Philip J Pellegrino PsyD 1 Training Objectives Identify the specific physiological effects of drug use on the brain and neurotransmission Develop an understanding of the Disease Model ID: 728119
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This is Your Brain on Drugs
Philip J. Pellegrino, Psy.D.
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Training Objectives
Identify the specific physiological effects of drug use on the brain and neurotransmissionDevelop an understanding of the “Disease Model”
Describe how the “Disease Model” applies to clinical practice
Describe how the “Disease Model” may not apply to clinical practice
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What is the Disease Model?
The idea that addiction is a biological/medical phenomena where the individual is unable to control their use of the substance
Certain individuals are predisposed for addiction and this is brought out by use of the substance
Individual is not held responsible for the development of the disease but is responsible for its treatment!
Miller and Kurtz (1994)
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Neurons
Receptor sites – Areas on the neuron where neurotransmitters attach and send messages to the neuronAxon – Messages travel from receptor sites down the axon to the dendrites
Axon Terminal – Where neurons make connections with the dendrites of other neurons
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Neurons (continued)
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Neurons (continued)
Synapse – Includes a space where neurotransmitters are released and
attach to terminals on the adjacent
neurons dendrites
Dendrites – Short fibers that contain receptor sites, which receive neurotransmissions
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Neurons (continued)
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Neurotransmitters
Dopamine – motor regulation, mood, concentration, reward, hormone controlSerotonin – Emotional processing, sleep, appetite, mood, pain processing
GABA – Inhibitory NT in the CNS
Endorphins – pain killers
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Neurotransmitters (continued)
Norepinephrine – Sensory processing, sleep, mood, learning, memory, anxiety
Acetylcholine – Memory, motor coordination, ANS functioning, neurotransmission
Endogenous
Cannabanoids
(
Anandamide
) – inhibits GABA, activates glutamate, inhibits hippocampal (memory) neurons
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Effects of Drugs
(Legal and Illegal)Reuptake Inhibitors – Blocks the reuptake of neurotransmitters back into the axon terminals
Agonists
Substances that mimic the effect of the neurotransmitter
Antagonists
Drugs that block or inhibit neurotransmitter release or reception
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Cocaine
Acts as a stimulantBlocks re-uptake of dopamine
Increased energy
Feelings of euphoria
Psychosis (dopamine hypothesis of schizophreniaDepression type withdrawal
Also thought to work on serotonin
Alterations in brain serotonin transporters
(White, 1998)
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Opiates
Endorphins/Enkephalins
The bodies natural pain killers (analgesic)
Euphoria
SedationOpiates vary on their agonist/antagonist properties
Endocannabinoids
Dopamine
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Nicotine
AcetylcholineIncreased blood pressure and heart rateFacilitates the release of other NT’s, particularly increased dopamine levels
Memory
potentiation
DopamineIs increased in the limbic system as the result of acetylcholine activation
Julien
(2005)
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THC
Andandamide agonist—THC mimics the effects of this endogenous cannabinoid
Memory impairment
Endorphins
Analgesic effectsDopamine
Pleasure, reward
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Alcohol
GABAActivates GABACauses muscle sedationInhibitions of motor skills
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Alcohol (continued)
Opioids, dopamine, and serotonin all considered to be involved with alcohol Dopamine and serotonin account for the rewarding effects
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Nervous System
CentralConsists of the brain and spinal cord and will be our main focusPeripheral
Autonomic and somatic
These are affected by substance use through specific effects on brain function
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Central Nervous System
BrainOld BrainCerebellum
and the limbic system
Cerebellum
is involved with simple functions/motor movementsLimbic system is involved with fear and anger, fight or flightMade up of
amygdala
,
substantia nigra
, the hippocampus, and the hypothalamus
New Brain
Frontal lobes
Reasoning, decision making, and high cognitive functioning
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Reward Pathway
Specific areas in the old brain (the brain’s Go) system are activated by substance useThese areas are typically associated with meeting most of our pleasurable needs (i.e., food, sex, etc.)
