3 replies to this topic

[medicineman]

http://www.sumanasin.../receptors.html

This will clear up alot of questions regarding how the racetams work, how calcium can cause toxic effects if unchecked, and how nmda antagonists work...

[cougar]

http://www.sumanasin.../receptors.html

This will clear up alot of questions regarding how the racetams work, how calcium can cause toxic effects if unchecked, and how nmda antagonists work...

Wonderful, great job medicineman. This is what I have been looking for. Thanks a lot.

[acantelopepope]

http://www.sumanasin.../receptors.html

This will clear up alot of questions regarding how the racetams work, how calcium can cause toxic effects if unchecked, and how nmda antagonists work...

Good video, but it didn't explain 'how calcium can cause toxic effects if unchecked,' did it?

Here's some additional information on NMDA/AMPA receptors taken from the springerlink encyclopedia of neuroscience:

Many other drugs have been investigated for possible
efficacy in the treatment of cognitive deficits, including
▶memantine, selegiline, modafanil, vitamin E, Ginkgo
biloba extracts and a variety of other herbal extracts,
and▶α-amino-3-hydroxy-5-methylisoxazole-4-propionic
acid (AMPA) receptor potentiators. Of these, only
memantine and AMPA receptor potentiators have been
shown to have any clinical effect [4]. Memantine
blocks the calcium ion channel associated with the
▶N-methyl-D-aspartate (NMDA) subtype of glutamate
receptor (an uncompetitive NMDA antagonist). Since
the NMDA receptor is involved in increases in synaptic
efficacy associated with LTP, it may at first seem
paradoxical that memantine could benefit cognition.
However, over-stimulation of theNMDAreceptor causes
neurotoxicity and therefore memantine may improve
cognition in diseases such as Alzheimer’s disease by
limiting this form of neural damage [3,4,6,7]. ▶Piracetam
is one of a number of AMPA receptor potentiators
that has been actively researched but is not yet prescribed
for Alzheimer’s disease. Along with aniracetam, it is a
pyrrolidone that increases the response of the AMPA
subtype of glutamate receptor [9]. Other AMPA receptor
potentiators, sometimes referred to as “▶ampakines,”
include benzylpiperidines such as CX-516 and CX-546,
which are in clinical trials [1,9].
Most of the drugs that are used clinically in the
treatment of cognitive disorders do not enhance cognition
in people without a neurological deficit. However, many
drugs that were first investigated for their general
nootropic effects, were then tested in patients with
Alzheimer’s disease and other neurological disorders to
determine whether they would have any beneficial
clinical effect. Some herbal drugs such as Ginkgo biloba
extracts have been claimed to improve memory in
both Alzheimer’s disease patients and in neurologically
intact individuals; however, there is no convincing
evidence for a consistent effect in either case [4,10].
Summary of Nootropic Sites of Action
Where in the brain do nootropic drugs act to produce
their effects? Many areas of the brain are involved in the Areas such as the hippocampus and other areas of the
medial temporal lobe are believed to be important for
encoding new memories; the neocortex is thought to be
important for long-term storage of memories [1,2].
Molecular Mechanisms of Action of Nootropic Drugs
The precise mechanisms of the formation and retrieval
of memories are not understood and therefore the
precise mechanisms of action of nootropic drugs are not
known. However, it is well established that acetylcholine
is important for the formation new memories.
Activation of acetylcholine receptors causes intracellular
changes in neurons that result in the activation of
proteins such as the cyclic adenosine monophospshate
(cAMP) response element binding protein (▶CREB),
which many researchers regard as a form of “molecular
switch” that converts short-term memories into longterm
ones [2]. The neural model of memory, LTP, has
been used to better understand the increases in synaptic
efficacy that are likely to underlie the formation of
memories. In LTP, the activation of post-synaptic
NMDA receptors is thought to be a critical step in
producing the biochemical changes that lead to enhanced
synaptic efficacy. While excessive activation of NMDA
receptors results in excessive calcium influx and
neurotoxicity, a smaller elevation of NMDA receptor
activation may enhance memory. For example, the
ampakines have been developed so that they elevate
NMDA receptor activation indirectly, by potentiating
AMPA receptor activity, which then leads to increased
depolarization, thus lowering the threshold for NMDA
receptor activation [1,9]. The downstream effects of
AMPA receptor modulation include an increase in
growth factors such as brain-derived neurotrophic factor
(BDNF), which is known to be important in synaptic
plasticity [9].While still in clinical trials, these drugsmay
be one class of nootropic drug that is used to treat
Alzheimer’s disease and other related neurological
disorders in the future. Other possibilities include drugs
that modulate dopaminergic and serotonergic function.
Many researchers believe that no one drug with a single
mechanism of action is likely to provide successful
therapy for cognitive disorders.
Will the same nootropic drugs that are used to treat
cognitive disorders be useful for enhancing cognition in
healthy individuals? It is possible but more likely that
there are natural limits to the extent that the normal
neurochemical machinery of memory can be enhanced
before adverse side effects develop.

[cougar]

Here's some additional information on NMDA/AMPA receptors taken from the springerlink encyclopedia of neuroscience:

Very helpful, I'm downloading this book now. Thanks.