BIOLOGICAL BASIS OF BEHAVIOR
Psychology 321
Spring, 2005 HGH 225
Dr. John M. Morgan MWF, 8am to 9:00
Wendy Horn
Diana Pineda
Nicollette Schlick
Butterfield
Biological Bases of Behavior-Marijuana Report
Marijuana is the dried leaves and flowers of the hemp plant
Cannabis sativa. Like all plants, it's sensitive to the environment
where it grows. Some of the names for it are Mary Jane, pot, weed,
grass, herb, ganja or skunk. The brain has many responses to marijuana.
Marijuana can cause people to lose focus on events around them. For
some it makes them more aware of their physical sensations. For others,
there are numerous other effects. All forms of marijuana are mind-
altering
All of the changes are caused by chemicals that affect the brain.
More than 400 chemicals are in the average marijuana plant. When
smoked, heat produces even more chemicals. Different weather and soil
conditions can change the amounts of the chemicals inside the plant.
Marijuana grown in one place might be chemically stronger than grown in
another. Marijuana's effects on the user depend on it's strength or
potency, which is related to the amount of THC it contains.
Marijuana causes some parts of the brain, such as those governing
emotions, memory, and judgment, to lose balance and control. Marijuana
can speed the heart rate up to 160 beats per minute. Dilated blood
vessels make the whites of the eyes turn red. Panic feelings may be
accompanied by sweating, dry mouth, or trouble breathing. Much like
tobacco smokers, marijuana smokers may experience a daily cough and
more frequent chest colds. Animal studies have found that THC can
damage the cells and tissues in the body that help protect against
disease. When the immune cells are weakened you are more likely to get
sick.
When someone uses marijuana, these chemicals travel through the
bloodstream and quickly attach to special places on the brain's nerve
cells. These places are called receptors, because they receive
information from other nerve cells and from other chemicals. When a
receptor receives information, it causes changes in the nerve cell.
The chemical in marijuana that has a big impact on the brain is
called THC (tetrahydrocannabinol). It is the main active chemical in
marijuana. Scientists recently discovered that some areas in the brain
have a lot of THC receptors, while other have very few or none. These
clues are helping researchers figure out exactly how THC works in the
brain.
One region of the brain that contains a lot of THC receptors is
the hippocampus, which processes memory. When THC attaches to receptors
in the hippocampus, it weakens short-term memory.
The hippocampus also communicates with other brain regions that
process new information into long-term memory. In the brain, under the
influence of marijuana, new information may never register, and may be
lost from memory.
In some people, marijuana can cause uncontrollable laughter one
minute and paranoia the next. That's because THC also influences
emotions, probably by acting on a region of the brain called the limbic
system. THC can make something as simple as driving a car really
dangerous.
Some of THC's effects are useful in the world of medicine, like
preventing nausea and blocking pain. The trick is for scientists to get
these results without the harmful effects.
Researchers recently found out the brain makes a chemical,
anandamide, that attaches to the same receptors as THC. This discovery
may lead to the development of medications that are chemically similar
to THC but less harmful, and they may be used for treating nausea and
pain.
As implied by the word hallucinogen, marijuana may cause people
to hallucinate and have imagined experiences that seem real. The word
hallucinate comes from Latin words meaning "to wander in the mind."
That is why some people refer to hallucinating as tripping. The trips
caused by marijuana can last for hours. Parts of these trips can feel
really good, and other parts can feel terrible. Hallucinogens
powerfully affect the brain, distorting the way our five sense work and
changing our impressions of time and space. People who use these drugs
a lot may have a hard time concentrating, communicating, or telling the
difference between reality and illusion.
Your brain controls all of your perceptions-the way you see,
hear, smell, taste, and feel. The brain communicates with the rest of
your body. Chemical messengers transmit information from nerve cell to
nerve cell in the body and the brain. Messages are constantly being
sent back and forth with amazing speed.
Your nerve cells are called neurons, and their chemical
messengers are called neurotransmitters. When neurotransmitters attach
to special places on nerve cells (called receptors), they cause changes
in the nerve cells. This communication system can be disrupted by
chemicals like hallucinogens, and the results are changes in the way
you sense the world around you.
Scientists are examining the possibility that long-term marijuana
use may create changes in the brain that make a person more at risk of
becoming addicted to other drugs, such as alcohol or cocaine. Further
research is needed to predict who will be at greatest risk.