These areas react quicker and are more need driven than the NEW brain areas
They are typically located within the limbic system and bypass the reasoning frontal lobes
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Brain Diagram
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Reward Pathway
The Reward Pathway is also called the mesolimbic reward system This system contains the ventral tegmental area, the basal forebrain, and the extended
amygdala
Dopamine is the main neurotransmitter involved in communicating between these parts of the brain
Koob
(2006), Cami & Farre (2003), Lingford, Hughes, & Nutt (2003)
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Reward Pathway (continued)
Drug use is continued due to the positive reinforcing effects of the substance use on these areas of the brainAnimal models
Animals self-administer substances such as cocaine, opiates, and alcohol
Rats starving themselves for drug rewards
Brain stimulation of the reward pathway
Rocha et al. (1998)
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Use to Abuse to Addiction
Koob (2006) modelExplains how use progresses from recreation to dependence/addiction
This model explains that use begins as positively reinforcing in the brain and then becomes negatively reinforcing after repeated use
There is an escalation in use until the substance is used to get rid of aversive feelings such as dysphoria, withdrawal, etc.
Koob
(2001)
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Abuse to Addiction
Koob explains that we can use behavioral models to describe how use goes from abuse to addictionPositive reinforcement circuit
Involves the reinforcing effects of the amygdala and the limbic reward pathway
Behavioral psychology—Thorndike’s “Law of Effect”…That which tends to be rewarded will be repeated!
Koob
(2003)
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Abuse to Addiction
Negative ReinforcementOver time the drug produces negative affect and negative physiological effectsUse serves the purpose of getting rid of these negative experiences
Involves the hypothalamus,
amygdala
(fear, anxiety, anger) and the brain stem (sleep, restlessness)
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Abuse to Addiction (continued)
Obsessive Compulsive/Impulse ControlThe addictive nature of use then involves behaviors similar to Obsessive-Compulsive Disorder (OCD)
The behaviors becomes compulsive in response to thoughts, feelings and situations
Involves the striatum and the dorsal pre-frontal cortex
What we think of when the individual “loses” control over their substance use
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Stages of Abuse to Addiction
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Brain’s Stop and Go System
Conceptualization by Childress (2006)The old brain is considered the “GO” system
The new brain is considered the “STOP” system
Changes in the brain during adolescence may provide a vulnerability
Increase in the GO (hormones, sex drive, etc.)
The STOP system is not fully developed
What does this mean for Job Corps students?
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Competing Systems
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Competing Systems (continued)
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STOP and GO System
Suggests the idea of specific brain differences between “normals” and individuals predisposed to addiction issues (main premise of the disease model)
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GO
Dopamine is considered to be the main neurotransmitter involved in the GO/reward systemMost substances increase dopamine in reward system
Low levels of dopamine (D2) receptors found in brain imaging of drug addicts
Is this the result of drug use or does it pre-date drug use?
Some research suggests that it predates
Volkow
(2004b), Childress (2004)
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Go and Craving
Go system is cravingSensory cues provide activation of this system
Again the limbic system, in particular the nucleus
accumbens
This creates a sensation and state for a need to act on getting the drug
The brain is on GO!
Childress (1999), Cami & Fare (2003)
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STOP System
Difficulties in the frontal regions found in addicted individuals. Can explain the difficulties of controlling the GO systemLower metabolism
Decreased blood flow
Less dense gray matter
Franklin et al. (2002), Volkow (2004a)
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STOP System
AD/HD and conduct disorder have been linked to frontal lobe deficitsThese disorders also have a correlation with substance use disorders
Does this predate or is it the effects of the substance use?
