Science of Addictive Disorders |
| The Reward-Reinforcement Circuitry of the Meso-Limbic and Medial Frontal Cortices of the Brain. |
Recent rigorous research under Dr. Nora Volkow and Dr. Elliot Gardner at the National Institute on Drug
Abuse has validated the anatomical (Limbic) reward-reinforcement (RR) circuitry for addictive chemicals
that is also activated in many compulsive behavioral disorders. The circuit has two parts-a "more
switch" and a corresponding "stop switch"-that is comprised of 4 major brain cortices and consists of 3
phases.
Phase I: Cravings for drugs experienced by a chemically dependent individual is often the first phase of
the RR circuitry. There are two major types of drug craving-Endogenous and Environmental Cued or
Triggered Craving. Endogenous Craving results from neurotransmitter imbalances induced by drug
use. Environmental Cued Craving results from anticipation of drug use induced by cues or triggers
(often: odors, auditory stimulus or visual sensory experiences) that activate recall of various past
memories of drug experiences. When a cue is experienced, the Amygdalal is activated to recall
emotional memories and the Ventral Tegmental Area releases dopamine that then activates the shell of
the NAc Septi resulting in a subtle yet powerful drive to do more which during Phase I is actually a
craving to do a drug(s) or a compulsive behavior.
Phase II: Addictive psychoactive substances activate dopamine activity at dopamine-2 receptors in the
Nucleus Accumbens (NAc) Septi. Dopamine is released by the Ventral Tegmental Area of the Limbic
RR circuit that can also result in endorphin or GABA activity at the Lateral Hypothalamus. When the NAc
Septi is activated, individuals experience a very primitive and compulsive need to activate it even more.
This "more switch" is more active and powerful in those with a compulsivity disorder like chemical
dependency.
Phase III: As brain dopamine levels increase, Orbito Frontal Cortex (OFC) in the medial prefrontal areas
of the brain is activated in non-addicts. This results in an endorphin mediated feedback mechanism
that curb the drive for more in the NAc and also suppresses emotional responses in the Amygdalal of
the Limbic System as well. An addict's OFC does not respond and thus, has no reins of its drive for
more drug exposure. This has been called a physiologic "Deficit of Self-Control".
RECOMMENDED REFERENCE: Inaba & Cohen, Uppers, Downers, All Arounders,
5th Ed., Chapter2
Source: Neuroscientific Models of Addiction and Impulsive Control Behavioral
Disorders....Darryl Inaba
Abuse has validated the anatomical (Limbic) reward-reinforcement (RR) circuitry for addictive chemicals
that is also activated in many compulsive behavioral disorders. The circuit has two parts-a "more
switch" and a corresponding "stop switch"-that is comprised of 4 major brain cortices and consists of 3
phases.
Phase I: Cravings for drugs experienced by a chemically dependent individual is often the first phase of
the RR circuitry. There are two major types of drug craving-Endogenous and Environmental Cued or
Triggered Craving. Endogenous Craving results from neurotransmitter imbalances induced by drug
use. Environmental Cued Craving results from anticipation of drug use induced by cues or triggers
(often: odors, auditory stimulus or visual sensory experiences) that activate recall of various past
memories of drug experiences. When a cue is experienced, the Amygdalal is activated to recall
emotional memories and the Ventral Tegmental Area releases dopamine that then activates the shell of
the NAc Septi resulting in a subtle yet powerful drive to do more which during Phase I is actually a
craving to do a drug(s) or a compulsive behavior.
Phase II: Addictive psychoactive substances activate dopamine activity at dopamine-2 receptors in the
Nucleus Accumbens (NAc) Septi. Dopamine is released by the Ventral Tegmental Area of the Limbic
RR circuit that can also result in endorphin or GABA activity at the Lateral Hypothalamus. When the NAc
Septi is activated, individuals experience a very primitive and compulsive need to activate it even more.
This "more switch" is more active and powerful in those with a compulsivity disorder like chemical
dependency.
Phase III: As brain dopamine levels increase, Orbito Frontal Cortex (OFC) in the medial prefrontal areas
of the brain is activated in non-addicts. This results in an endorphin mediated feedback mechanism
that curb the drive for more in the NAc and also suppresses emotional responses in the Amygdalal of
the Limbic System as well. An addict's OFC does not respond and thus, has no reins of its drive for
more drug exposure. This has been called a physiologic "Deficit of Self-Control".
RECOMMENDED REFERENCE: Inaba & Cohen, Uppers, Downers, All Arounders,
5th Ed., Chapter2
Source: Neuroscientific Models of Addiction and Impulsive Control Behavioral
Disorders....Darryl Inaba
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