The locations of the cannabinoid receptors are most revealing of
the way THC acts on the brain, but the importance of this determination
is best understood in comparison with the effects of other drugs on the
brain.
Neurons are brain cells which process information.
Neurotransmitter chemicals enable them to communicate with each other
by their release into the gap between the neurons. This gap is called
the synapse. Receptors are actually proteins in neurons which are
specific to neurotransmitters, and which turn various cellular
mechanisms on or off. Neurons can have thousands of receptors for
different neurotransmitters, causing any neurotransmitter to have
diverse effects in the brain.
Drugs affect the production, release or re-uptake (a regulating
mechanism) of various neurotransmitters. They also mimic or block
actions of neurotransmitters, and can interfere with or enhance the
mechanisms associated with the receptor.
Dopamine is a neurotransmitter which is associated with extremely
pleasurable sensations, so that the neural systems which trigger
dopamine release are known as the "brain reward system." The key part
of this system is identified as the mesocorticolimbic pathway, which
links the dopamine-production area with the nucleus of accumbens in the
limbic system, an area of the brain which is associated with the
control of emotion and behavior.
Cocaine, for example, blocks the re-uptake of dopamine so that
the brain, lacking biofeedback, keeps on producing it. Amphetamines
also block the re-uptake of dopamine, and stimulate additional
production and release of it.
Opiates activate neural pathways that increase dopamine
production by mimicking opioid-peptide neurotransmitters which increase
dopamine activity in the ventral tegmental area of the brain where the
neurotransmitter originates. Opiates work on three receptor sites, and
in effect restrain an inhibitory amino acid, gamma-aminobutyric acid,
that otherwise would slow down or halt dopamine production.
All of these substances can produce strong reinforcing properties
that can seriously influence behavior. The rewarding properties of
dopamine are what accounts for animal studies in which animals will
forgo food and drink or willingly experience electric shocks in order
to stimulate the brain reward system. It is now widely held that drugs
of abuse directly or indirectly affect the brain reward system. The key
clinical test of whether a substance is a drug of abuse potential or
not is whether administration of the drug reduces the amount of
electrical stimulation needed to produce self-stimulation response, or
dopamine production. This is an indication that a drug has reinforcing
properties, and that an individual's use of the drug can lead to
addictive and other harmful behavior.
While there are cannabinoid receptors in the ventromedial
striatum and basal ganglia which are areas associated with dopamine
production, no cannabinoid receptors have been found in dopamine-
producing neurons, and as mentioned above, no reinforcing properties
have been demonstrated in animal studies.
There are virtually no reports of fatal cannabis overdose in
humans. The safety reflects the paucity of receptors in medullary
nuclei that mediate respiratory and cardiovascular functions. This is
also why cannabinoids have great promise as analgesics or painkillers,
in that they do not depress the function of the heart or the lungs. In
this respect, they are far superior to opiates, which decrease the
entire physiological system because the receptors are all over the
medulla as well as the brain.
Marijuana is distinguished from most other illicit drugs by the
locations of its brain-receptor sites for two predominant reasons. The
lack of receptors in the medulla significantly reduces the possibility
of accidental, or even deliberate, death from THC, and the lack of
receptors in the mesocorticolimbic pathway significantly reduces the
risks of addiction and serious physical dependence.
None of the medical tests currently used to detect brain damage
in humans have found harm from marijuana, even from long term high-dose
use. An early study reported brain damage in rhesus monkeys after six
months exposure to high concentrations of marijuana smoke.
Marijuana produces immediate, temporary changes in thoughts,
perceptions, and information processing. The cognitive process most
clearly affected by marijuana is short-term memory. In laboratory
studies, subjects under the influence of marijuana have no trouble
remembering things they learned previously. However, they display
diminished capacity to learn and recall new information. This
diminishment only lasts for the duration of the intoxication. There is
no convincing evidence that heavy long-term marijuana use permanently
impairs memory or other cognitive functions.
Many active drugs enter the body's fat cells. What is different
(but not unique) about THC is that it exits fat cells slowly. As a
result, traces of marijuana can be found in the body for days or weeks
following ingestion. However, within a few hours of smoking marijuana,
the amount of THC in the brain falls below the concentration required
for detectable psychoactivity. The fat cells in which THC lingers are
not harmed by the drug's presence, nor is the brain or other organs.
The most important consequence of marijuana's slow excretion is that it
can be detected in blood, urine, and tissue long after it is used, and
long after its psychoactivity has ended.