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Withdrawal and Dopamine
Reductions in brain dopamine are noticed in the mesolimbic system six months post abstinenceReduced receptors
Thought to lead to drug craving
Volkow
(2004)
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Disease Model
How does all of this information fit into the Disease Model
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Disease Model
Development of compulsive uncontrollable use over timeThe impact of use on the brain/biological structures changes the function of the brain
Physiological/biological changes makes it more difficult for the individual to STOP engaging in drug taking behaviors
Brain differences between addicts and non-addicts
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Disease Model
What may be some of the issues with the Disease Model?
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Disease Model
Does all drug use lead to compulsive uncontrollable use?What came first, the c
hicken or the egg?
What makes for the differences between those who become addicts and those who do not?
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Job Corps
How does this information apply to our students?How does this information not apply to our students?
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How does this apply to our students?
Provides education on how substance use can lead to changes in brain functionProvides specific education on specific effects of substances
Allows us to determine at-risk students
Risk factors?
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How does this not apply to our students?
Not all drug use leads to a disease stateAre there drug and alcohol problems that are not a disease?
No one size fits all
Tx
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References
Cami, J., & Farre (2003). Drug Addiction. New England Journal of Medicine, 349, 975-986.
Childress, A.R. (2006). What can human brain imaging tell us about vulnerability to addiction and relapse? In W.R
. Miller & K.M. Carroll (Eds.)
Rethinking Substance Abuse: What the Science Shows and What we Should Do About it (.46-60)
New YorK: Guilford Press
.
Childress, A.R., Mozley, P.D., McElgin, W., Fitzgerald, J., Reivich, M., & O’Brien, C.P. (1999). Limbic activation during cue-induced cocaine craving.
American Journal of Psychiatry, 156
, 11-18.,
Franklin, T.R., Acton, P.D.,
Maldjian
, J.A., Gray, J.D., Croft, J.E.,
Dackis
, C.A., et al. (2002). Decreased gray matter concentration in the insular, orbitofrontal, cingulate, and temporal cortices of cocaine patients.
Biological Psychiatry, 51
134-142.
Julien
, R.M. (2005).
A Primer of Drug Action, Tenth E
dition
. A comprehensive guide to the actions, uses, and side effects of psychoactive drugs.
New York: Worth Publishers.
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References
Koob, G.F. (2003). Neuroadaptive mechanisms of addiction: Studies on the extended Amygdala. European
Neuropsychopharmacology
, 13, 442-452.
Koob, G.F. (2006). The neurobiology of addiction: A hedonic calvinist view. In W.R. Miller & K.M. Carroll (Eds.)
Rethinking Substance Abuse: What the Science Shows and What we Should Do About it
(.25-45) New YorK: Guilford Press.
Koob, G.F., and M.
LeMoal
(2001). Drug addiction,
dysregulation
of reward, and
allostasis
.
Neuropsychopharmacology
, 24
, 97-129
.
Leshner
, A.I. (1997). Drug abuse and addiction treatment research: The next generation.
Archives of General Psychiatry, 54
, 691-694
.
Lingford
-Hughes, A., & Nutt, D. (2003). Neurobiology of Addiction and Implications for treatment.
British Journal of Psychiatry, 182
, 97-100.
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References
Miller, W.R., & Kurtz, E. (1994). Models of alcoholism used in treatment: Contrasting AA and other perspectives with which it is often confused. Journal of Studies on Alcohol, 55
, 159-166.
Rocha, B.A., et al. (1998). Cocaine Self-administration in dopamine-transporter
Knockout-mice. Nature Neuroscience, 1, 132-137
.
Volkow, N.D., Fowler, J.S., & Wang G.J. (2004). The addicted human brain viewed in the light of imaging studies: Brain circuits and treatment strategies.
Neuropharmacology, 47,
3-13.
Volkow, N.D., Fowler, J.S., Wang, G.J., Swanson, J.M. (2004). Dopamine in drug abuse and addiction: Results from imaging studies and treatment implications.
Molecular Psychiatry, 9
, 557-569.
White
, F.J. (1998). Cocaine and the Serotonin Saga.
Nature, 393
. 118-119.
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