SpunkySkunk347
Bluelighter
- Joined
- Jan 15, 2006
- Messages
- 1,717
Since amphetamine releases dopamine from storage vesicles by reversing the reuptake of dopamine, why doesn't amphetamine "create" thought?
Wouldn't the released dopamine trigger an action potential in the post-synaptic neuron?
Since the pre-synaptic neuron didn't actually send the "message" itself (since the neuron didn't naturally release the dopamine, the amphetamine did), wouldn't this cause for a signal to be generated "out of thin air" without having any rhyme or reason for its existence? And since these "artificially created signals" weren't actually supposed to occur, wouldn't this cause the entire dopaminergic neural system to be out of synchronicity - and in turn cause a collapse of an individual's train of thought?
Maybe my understanding of neurology is completely bogus - one thing I was considering is that the neurotransmitters do not generate a signal themselves, but merely enhance any incoming signals from the pre-synaptic neuron. If that's the case, then just delete this thread because I am an idiot.
However, excluding that dopamine doesn't generate the signal itself (and can't trigger an action potential by itself), what are the explanations to my originally proposed problem?
One explanation is that the constant input of new incoming stimulation causes the dopaminergic neural pathways to "re-synchronize" themselves before any significant level of "brain incoherence" were to occur.
Another explanation is that amphetamine does not affect enough neurons on the scale of the whole brain in order to cause a noticeable level of incoherence - and the minor level of "incoherence" that does occur is actually what is responsible for amphetamine's effects. The dose of amphetamine is merely not high enough to generate a noticeable lack of synchronicity in the mind's train of thought.
Even yet another explanation is that the dopaminergic pathways activated by amphetamine are not responsible for thought itself, but are responsible for the motivation of maintaining a certain thought.
An abstract explanation would be that our concept of "thought" is flawed, but is really our brain's "self-evaluation" of a planned act of speaking before that speaking occurs (this is to ensure that the speaking will make logical sense, and allows the mind to "remold" a potential act of speech).
What exactly is this "incoherence" I am referring to? Well, it basically means that amphetamine causes the brain to generate activity on its own without any incoming stimulus. In a situation where an individual on amphetamine completely lacked any external stimulus, the mind would begin to generate its own thoughts (and due to the lack of any actual external stimulus, the thoughts would be incoherent and random) - the individual would be unable to figure out why he was having such strangely incoherent thoughts, and would be unable to stop them or control them.
If all this is true, then why doesn't amphetamine cause a person to become insane and have disorganized thought patterns that are generated for no particular reason?
The answer is explained by 5-HT. Serotoninergic pathways inhibit the activity of dopaminergic pathways. Whenever a significant level of amphetamine-induced "dopaminergic incoherence" occurs, the brain lets serotonergic pathways step in and inhibit the dopaminergic pathways that were causing the incoherence.
This supports a hypothesis I posted on this forum a few months back. The hypothesis was that "amphetamine psychosis is caused by a depletion of serotonin and possibly amphetamine's indirect anti-cholinergic activity in the striatum haulting the striatum's interneuronal abilities" as opposed to the popular belief that amphetamine psychosis is caused by an excess of dopamine. The popular belief is still partially true, that excessive dopamine activity is responsible for the "disorganized thinking" of amphetamine psychosis; but with normal serotonin levels, such excessive dopamine activity could be naturally inhibited.
Since serotonin vesicles are depleted much faster than dopamine vesicles (as well as the fact that they take much longer to replenish), amphetamine psychosis occurs when the brain's serotonergic activity has dropped significantly below the amount required to successfully inhibit dopaminergic activity.
Anti-cholinergic activity in the striatum also could explain this - the striatum is left incapable of generating interneuronal signals (that are normally mediated by acetylcholine) that normally allow for sensations of "reward" to occur. What exactly are these sensations of reward? The cholinergic inter-neurons from the striatum somehow (either directly or indirectly) revert dopaminergic activity (this dopaminergic activity we would relate to "deep contemplation" or "confusion") into "pleasure" or "satisfaction" (which is really just the peace of mind gained from no longer having to think about something). It is basically our brains way of "stopping a thought" once a problem has been solved - you wouldn't need to keep thinking about the solution for a problem if that problem had already been solved, now would you?
