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Drug craving
Definition of craving
 Although drug craving has been defined in numerous
  ways, it has generally been regarded as a desire to
  use a drug.
 It is a combination of thoughts and feelings. There is a
  powerful physiological components to craving that
  makes it a very powerful event and very difficult to
  resist.
 Craving is sometimes defined as a "subjectively
  experienced" desire or urge to approach and consume
  a particular substance
Drug craving
Brain Networks Associated
             With Craving
Drugs of abuse activates the brain’s “reward circuit.”

Neurons located in the nucleus accumbens extend to both
 the amygdala and the frontal cortex areas. The
 amygdala, which is highly connected to brain regions that
 control emotions (i.e., the limbic system), plays a role in
 the modulation of stress and mood. The frontal cortex
 areas integrate incoming sensory information, such as
 sights, smells, and sounds.
Drug craving
• Integration of sensory
             Prefrontal     information
               cortex     • reward memory is
                            thought to be located




 Neucleus                      • plays a role in the
accumbence        amygdala       modulation of stress
                                 and emotions




                          • which plays a role in
              basal
                            repetitive thought and
             ganglia
                            behavior patterns
 Neurons located in the amygdala also send information to
 the DLPC and the basal ganglia. The DLPC sends
 information back to the basal ganglia (a connection that
 may play a role in obsessive-compulsive behaviors) and to
 the nucleus accumbens.

 Feedback from the DLPC to the nucleus accumbens may
 sensitize the latter to further drug exposure.
 Neuroscientists discovered drugs also alter connections in
  brain circuits that govern learning and memory, causing the
  formation of strong associations between the drug’s
  pleasurable sensation and the circumstances under which
  it was taken.
 Drugs also disrupt brain circuits involved in impulse control
  in the prefrontal cortex, making it more difficult for addicts
  to resist taking drugs. Conversely, research suggests
  existing deficiencies in prefrontal function increase the risk
  of drug addiction.
 This finding may help explain why adolescents are more
  susceptible to addiction — the prefrontal cortex does not
  become fully developed until people reach their mid-20s.
Drug craving
Craving Cycle
Stage I: Set-up behaviors:
Including: Physical factors, Psychological factors & Social factors.

Stage II: Trigger Events for Craving:
 Thought Triggers.
 Feeling Triggers.
 Behavioral Triggers.
 Situational Triggers.


Stage III: The Craving Cycle:
Gorski (2001) proposed the craving cycle as a series of self reinforcing
  thoughts and behaviors that continue to activate and intensify the craving
  response.
This cycle is marked by obsession, compulsion, physical craving, and drug-
  seeking behavior.
Anti- Craving medications
Neurotransmitters …………
Neurotransmitter         Site

Dopamine           Ventral tegmental area, nucleus accumbens

Opioid Peptides    Nucleus accumbens, amygdala, ventral
                   tegmental area

GABA               Amygdala, bed nucleus of stria terminalis

Glutamate          Nucleus accumbens
Opioid system:
 The mu subtype appears to be a key in opiate addiction: for
  mice lacking this receptor, morphine is no longer rewarding or
  reinforcing.
 Neuroimaging studies suggest that alterations in mu receptor
  level may be fundamental to addiction. Increased receptor
  levels in the anterior cingulate was found in recently abstinent
  humans addicted to cocaine or opiates; which may reflect
  elevated mu opiate receptor levels or decreased endogenous
  opioid levels leading to craving.
 Roles for kappa and delta opiate receptors in addiction are
  also evident. Unlike mu receptors, kappa receptor stimulation
  reduces dopamine function in the NAcc. This may possibly
  result in dysphoria. In animal models, delta antagonists can
  reduce self-administration of alcohol, suggesting that this
  receptor also plays a key role in reinforcement.
GABA Systems
Gamma-aminobutyric acid (GABA) is the primary inhibitory
neurotransmitter in the brain.

Sedative-hypnotic drugs including alcohol, benzodiazepines
(e.g., Valium®), and barbiturates have long been hypothesized
to modulate receptors in GABA systems.
Supporting this concept, experimental drugs that decrease the
function of GABA receptors reduce alcohol consumption by rats.
Microinjections of GABA antagonists into various rat brain.

Regions suggest that an important brain area for alcohol- GABA
interactions is the central nucleus of the amygdala, a structure
that communicates with the basal forebrain structures and is
associated with emotion and stress.
NALTREXONE (ReVia®; Vivitrol®)
  opioid antagonist medication that binds to opioid receptors
   but does not activate them.
  useful for highly motivated recently detoxified patients who
   want total abstinence .

