News (Media Awareness Project) - CN SN: Marijuana May Not Be Cure-All Once Thought |
Title: | CN SN: Marijuana May Not Be Cure-All Once Thought |
Published On: | 2004-08-13 |
Source: | Regina Leader-Post (CN SN) |
Fetched On: | 2008-08-22 02:22:57 |
MARIJUANA MAY NOT BE CURE-ALL ONCE THOUGHT
SASKATOON -- Marijuana researchers have found that a component of pot may
intensify the severity of the most common type of epileptic seizures.
The finding was a surprise for research group leader Dr. Michael Corcoran at
the University of Saskatchewan, who said this week he expected findings
would support older research that had suggested high doses of THC, the
psychoactive ingredient of cannabis, could suppress grand-mal type seizures.
Now Corcoran suspects that the effects of THC or its synthetic form, known
as cannabinoids, may depend on the part of the brain where the seizure
occurs. The regions of the brain which are susceptible to epilepsy are
mainly those involved in learning and memory, he said.
Corcoran's experiments on rats have shown that seizures which begin in the
temporal lobes appear to last longer and be more severe after cannibinoids
are administered.
He thinks studies conducted in the 1980s, which suggested some seizures may
be suppressed by marijuana, may have had a greater concentration of a THC
component that acts on the brain stem where grand-mal seizures originate.
Research conducted in the past decade has found that there are at least two,
possibly three, different types of receptors on cellular membranes for
marijuana-like compounds, including some on nerve cells.
These "cannabinoid receptors" normally are acted upon by various
naturally-occuring marijuana-like substances called "endogenous
cannabinoids."
One of those endogenous cannabinoids has been aptly labelled andomide, a
term derived from the Sanskrit word meaning bliss, Corcoran noted.
Identifying and cloning the receptor allowed researchers to design
artificial drugs that act very selectively at that receptor, to turn it on
or block the action of cannabinoids, Corcoran said.
Using a process called kindling, Corcoran gradually induces epilepsy in rats
by administering low doses of electricity to the brain. Once epilepsy has
been induced, the brain becomes more susceptible to seizures than a normal
brain.
Corcoran found that administering cannibinoids before kindling caused rats
to develop epilepsy much sooner than those which didn't get the marijuana
component.
"It's really completely the opposite of what I expected," he said.
"Instead of finding potentially useful anti-epileptic effects, we found the
opposite."
Still, Corcoran is not saying people who smoke pot are more likely to
develop epilepsy.
The true effects won't be known unless clinical trials are done on humans
and those could result in other findings.
A classic example is Thalidomide, an anti-morning sickness drug which had
devastating side-effects of causing congenital deformities of the limbs in
humans, though no such side-effect had shown up in animals.
The results of the older studies were not particularly impressive because
they required such high doses that side-effects resulted, Corcoran said.
SASKATOON -- Marijuana researchers have found that a component of pot may
intensify the severity of the most common type of epileptic seizures.
The finding was a surprise for research group leader Dr. Michael Corcoran at
the University of Saskatchewan, who said this week he expected findings
would support older research that had suggested high doses of THC, the
psychoactive ingredient of cannabis, could suppress grand-mal type seizures.
Now Corcoran suspects that the effects of THC or its synthetic form, known
as cannabinoids, may depend on the part of the brain where the seizure
occurs. The regions of the brain which are susceptible to epilepsy are
mainly those involved in learning and memory, he said.
Corcoran's experiments on rats have shown that seizures which begin in the
temporal lobes appear to last longer and be more severe after cannibinoids
are administered.
He thinks studies conducted in the 1980s, which suggested some seizures may
be suppressed by marijuana, may have had a greater concentration of a THC
component that acts on the brain stem where grand-mal seizures originate.
Research conducted in the past decade has found that there are at least two,
possibly three, different types of receptors on cellular membranes for
marijuana-like compounds, including some on nerve cells.
These "cannabinoid receptors" normally are acted upon by various
naturally-occuring marijuana-like substances called "endogenous
cannabinoids."
One of those endogenous cannabinoids has been aptly labelled andomide, a
term derived from the Sanskrit word meaning bliss, Corcoran noted.
Identifying and cloning the receptor allowed researchers to design
artificial drugs that act very selectively at that receptor, to turn it on
or block the action of cannabinoids, Corcoran said.
Using a process called kindling, Corcoran gradually induces epilepsy in rats
by administering low doses of electricity to the brain. Once epilepsy has
been induced, the brain becomes more susceptible to seizures than a normal
brain.
Corcoran found that administering cannibinoids before kindling caused rats
to develop epilepsy much sooner than those which didn't get the marijuana
component.
"It's really completely the opposite of what I expected," he said.
"Instead of finding potentially useful anti-epileptic effects, we found the
opposite."
Still, Corcoran is not saying people who smoke pot are more likely to
develop epilepsy.
The true effects won't be known unless clinical trials are done on humans
and those could result in other findings.
A classic example is Thalidomide, an anti-morning sickness drug which had
devastating side-effects of causing congenital deformities of the limbs in
humans, though no such side-effect had shown up in animals.
The results of the older studies were not particularly impressive because
they required such high doses that side-effects resulted, Corcoran said.
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