Side Effect Behavior Changes and Primary Behavior changes with
Marijuana
There are many side effects associated with Marijuana. Marijuana
affects sensory, psychomotor, and cognitive function. For motor
performance, marijuana intoxication may be difficult to read in an
experienced user, except in difficult performance tasks or for those
tasks in which they have had little previous training. However,
intoxication of marijuana on an inexperienced person can be easily
detectable on some performance measures. Another problem with assessing
marijuana on a person's behavior is that this drug is commonly used
with other drugs such as alcohol. Making it difficult and/or distorting
the causality of the use of marijuana. It then makes studies
inconsistent.
The effects from the smoking of cannabis products are felt
within minutes and reach their peak in 10-30 minutes. Typical marijuana
smokers experience a high that lasts approximately two hours. Most
behavioral and physiological effects return to baseline levels within
3-5 hours after drug use. The initial effects felt include a dry
mouth, rapid heartbeat, some loss of coordination and poor sense of
balance, and slower reaction time. Blood vessels in the eye expand, so
the user's eyes may become bloodshot. Marijuana use also raises blood
pressure slightly and can double the normal heart rate. This effect can
be greater when marijuana is mixed with other drugs such as PCP. Some
users may have a negative reaction to marijuana. Someone new to the
drug or in a strange setting may suffer acute anxiety and have paranoid
thoughts. This is more likely to happen with higher doses of THC. These
feelings eventually wear off. In rare cases a user who has taken a very
high dose of the drug can have severe psychotic symptoms and need
emergency medical treatment. These negative reactions are more likely
to occur when marijuana is mixed with other drugs such as PCP.
Physical side effects of marijuana may include any mixture of
the following: dry mouth, nausea, headache, Nystagmus, tremors,
decreased coordination, increased heart rate, altered pulmonary status,
altered body temperature (users often report getting severely cold
while intoxicated), reduced muscle strength, decreased cerebral blood
flow, and increased food consumption. Psychological side effects of
marijuana may include any mixture of the following: anxiety and panic,
paranoia, confusion, aggressiveness, hallucinations, sedation, altered
libido, possible suicidal ideation, depersonalization, poor sense of
time, worsened short term memory, addictive behaviors, and
Amotivational syndrome.
The short-term effects of marijuana use include problems with
memory and learning, distorted perception, difficulty in thinking and
problem solving, and loss of coordination. Heavy users may have
decreased ability to concentrate, shifting their attention to meet the
demands of changes in the environment, and in registering, processing
and using information. Performance studies indicate that sensory
functions are not highly impaired, however perceptual functions are
significantly affected. The ability to concentrate and hold attention
are decreased during marijuana use, and impairment of hand- eye
coordination is dose related over a wide range of doses. People who use
marijuana can sometimes force themselves to concentrate on simple tasks
for brief periods of time. Impairment of performance was usually
observed for up to 1-2 hours following the use of marijuana.
Marijuana has another side effect; it can seriously alter
driving. In some studies marijuana was shown to impair the driver for
up to three hours. Decreased car handling performance, increased
reaction time and distance estimation, inability to maintain headway,
lateral travel, subjective sleepiness, and motor incoordination have
all been reported. Some drivers are reported to improve their
performance for brief periods of time by over compensating for the
users self-perceived impairment. The more demands put upon the driver,
the more impairment the driver has. Mixing alcohol with marijuana may
dramatically increase the effects than either drug on its own.
The primary effects of marijuana are behavioral because the drug
affects the central nervous system. Popular use of this drug has arisen
from its effects of euphoria, sense of relaxation, increased visual,
auditory, and taste perceptions that may occur with marijuana use.
Unpleasant effects that can happen include depersonalization, changed
body image, disorientation and acute panic reactions or severe
paranoia.
Visual tracking is impaired and the sense of time is typically
prolonged. Learning may be greatly affected because the drug diminishes
the ability to concentrate attention. Studies have shown that learning
may become "state-dependent" that the information acquired or learned
while under the influence of marijuana is best recalled in the same
state of drug influence. Amotivational syndrome (mentioned previously)
is the characterization by a loss of energy, a lack of concentration,
impaired memory (especially in short term memory), decreased
effectiveness and performance at school and work, and a general lack of
ambition and drive to work towards long- term goals. It has been
observed that the lack of motivation observed in some individuals more
likely results from previous psychological problems and polydrug use
rather than marijuana use alone. Researchers have found a controversy
in this because they can't seem to find a primary cause for the lack of
motivation.