  How it works: Naltrexone blocks the part of your brain that
   feels pleasure when taking narcotics. Because it blocks the
   opioid receptors it prevents the body from responding to
   opiates
  It can be taken by mouth once daily or every other day, has
   minimal side effects and is not addicting.
  A favorable treatment outcome requires some form of
   psychotherapy, careful monitoring of medication compliance
   and effective behavioral interventions.
  Side effects: Nausea, vomiting, diarrhea, constipation,
   headache, dizziness.
METHADONE (Dolophine®; Methadone
Diskets®)
 Methadone blocks the receptors in the brain that are affected by
  opiates such as heroin, enabling users to gradually detoxify
  from opiates without experiencing painful withdrawal symptoms.
 Methadone occupies the receptors in the brain that opiates use,
  blocking the high feeling that opiates provide and making the
  user feel more stable.
 This reduces the drug cravings and withdrawal symptoms that
  often lead to relapse. Because Methadone’s effects last
  between 24 and 36 hours, most patients can be maintained on
  one daily dose.
 Side effects: Drowsiness, weakness, nausea, constipation,
  headache, loss of appetite.
BUPRENORPHINE (Buprenex®; Subutex®,
Suboxone)
  Buprenorphine hydrochloride is a semi-synthetic partial µ-
     opioid receptor agonist
    Approved for treatment of pain and as a maintenance
     treatment for opioid dependence .
    Several studies have shown that a dose of 8 mg of
     Buprenorphine daily, administered sublingually is roughly
     equivalent of a 60 mg daily dose of methadone.
    SUBOXONE :Buprenorphine and Naloxone
    Because Naloxone has poor oral and sublingual bio-
     availability, it does not interfere with the effects of sublingually
     administered Buprenorphine. This combined preparation
     appears to be as effective as Buprenorphine alone and is less
     likely to be abused by patients
Baclofen
 a GABA B receptor agonist that inhibits the release of several
  neurotransmitters, including dopamine, noradrenaline, 5HT, and
  glutamate .
 Baclofen, through inhibition of somatodendritic dopamine
  release, prevents development of cocaine-induced behavioral
  sensitization and abolishes the motor-stimulant actions of
  cocaine.
 Baclofen was recently shown to attenuate the reinforcing effects
  of cocaine in rats.
 Other studies suggest that baclofen may be a fast acting
  treatment for the affective state that occurs during cocaine
  abstinence and, hence, may promote greater engagement in
  psychosocial treatment.
Antalarmin
 Corticotropin releasing hormone antagonist
 inhibit CRF-stimulation of cAMP or CRF-stimulated ACTH
  release from cultured rat anterior pituitary cells.
 sauvagine binding to CRF1 receptors in brain sections
  demonstrating their ability to cross the blood-brain-barrier.
  In in vivo studies, peripheral administration of these
  compounds attenuate stress-induced elevations in plasma
  ACTH levels in rats demonstrating that CRF1 receptors
  can be blocked in the periphery
 In several experiments on rats; Antalarmin prevent dose
    escalation with prolonged use, suggesting that it might
    stabilise cocaine use and prevent it increasing over time,
    although without consistently reducing it.
 Antalarmin also showed positive effects in reducing
    withdrawal syndrome from chronic opioid use, and
    significantly reduced self-administration of ethanol in
    ethanol-addicted rodents.