Since the striatum's ability to do this is left compromised by amphetamine, dopaminergic activity continues unimpeded and accumulates to critical levels - the individual experiencing this is unable to feel "satisfaction" and is unable to stop thoughts/activities due to a feeling that "something still needs to be done" or "the thought is still incomplete"; individuals are unable to "let go" of a thought.
_ _ _ _
Why is Amphetamine considered "more psychogenic" than DRIs such as Cocaine?
As noted above, amphetamine is capable of "generating mental activity" by itself, even in the absence of external stimulation. Amphetamine is perceived to be "more psychogenic" than cocaine and other DRIs because amphetamine releases dopamine itself, where as cocaine and DRIs merely increase the concentrations of dopamine that neurons have released themselves.
Amphetamine creates "artificial activity", where as cocaine only enhances activity that was already there.
This is why amphetamine psychosis is perceived to be different than a cocaine-induced psychosis. The psychosis resulting from prolonged use of dopamine re-uptake inhibitors is mostly due to mental exhaustion, fatigue, and sleep deprivation. A DRI-induced psychosis will mostly exaggerate thought processes where as an amphetamine-induced psychosis will generate its own thought processes.
Amphetamine induced-psychosis will cause a significant amount of memory impairment, and the individual will feel as if they are "trapped in introspection" that is beyond their control as the amphetamine begins to generate more and more thoughts that are beyond the control of the individual.
Cocaine-induced psychosis is more noted for long-term memory impairment (not remembering much of what happened after you crash and wake up) because it is mostly fatigue-related - where as amphetamine is more noted for short-term memory impairment as well as long-term. This is, again, mostly because of amphetamine's indirect anticholinergic activity.
Another unique aspect of amphetamine psychosis is its tendency to create "thought paralysis" in which an individual is unable to shift out of a certain mental state, and is essentially "trapped" in introspection. Once again, this appears to be due to anti-cholinergic activity in the striatum combined with serotonin-depletion.
One partially successful thing I have found that will eliminate the "uncontrollable thoughts" associated with amphetamine psychosis, is to ingest foods containing tryptophan - specifically milk. Although this will not completely resolve the amphetamine psychosis, it will allow for an individual to "relax" and have more control over their thoughts. They will transition to more of a "surreal like" state instead of a "confused and irritated" state.
Wow okay good god I am done typing this long ass thread.
Wouldn't the released dopamine trigger an action potential in the post-synaptic neuron?
Since the pre-synaptic neuron didn't actually send the "message" itself (since the neuron didn't naturally release the dopamine, the amphetamine did), wouldn't this cause for a signal to be generated "out of thin air" without having any rhyme or reason for its existence? And since these "artificially created signals" weren't actually supposed to occur, wouldn't this cause the entire dopaminergic neural system to be out of synchronicity - and in turn cause a collapse of an individual's train of thought?
Maybe my understanding of neurology is completely bogus - one thing I was considering is that the neurotransmitters do not generate a signal themselves, but merely enhance any incoming signals from the pre-synaptic neuron. If that's the case, then just delete this thread because I am an idiot.
However, excluding that dopamine doesn't generate the signal itself (and can't trigger an action potential by itself), what are the explanations to my originally proposed problem?
One explanation is that the constant input of new incoming stimulation causes the dopaminergic neural pathways to "re-synchronize" themselves before any significant level of "brain incoherence" were to occur.
Another explanation is that amphetamine does not affect enough neurons on the scale of the whole brain in order to cause a noticeable level of incoherence - and the minor level of "incoherence" that does occur is actually what is responsible for amphetamine's effects. The dose of amphetamine is merely not high enough to generate a noticeable lack of synchronicity in the mind's train of thought.
Even yet another explanation is that the dopaminergic pathways activated by amphetamine are not responsible for thought itself, but are responsible for the motivation of maintaining a certain thought.
An abstract explanation would be that our concept of "thought" is flawed, but is really our brain's "self-evaluation" of a planned act of speaking before that speaking occurs (this is to ensure that the speaking will make logical sense, and allows the mind to "remold" a potential act of speech).
What exactly is this "incoherence" I am referring to? Well, it basically means that amphetamine causes the brain to generate activity on its own without any incoming stimulus. In a situation where an individual on amphetamine completely lacked any external stimulus, the mind would begin to generate its own thoughts (and due to the lack of any actual external stimulus, the thoughts would be incoherent and random) - the individual would be unable to figure out why he was having such strangely incoherent thoughts, and would be unable to stop them or control them.