Psychological effects of marijuana are still being studied to
see if there can be any use of it for psychological disorders. Studies
suggested that measures of mood, cognition and psychomotor performance
should be incorporated into clinical trials evaluating the efficacy of
marijuana or cannabinoid drugs for a given medical condition,
concluding that psychological effects of cannabinoids, such as anxiety
reduction, sedation, and euphoria can influence their potential
therapeutic value. Those effects are potentially undesirable for
certain patients and situations, and beneficial for others. In addition
psychological effects can complicate the interpretation of other
aspects of the drug effect.
There have been suggestions that marijuana induces several
psychopathological states, a "marijuana psychosis" has not been
successfully characterized. Marijuana can exacerbate pre-existing
mental disorders such as with schizophrenics, who use this drug to self
medicate even after recognizing its harmful effects. Schizophrenics
abusing marijuana are more difficult to treat effectively. Another
state is depression. Marijuana is linked to depression directly if you
already have symptoms or inherit depression from a family member. It
can increase signs of depression making it severely hard to get out of
the negative state that they are in. It can get so severe that suicidal
thoughts will enter their mind or worse.
Tolerance and dependence are also primary behavior changes
associated with marijuana. This manifests through decreases in
cardiovascular and autonomic functions, increases intraocular pressure,
sleep disturbances and mood changes. Behavioral tolerance is achieved
by consuming high amounts of THC administered over a period of time. A
greater tolerance may be developed with increased amounts of the drug.
If the doses are small and infrequent, little behavioral tolerance
seems to develop. It is inconclusive whether chronic marijuana use
results in severe withdrawal symptoms, but numerous case reports
attests to the development of dependence. The major complaints by
marijuana dependent individuals are: loss of control over drug use,
cognitive and motivational impairments, lowered self- esteem,
depression, and spousal discord.
I personally interviewed two chronic users of marijuana and
asked why they primarily use this drug. Anonymous Female said that she
started using marijuana out of curiosity. She then she would use it as
a substitution for alcohol to not appear as impaired as other persons
who were consuming alcohol. She now currently uses it to feel relaxed
after a stressful day. She said that she does not feel as if she is
physically addicted to it, but as the years progress and get more
stressful she turns to marijuana as a stress reliever more than any
other narcotic. She also feels that it is the safest substance to use
since there haven't been any studies concluding that there has ever
been a marijuana overdose. Anonymous Male has been smoking marijuana
for 10 years and is now feeling ready to quit. He stated that he hates
that he is around marijuana everywhere he goes, because it continually
makes it harder for him to quit. He thinks that smoking marijuana
brings on his minor and major paranoia and anxiety attacks. He believes
that if he quits he will no longer feel so unsure and indecisive about
the way he is choosing to live his life.
In conclusion, the numerous studies of marijuana are found to be
inconclusive due to the wide variety of findings which appear to
contradict one another. Also, many different people feel, and or
believe so many different things about this drug that it is hard to
find the negative effects to be due to marijuana use, when it
counteracts other's positive experiences with the drug. There appears
to be many variables not looked at in the studies such as people's
behaviors before any use of marijuana.
Effects Reported by Users and/or Survivors of Marijuana
It is estimated that approximately 14% of adolescents and 7% of
adults meet the Diagnostic and Statistical Manual of Mental Disorders
criteria for Marijuana Dependence (Kouri & Pope, 2000). There is a
minority of Marijuana users and survivors in our population.
Preclinical studies have found that there is an existence of a
Marijuana withdraw syndrome in long term heavy marijuana users. In
other words, a person can become physically dependent on Marijuana.
Kouri and Pope's (2000) findings were significant. They found that
heavy marijuana users experience several withdraw symptoms during an
attempt to detoxify. The symptoms appear about 24 hours after the
last use of marijuana. This means that a person will begin to feel
irritated and anxious almost one day after they smoke.
Unfortunately the study revealed that the withdraw symptoms were most
unbearable during the first 10 days yet, lasted the entire 28 days
that the study lasted. Although these withdraw symptoms are not life
threatening they effect a persons mood and happiness. The symptoms
that they experienced were irritability, sleeplessness and anxiety.
These symptoms are almost opposite to the side affects of smoking
marijuana. Therefore, it is easy to see why people relapse from
quitting. There is controversy on whether this withdraw syndrome
exists because not all people who stop using the drug experience
these types of withdraws. It is important to note that users
reported attempting to quit in the past they have failed due to the
withdraw symptoms. Even if these symptoms are not as bad as heroin
withdraws they still are bothersome enough to lead a person to
relapse.
