humans
  • Functional brain imagery of brain activity after
    administration of a learned reward in humans has
    found changes in brain activity in the nucleus
    accumbens, medial orbitofrontal cortex and
    anterior cingulate cortex.

15
What about ICSS in Humans
  • In humans, a well-known case was B-19, a young
    man implanted with stimulation electrodes by
    Heath and colleagues in the 1960s.
  • B-19 self-stimulated at very high rates and
    would be upset when the stimulation was
    disallowed.
  • Appeared to produce feelings of pleasure,
    alertness, and warmth.
  • He also reported sexual arousal and described a
    compulsion to masturbate (p. 6, Heath, 1972).

16
But was this pleasure?
  • Perhaps not.
  • B19s electrode stimulation evoked desire to
    stimulate again and strong sexual arousal while
    never producing sexual orgasm or clear evidence
    of actual pleasure sensation.
  • Alternatively The stimulation may not have
    affected reward but may have produced a want
    to do sexual acts.

17
The Incentive-Sensitization Theory 'wanting' is
not 'liking'
  • The neural system are proposed to be separate ..
    (Robinson and Berridge)

18
Then what is the role of meso-cortical,
mesolimbic DA systems?
  • ..to increase the salience' of stimuli and
    events associated with activation of the system.
  • Stimuli are imbued with salience, making them
    attractive, 'wanted', incentive stimuli.

19
The Incentive-Sensitization theory and Drug
Addiction ?
  • Drug-induced sensitization of DA pathways cause
    pathological incentive motivation (wanting) for
    drugs (Robinson and Berridge, 2008)
  • Dopamine normally functions to trigger reward
    wanting. In drug dependence, drugs alter
    this system.
  • Repeated use of such drugs makes the dopamine
    system hyper-responsive to drug cues
  • Drug cues become difficult for addicts to
    ignore, and lead to intense wanting (cravings
    and/or relapse).

20
The Incentive-Sensitization theory and Implicit
perceptions?
  • The incentivesensitization theory holds that
    drugs can activate wanting in the absence of
    conscious awareness.
  • Activation of the DA pathways can sometimes
    produce goal-directed
  • behavior (wanting) not only in the absence of
    subjective pleasure, but in the absence of
    conscious awareness of wanting itself.

21
Evidence supporting the Incentive-Sensitization
Theory
  • Lesions studies, and studies using selective
    dopamine agonists or antagonists, as well as
    other similar manipulations have no effect on
    rats judgements of hedonic properties of taste
    stimuli1 (for reviews, see Berridge ).
  • Many studies show that dopamine and accumbens
    neurons often become most active in anticipation
    of rewards, not during the reward phase
  • DA systems are also activated by aversive,
    stimuli and events.
  • In humans DA antagonists, such as pimozide or
    haloperidol, do not reduce amphetamine-induced
    pleasure.

22
But What About Pleasure?
  • Rewarding/pleasurable stimuli activate Opioid,
    anandamine ( an endogenous cannabis-like
    neurotransmitter) and GABA release in the
    Accumbens.
  • Crucial for pleasurable feelings associated with
    delicious foods, sex, drugs, and other rewards (a
    role previously thought to be played mostly by
    brain dopamine systems).

23
Evidence for separate pleasure circuits?
  • Enjoyable sweet tastes produce characteristic
    licking responses in rats. Aversive bitter
    tastes produce gaping and head shaking.
  • An opioid drug (Damgo) was micro-injected into
    the VTA of rats
  • Rats ate much more food and had significantly
    greater number of "liking" expressions when they
    tasted the food.
  • "Liking" expressions were defined as positive
    facial lip licking expressions that are similar
    in rats, monkeys, apes and even human infants.

24
PLEASURE/LIKING?
  • In this fashion Several brain areas have been
    found to produce changes in Liking
  • E.g... activation of opioid circuits in the
    nucleus accumbens (e.g., by microinjecting
    morphine there) causes increased pleasure
    liking.
  • Thus the VTA- Accumbens pathway appears important
    in wanting (DA) and Liking (opioids etc)

25
Relation of incentive sensitization to cognitive
dysfunction
  • Other brain changes contribute importantly to
    addiction too, including damage or dysfunction in
    cortical mechanisms that underlie cognitive
    choice and decision making (Robinson Berridge
    2000, 2003).
  • Many studies have indicated changes in executive
    functions, involving how alternative outcomes
    are evaluated and decisions and choices made,
    occur in addicts and animals given drugs (Jentsch
    Taylor 1999 Rogers Robbins 2001 Bechara et
    al. 2002 Schoenbaum Shaham 2008).
  • The impairment of executive control plays an
    important role in making bad choices about drugs,
    especially when combined with the pathological
    incentive motivation for drugs induced by
    incentive sensitization.
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