If all this is true, then why doesn't amphetamine cause a person to become insane and have disorganized thought patterns that are generated for no particular reason?
The answer is explained by 5-HT. Serotoninergic pathways inhibit the activity of dopaminergic pathways. Whenever a significant level of amphetamine-induced "dopaminergic incoherence" occurs, the brain lets serotonergic pathways step in and inhibit the dopaminergic pathways that were causing the incoherence.
This supports a hypothesis I posted on this forum a few months back. The hypothesis was that "amphetamine psychosis is caused by a depletion of serotonin and possibly amphetamine's indirect anti-cholinergic activity in the striatum haulting the striatum's interneuronal abilities" as opposed to the popular belief that amphetamine psychosis is caused by an excess of dopamine. The popular belief is still partially true, that excessive dopamine activity is responsible for the "disorganized thinking" of amphetamine psychosis; but with normal serotonin levels, such excessive dopamine activity could be naturally inhibited.
Since serotonin vesicles are depleted much faster than dopamine vesicles (as well as the fact that they take much longer to replenish), amphetamine psychosis occurs when the brain's serotonergic activity has dropped significantly below the amount required to successfully inhibit dopaminergic activity.
Anti-cholinergic activity in the striatum also could explain this - the striatum is left incapable of generating interneuronal signals (that are normally mediated by acetylcholine) that normally allow for sensations of "reward" to occur. What exactly are these sensations of reward? The cholinergic inter-neurons from the striatum somehow (either directly or indirectly) revert dopaminergic activity (this dopaminergic activity we would relate to "deep contemplation" or "confusion") into "pleasure" or "satisfaction" (which is really just the peace of mind gained from no longer having to think about something). It is basically our brains way of "stopping a thought" once a problem has been solved - you wouldn't need to keep thinking about the solution for a problem if that problem had already been solved, now would you?
Since the striatum's ability to do this is left compromised by amphetamine, dopaminergic activity continues unimpeded and accumulates to critical levels - the individual experiencing this is unable to feel "satisfaction" and is unable to stop thoughts/activities due to a feeling that "something still needs to be done" or "the thought is still incomplete"; individuals are unable to "let go" of a thought.
_ _ _ _
Why is Amphetamine considered "more psychogenic" than DRIs such as Cocaine?
As noted above, amphetamine is capable of "generating mental activity" by itself, even in the absence of external stimulation. Amphetamine is perceived to be "more psychogenic" than cocaine and other DRIs because amphetamine releases dopamine itself, where as cocaine and DRIs merely increase the concentrations of dopamine that neurons have released themselves.
Amphetamine creates "artificial activity", where as cocaine only enhances activity that was already there.
This is why amphetamine psychosis is perceived to be different than a cocaine-induced psychosis. The psychosis resulting from prolonged use of dopamine re-uptake inhibitors is mostly due to mental exhaustion, fatigue, and sleep deprivation. A DRI-induced psychosis will mostly exaggerate thought processes where as an amphetamine-induced psychosis will generate its own thought processes.
Amphetamine induced-psychosis will cause a significant amount of memory impairment, and the individual will feel as if they are "trapped in introspection" that is beyond their control as the amphetamine begins to generate more and more thoughts that are beyond the control of the individual.
Cocaine-induced psychosis is more noted for long-term memory impairment (not remembering much of what happened after you crash and wake up) because it is mostly fatigue-related - where as amphetamine is more noted for short-term memory impairment as well as long-term. This is, again, mostly because of amphetamine's indirect anticholinergic activity.
Another unique aspect of amphetamine psychosis is its tendency to create "thought paralysis" in which an individual is unable to shift out of a certain mental state, and is essentially "trapped" in introspection. Once again, this appears to be due to anti-cholinergic activity in the striatum combined with serotonin-depletion.
One partially successful thing I have found that will eliminate the "uncontrollable thoughts" associated with amphetamine psychosis, is to ingest foods containing tryptophan - specifically milk. Although this will not completely resolve the amphetamine psychosis, it will allow for an individual to "relax" and have more control over their thoughts. They will transition to more of a "surreal like" state instead of a "confused and irritated" state.
Wow okay good god I am done typing this long ass thread.
