The Chemistry of Drugs

The Chemistry of Drugs

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The Chemistry of Drugs

Delta 9 Tetrahydrocannabinol is the primary psychoactive
constituent of Cannibis sativa, and is bound to two cannabinoid
receptors: CB1 receptors, located primarily in the brain, and CB2
receptors, located primarily in the periphery (Wiley & Martin
2002). A cannabinoid is defined as a substance that has
pharmacological properties that resemble those of delta 9 THC i.e.
" a drug that binds to CB1 and /or CB2 receptors in vitro and
produces a profile of in vivo effects in the tetrad model" (Wiley
2002). THC inhibits the function of the enzyme adenylate cyclase
which is involved in the transmission of pain messages. While
there are over 60 cannibinoids identified in the plant Cannabis
sativa, Delta 9 tetrahydrocannabinol is the primary mood altering
psychoactive agent in marijuana. Marijuana effects acetylcholine
synthesis and turnover in the limbic region of the brain and in
the cerebellum. (Harwood 2005)

Eldreth, Matochik Cadet, and Bolla (2004) used PET 15 and a
modified version of the Stroop task to determine if 25 day
abstinent heavy marijuana users experienced persistent deficits in
executive cognitive functioning and brain activity. The
performance on a modified version of the Stroop task and brain
activity was compared between 25 day abstinent, heavy users, and a
matched comparison group. The 25 day abstinent users showed no
deficits in performance on the modified version of the Stroop task
when compared to the comparison group. They also found that
despite the lack of performance differences, the anterior
cingulated cortex and the left lateral prefrontal cortex had
hyperactivity in the hippocampus bilaterally, when compared to the
comparison group. The results suggested that users display
persistent metabolic alterations in brain regions responsible for
executive cognitive functioning. (Eldreth, Matochik, Cadet, &
Bolla 2004).

When performing the Stoop task, marijuana users were found to
have greater activation compared to the comparison group in the
left and right hippocampus. Marijuana users also failed to
activate to the same extent as the comparison group in the left
lateral prefrontal cortex and the left perigenual anterior
cingulated cortex.

According to Gardner (2002) drugs that are addictive to
humans are similar to animal model systems in five ways. First,
drugs enhance electrical brain stimulation reward in the core
meso-accumbens reward circuitry of the brain, a circuit
encompassing that portion of the medial forebrain bundle which
links the ventral tegmental area of the mesencephalic midbrain

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with the nucleus accumbens of the ventreal limbic forebrain. The
next similarity is that they enhance neural firing of a core
dopamine component of this meso accumbens reward circuit. They
also enhance dopamine tone in this reward relevant meso accumbens
dopamine circuit with resultant enhancement of extracellular Ach
DA. They produce conditioned place preference, a behavioral model
of incentive motivation. And finally they are self administered
and they trigger reinstatement of drug seeking behavior and
pharmacologically detoxified from their self administered drug.
(Gardner 2002).

Addictive drugs enhance brain reward processes by acting at
different anatomic sites within the brain's reward circuitry,
different addictive drugs enhance brain reward processes by acting
through different mechanisms within the brain's reward circuitry.
(Gardner 2002). THC's site of action is in the vicinity of the
reward relevant ACH Dopamine axon terminals. (Gardner 2002)

Cannabinoids enhance AcH Dopamine by acting at various brain
loci: 1. within the AcH acting on mechanisms closely linked to
axon terminal Dopamine releas; 2. within the VTA acting on
endogenous opiod mechanisms not linked to activation of neuronal
firing but rather linked to mechanisms of Dopamine synthesis,
transport and release and 3. within the VTA acting on
nonendogenous opiod mechanisms linked to activation of neuronal
firing. (Gardner 2002).

In a study by Oleary et al 2002, researchers found that
smoking marijuana significantly increased heart rate and blood
pressure and resulted in extensive changes in regional cerebral
blood flow in comparison to presmoking conditions and to the
conditions following smoking placebo. The regional cerebral blood
flow changes observed reflected the direct changes caused by
smoking marijuana upon brain metabolism and blood flow as well as
less direct effects resulting from its intoxicating and mood
enhancing effects.(Oleary et al. 2002).

The molecular structure is unlike that of any known
transmitter but it does not seem related to steroids(similar to
testosterone and estradiol that seem to be involved in depression.
(Palfai & Jankiewicz 1991). Cannabinoids are increased by the
synthesis of catecholamines in the brain through a direct action
on neurons. There is also a decrease in Ach synthesis. The
greatest density of cannabinoids are found in the basal ganglia,
hippocampus, and cerebellum (Palfai & Jankiewicz 1991).


Eldreth,D. Matochik,J. Cadet,J. & Bolla,K.(2004) Abnormal brain
activity in prefrontal brain regions in abstinent users.
NeuroImage, 23, 914-920.

Gardner, E. (2002). Addictive potential of cannabinoids: the
underlying neurobiology. Intramural Research Program, National
Institute of Health and Human services. Baltimore Maryland.

Harwood,T.(2005). Lecture Notes handout. Personal Communication.
Oleary et al. (2002). Effects of smoking on brain perfusion and
cognition. Neuropsychopharmacology, 26, 802-816.

Palfai, T. & Jankiewicz (1991) Drugs and human behavior. Iowa: WM
C Brown.

Wiley,J. Martin, B. (2002). Cannabinoid pharmacology: implications
for additional cannabinoid receptor subtypes.
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