In another study conducted by Williams (2004)it was
investigated if cognitive deficits continued after the use of
marijuana stops in long term heavy marijuana users. He found that
these symptoms still lingered on when he tested his participants for
verbal memory, visual memory, executive cognitive functioning and
manual dexterity (Williams, 2004). This means that as persons short
term memory is affected by the long term use of heavy marijuana
smoking. The study also revealed that some people are at higher
cognitive risk from smoking marijuana than others. It was found that
people with a lower IQ would score lower than those with a high IQ.
The interesting part is that in this group all participants continued
to smoke however, those with a low IQ scores continued to decrease
while those with a high IQ continued to score the same. This means
that the impact of the drug on a brains function is more evident in
those with fewer cognitive (low IQ's) resources. A person's who
smokes marijuana has deficits in their cognitive abilities. It should
be noted that those who smoke marijuana daily may be functioning at a
lower intellectual level.
Depression, Anxiety, and personality disorders have been
associated with heavy marijuana use. It is unclear if people who are
more vulnerable to these mental illnesses are more likely to be
attracted to this marijuana or if marijuana causes these illnesses.
Whatever the case, one should be cautious when considering smoking
marijuana, the truth is that it is a risk. It is important to note
that although one cannot overdose while taking the drug it can still
affect many areas of ones life. Studies have also demonstrated that
students who smoke marijuana get lower grades and are less likely to
graduate from high school (NIDA website, pg3). As mentioned above
one of the reasons why these students get bad grades is because
marijuana affects ones memory, and learning. Those students that
smoked marijuana heavily had a hard time shifting their attention and
organizing their work in the classroom. Of course it must be pointed
out that regardless of age, heavy marijuana users will experience
learning and social behavior problems. For example, adults who are
involved in heavy marijuana use usually begin to struggle at the
workplace. Many times there are increased absences, tardiness and
accidents.
Part of the Neuron Affected
The sensations of relaxation, time perception, increase in
appetite, and amplified visual and auditory perceptions produced by
tetrahydrocannabinol (THC) are attributed to the cannaboid receptors
in the brain. There are two subtypes CB1 and CB2, they appear to be
located in the nervous system and periphery (Breivogel & Childers,
1998). A brain chemical that binds to the cannabinoid receptor has
been identified: anandamide (Kalat, 2004). This chemical is involved
in regulating mood, memory, appetite, pain, cognition and emotions.
Anandamide binds to the cannabinoid receptors. There are two types
of cannabinoid receptors; CB1 and CB2 (Breivogel & Childers, 1998).
The CB1 receptor is the most common among the neural receptors
(Ameri, 1999). The highest density of CB1 receptors is in the basal
ganglia and the molecular layer of the cerebellum. This explains why
when someone who has recently been under the influence of marijuana
is affected cognitively and memory wise. In chronic Marijuana users,
the loss of CB1 in the brains arteries reduces the blood flow, and
also glucose and oxygen to the brain. This explains why some
survivors have attention deficits, memory loss and learning
diabilities. The cannabinoid CB2 receptor can be found in the
periphery,Spleen and tonsils but has not been detected in the central
nervous system (Ameri, 1999). The CB1 and CB2 receptors are actually
very similar. Although the anandamide tends to bind to the CB1
receptor rather than the CB2 receptor they are still very similar.
When THC enters the body, it begins to affect the normal
functions of the brain. Immediately the cannabinoids increase the
activity of dopamine neurons in especially those in the midbrain
ventral tegmental area (French, Dillon, & Wu, 1997). The release of
anandamide is followed by "rapid uptake into the plasma and
hydrolysis by fatty-acid amidohydrote" (French, Dillon, & Wu, 1997).
This activity affects the potassium and calcium channels so as to
reduce the amount of neurotransmitters released. These findings
demonstrate that the dopamine neurons that are being affected are in
the midbrain and there are very few cannabinoid binding sites at the
VTA. Since these receptors do not appear in this area of the brain,
it is then assumed that the effects of THC on the neuron occurs
through an alteration of the transmitter (French, Dillon, & Wu,
1997). The barins neural networks overall are affected by this as
well. Since the dopaminergic neurons do not have these receptors
they are usually affected by those GABA neurons that do have them.
