^ Shaolin, would LSD change your ability to process memories to a similar degree as MDMA? I read an editorial from the New Scientist a while ago about MDMA's affects on the brain and, in particular, cognitive function and memory. I think that, in terms of memory, MDMA users (or past users) scored slightly worse than the control, but I don't think it was an incredibly significant difference. Is there reason to believe that LSD would be 'worse' for your memory than MDMA?
Obviously there would be cause for concern if all LSD users turned into goldfish - has it been proven that LSD users do have a worse memory, in a practical, rather than neurological, sense?
i dont know alot about LSD, but from what i know, its effects on mental memory thought processes is not a threat, however, the synapses that control visual memory are effected greatly.
MDMA on the other hand is shown through numerous articles to be neurotoxic. This is probably the cause of memory, emotional, and anxiety problems associated with abuse of MDMA.
But to the original question Bonsai, the genes effected can regulate whether or not the cells deem it necessary for synaptic plasticity to take place, whether you want it or not. Suppose you take a new kind of psychedelic you've never had before, and you take a average dose, or more, does'nt matter. If your brain cannot handle the agonisitic properties of a psychedelic substance, or agonism of 5-ht2 receptors via over stimulation from regular 5-ht (serotonin), FROM RESEARCH ARTICLES THEY SUGGEST, your brain will try to adapt to the environment via extending synaptic connections, making your brain easier to process the uncoupled, destabilized environment in which a psychedelic drug puts your brain at.
I strongly believe HPPD to be only a worry in genetical susceptible people.
Alot of people report lingering visuals after a trip for a day or two, or even a week or two, but it goes away. This tells me that new/reinforced excitatory pathways were formed, but for whatever reason, their genetics recognized that these new forms are useless and no longer needed, so their brain "broke" the connections, and the visuals stabilized. HPPD is just a severe case of increased excitatory synaptic connections in the visual cortex via EXPRESSED soft coding gene. Thats just my opinion but i've dont alot of reading on Chemically induced long term potentiation in the brain and this is the only scenario that makes sense to me.
I can stress my point through my personal experiences and the experiences of others with HPPD through the use of AED (antiepileptic drugs) like keppra, in which theres evidence to suggest that the chemical, keppra, slows down excitatory synaptic activity by numerous means, and a prolonged state of this (continuous chronic administration of the drug) eventually causes new areas for the drug to bind to inhibitory receptors, and the more the drug attaches to its binding spots, one of them being a protein that transports neurotransmitters from neuron to neuron, the more its inhibitory effects are seen. Some people with HPPD have taken keppra and its almost a magic bullet, in the sense that dissociation is lifted, and visuals slowly start to improve over time. This is more evidence to me that long term potentiation is the cause for a visual disorder that lasts for so long, because decreases in synaptic activity at these over-stimulated inhibitory sites over long periods of time via chronic administration of an AED, IN THEORY, should break the newly formed synaptic contacts, or decrease the volume of the excitatory dendritic synaptic connections, therefore calming the constant state of excitation, and inhibitory afferents are now once again leveled off with excitation, recreating the balanced state of equilibrium in the negative feedbackloops of the excitatory and inhibitory serotonergic system in the visual cortex.
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