Drug craving

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Drug craving

  • 2. Definition of craving  Although drug craving has been defined in numerous ways, it has generally been regarded as a desire to use a drug.  It is a combination of thoughts and feelings. There is a powerful physiological components to craving that makes it a very powerful event and very difficult to resist.  Craving is sometimes defined as a "subjectively experienced" desire or urge to approach and consume a particular substance
  • 4. Brain Networks Associated With Craving Drugs of abuse activates the brain’s “reward circuit.” Neurons located in the nucleus accumbens extend to both the amygdala and the frontal cortex areas. The amygdala, which is highly connected to brain regions that control emotions (i.e., the limbic system), plays a role in the modulation of stress and mood. The frontal cortex areas integrate incoming sensory information, such as sights, smells, and sounds.
  • 6. • Integration of sensory Prefrontal information cortex • reward memory is thought to be located Neucleus • plays a role in the accumbence amygdala modulation of stress and emotions • which plays a role in basal repetitive thought and ganglia behavior patterns
  • 7.  Neurons located in the amygdala also send information to the DLPC and the basal ganglia. The DLPC sends information back to the basal ganglia (a connection that may play a role in obsessive-compulsive behaviors) and to the nucleus accumbens.  Feedback from the DLPC to the nucleus accumbens may sensitize the latter to further drug exposure.
  • 8.  Neuroscientists discovered drugs also alter connections in brain circuits that govern learning and memory, causing the formation of strong associations between the drug’s pleasurable sensation and the circumstances under which it was taken.  Drugs also disrupt brain circuits involved in impulse control in the prefrontal cortex, making it more difficult for addicts to resist taking drugs. Conversely, research suggests existing deficiencies in prefrontal function increase the risk of drug addiction.  This finding may help explain why adolescents are more susceptible to addiction — the prefrontal cortex does not become fully developed until people reach their mid-20s.
  • 11. Stage I: Set-up behaviors: Including: Physical factors, Psychological factors & Social factors. Stage II: Trigger Events for Craving:  Thought Triggers.  Feeling Triggers.  Behavioral Triggers.  Situational Triggers. Stage III: The Craving Cycle: Gorski (2001) proposed the craving cycle as a series of self reinforcing thoughts and behaviors that continue to activate and intensify the craving response. This cycle is marked by obsession, compulsion, physical craving, and drug- seeking behavior.
  • 13. Neurotransmitters ………… Neurotransmitter Site Dopamine Ventral tegmental area, nucleus accumbens Opioid Peptides Nucleus accumbens, amygdala, ventral tegmental area GABA Amygdala, bed nucleus of stria terminalis Glutamate Nucleus accumbens
  • 14. Opioid system:  The mu subtype appears to be a key in opiate addiction: for mice lacking this receptor, morphine is no longer rewarding or reinforcing.  Neuroimaging studies suggest that alterations in mu receptor level may be fundamental to addiction. Increased receptor levels in the anterior cingulate was found in recently abstinent humans addicted to cocaine or opiates; which may reflect elevated mu opiate receptor levels or decreased endogenous opioid levels leading to craving.  Roles for kappa and delta opiate receptors in addiction are also evident. Unlike mu receptors, kappa receptor stimulation reduces dopamine function in the NAcc. This may possibly result in dysphoria. In animal models, delta antagonists can reduce self-administration of alcohol, suggesting that this receptor also plays a key role in reinforcement.
  • 15. GABA Systems Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain. Sedative-hypnotic drugs including alcohol, benzodiazepines (e.g., Valium®), and barbiturates have long been hypothesized to modulate receptors in GABA systems. Supporting this concept, experimental drugs that decrease the function of GABA receptors reduce alcohol consumption by rats. Microinjections of GABA antagonists into various rat brain. Regions suggest that an important brain area for alcohol- GABA interactions is the central nucleus of the amygdala, a structure that communicates with the basal forebrain structures and is associated with emotion and stress.
  • 16. NALTREXONE (ReVia®; Vivitrol®)  opioid antagonist medication that binds to opioid receptors but does not activate them.  useful for highly motivated recently detoxified patients who want total abstinence .  How it works: Naltrexone blocks the part of your brain that feels pleasure when taking narcotics. Because it blocks the opioid receptors it prevents the body from responding to opiates  It can be taken by mouth once daily or every other day, has minimal side effects and is not addicting.  A favorable treatment outcome requires some form of psychotherapy, careful monitoring of medication compliance and effective behavioral interventions.  Side effects: Nausea, vomiting, diarrhea, constipation, headache, dizziness.
  • 17. METHADONE (Dolophine®; Methadone Diskets®)  Methadone blocks the receptors in the brain that are affected by opiates such as heroin, enabling users to gradually detoxify from opiates without experiencing painful withdrawal symptoms.  Methadone occupies the receptors in the brain that opiates use, blocking the high feeling that opiates provide and making the user feel more stable.  This reduces the drug cravings and withdrawal symptoms that often lead to relapse. Because Methadone’s effects last between 24 and 36 hours, most patients can be maintained on one daily dose.  Side effects: Drowsiness, weakness, nausea, constipation, headache, loss of appetite.
  • 18. BUPRENORPHINE (Buprenex®; Subutex®, Suboxone)  Buprenorphine hydrochloride is a semi-synthetic partial µ- opioid receptor agonist  Approved for treatment of pain and as a maintenance treatment for opioid dependence .  Several studies have shown that a dose of 8 mg of Buprenorphine daily, administered sublingually is roughly equivalent of a 60 mg daily dose of methadone.  SUBOXONE :Buprenorphine and Naloxone  Because Naloxone has poor oral and sublingual bio- availability, it does not interfere with the effects of sublingually administered Buprenorphine. This combined preparation appears to be as effective as Buprenorphine alone and is less likely to be abused by patients
  • 19. Baclofen  a GABA B receptor agonist that inhibits the release of several neurotransmitters, including dopamine, noradrenaline, 5HT, and glutamate .  Baclofen, through inhibition of somatodendritic dopamine release, prevents development of cocaine-induced behavioral sensitization and abolishes the motor-stimulant actions of cocaine.  Baclofen was recently shown to attenuate the reinforcing effects of cocaine in rats.  Other studies suggest that baclofen may be a fast acting treatment for the affective state that occurs during cocaine abstinence and, hence, may promote greater engagement in psychosocial treatment.
  • 20. Antalarmin  Corticotropin releasing hormone antagonist  inhibit CRF-stimulation of cAMP or CRF-stimulated ACTH release from cultured rat anterior pituitary cells.  sauvagine binding to CRF1 receptors in brain sections demonstrating their ability to cross the blood-brain-barrier. In in vivo studies, peripheral administration of these compounds attenuate stress-induced elevations in plasma ACTH levels in rats demonstrating that CRF1 receptors can be blocked in the periphery
  • 21.  In several experiments on rats; Antalarmin prevent dose escalation with prolonged use, suggesting that it might stabilise cocaine use and prevent it increasing over time, although without consistently reducing it.  Antalarmin also showed positive effects in reducing withdrawal syndrome from chronic opioid use, and significantly reduced self-administration of ethanol in ethanol-addicted rodents. 