Neuropharmacology of Alcohol Abuse

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Neuropharmacology of Alcohol Abuse
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A. Peaks in absorption 1. Highest Blood Levels
30-90 minutes after ingestion 2. Carbonated
alcoholic beverages increase absorption 3.
Drinking on an empty stomach increase
absorption 4. High alcohol concentration in
beverage
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DISULFIRAM
Metabolism of Alcohol
x
ADH
ALDH
Ethanol Acetaldehyde Acetic Acid CO2

• 1. Men
• a. 20 metabolized in the stomach by alcohol
  dehydrogenase
• b. 80 mainly metabolized by the liver
• More blood vessels due to increased muscle mass
  increasing
• diluting effect
• 2. Women
• a. 0 metabolized in the stomach mainly all
  metabolized by the
• liver
• b. Less blood vessels due to increase percentage
  of adipose
• tissue
• .

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Blood Alcohol Content (BAC)

• Amount of alcohol present in 100 mLs (or dL) of
  blood
• Percent from Latin per centum means by the
  hundred
• Thus, 80 mg of alcohol in 100 mLs may be
  expressed as 80 mg
• 80 mg is equal to 0.08g in 100 mLs which is 0.08
• Therefore a person with 0.19 BAC has 190 mg of
  ethanol in 100 mLs

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Effects of Ethanol on DA release
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Effects of Naltrexone
1. Self-administration studies
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Effects of Naltrexone
2. Microdialysis Studies
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B. 5-HT3 and nicotinic receptors
Ondansetron
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C. Neuronal Mechanisms withdraw and tolerance
Acomprosate
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Neuronal toxicities and Ethanol Use
1. Destruction of serotonergic terminals
-human studies - ALCOHOLIC DEMENTIA
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Neuronal toxicities and Ethanol Use

• Wernicke-Korsakoff Syndrome
• -vitamin B1 (thiamine) deficiency
• -Signs and Symptoms
• confusion
• disorientation
• abnormal eye movement
• difficulties in movement body coordination

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Neuronal toxicities and Ethanol Use

• Fetal Alcohol Syndrome (FAS)
• -teratogenic effects of ethanol that results in
• i. Growth retardation
• ii. Mental retardation
• iii. Skull and facial abnormalities