What the THC does is remove the inhibition of GABA and at the same
time excites or activates the dopamine neurons.
Effects on ion channels and synaptic terminals
In order to discuss how marijuana affects ion channels, it is
first necessary to give a general overview on the basic function of
the different ion channels. Since the neurons "membrane prevents
most large or electrically charged ions or molecules cannot cross the
membrane." (Karat, 2004) Examples of such ions are calcium and
potassium, whose ion channels are affected by marijuana, sodium and
chloride. Therefore this basic function is to allow certain ions or
molecules to pass into or out of the cellular membrane. Another
function of the ion channels is to regulate the amount of ions either
entering or exiting the ion channels by opening or closing gates.
These gates are open or closed depending on the amount of force
acting upon the amount of ions either being sucked in or released
through. This is determined by basically the depolarization or
polarization of the membrane, which in turn ends up affecting the
ions channel gates because they are voltage sensitive.
In order to determine whether the result of an ion influx, is
going to cause a depolarization of the neurons membrane and to what
extreme, it depends on a couple of different variables. The first
main factor is if the ions are entering or leaving the cellular
membrane. The second is what type of charge the ion holds, for
instance both potassium and sodium have positive charges. It is
basic process that scientists have investigated upon the effects of
marijuana on such ion channels and if such processes occur.
The discovery of cannabinoid led scientist to investigate what
brain chemicals bind with the cannaboid receptors. One of the
earliest chemicals identified in this process was anandamide that is
an agonist to the CB1 receptor. Later a more abundant cannabinoid
Sn2 arachidonylglcerol, abbreviated (2AG) was discovered. These two
cannabinoids play an important role in marijuana synthesis by acting
the cannabinoid receptors on the presynaptic terminal. However in
order for such an event to occur it is first necessary for the
postsynaptic terminal to be stimulated by transmitters, like
glutamate and GABA. After either glutamate or GABA acts on the
postsynaptic terminal, the postsynaptic neuron releases anandamide or
2AG. After the postsynaptic neuron releases either of these compounds
they return to the presynaptic terminal and temporarily decrease
further production of transmitters. It is these actions that lead to
the CB1 cannabinoid receptor located on the presynaptic terminal, to
decrease the opening of N type voltage gated Ca2+ channels. The
effects of this opening, it cause a depolarization wave to move down
the axon until it activates the voltage sensitive terminals of N type
and P/Q type calcium cannels. As a result the calcium channels
allows small amounts of calcium ions to enter into the terminal.
After this event, the amount of calcium present in the terminal
stimulates the release of a neurotransmitter into the synaptic cleft.
In addition to these calcium channels being voltage activated,
the channels are also regulated by CB1 and G1 proteins coupled protein
receptors. Therefore, after these calcium channels open on the presynaptic
side of the terminal, they inhibit the release of the neurotransmitter,
glutamate with the help of cannabinoids (see figure 1). After the
neurotransmitters are released into the synaptic cleft, they sit outside the
NMDA receptors on the post-synaptic terminal. It is this receptor, which after
activated allows calcium to enter through the receptor ion channel, causing the
membrane on the NMDA receptor to depolarize (see figure 2). It is this action,
which plays an important role in activating voltage sensitive calcium channels
on the postsynaptic terminal. As a result of these calcium N type and P/Q type
channels being activated the amount of calcium entering the membrane through
additional ion channels is greatly increased beyond the NMDA ion channel
receptors ability to channel calcium into the membrane. After this process of
the induced calcium influx upon the inside of the postsynaptic neuron the
endogenous cannabinoid system acts to regulate this influx of calcium. The
calcium regulation occurs as a result of the chemical synthesis of anandamide
in the response to the rise of intercellular calcium levels as a result of the
neurons exposure to glutamate excitotoxicity. Next, anandamide plays its role
in being a cannabinoid receptor agonist. Reducing the amount of stimulated
calcium entering through ion channels by voltage sensitive calcium channel
blockage. In addition to blocking the calcium channels the investigation upon
NMDA receptor blockade could also be effective in helping prevent calcium
influxes in causing damage in the postsynaptic terminal. "However it seems to
induce serious side affects like psychosis and cardiovascular problems
(Grotenhermen & Russo, 2002)." In addition to anandamide inhibiting N and P/Q
type calcium channels it also inhibits A type potassium ion channels. This
process occurs as a result of "cannabinoids ability to inhibit adenylatecyclase
and so suppress intracellular levels of cyclic AMP." (Brown, 1998).
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