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carovine? dissociative?

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caroverine? dissociative?

I stumbled across this in wiki, must be new or something. It's a drug for tinnitus and is an NMDA antagonist/AMPA antagonist.

Could this drug be a new dissociative, if so- does anyone know at what dose? It seems like an easy enough medication to obtain and would also most likely be available commercially so this may warrant some experimentation:).
 
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http://en.wikipedia.org/wiki/Caroverine

Its been investigated for a tinnitus cure and there have been limited clinical trials.

Might be worth looking for side effect profiles, as they will surely be available if the results of any trials have been publicised.


Volume 8, Issue 3, Pages 191-194 (1 August 1998)

Infusional high-dose application of the calcium-channel-blocking and antiglutamatergic agent caroverine in the treatment of alcohol withdrawal (DSM-III-R 291.80)

This abstract suggests there was no sedative effect, which might point to it not being too recreational, although it IS still a noncompetitive antagonist, although that article doesn't give any clues as to its binding site (I don't have the full text though), it says caroverine is a competitive AMPA antagonist at lower concentrations than it is an NMDA antagonist, so at doses required to produce dissociation if it indeed does so chances are it would either produce unconsciousness, or if not, then certainly impair AMPAr-dependent hippocampal LTP, and prevent one remembering a damned thing about any possible trip.
 
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thanks, I always wondered what ampa antagonism did, if blacking out is that then forget it(NoPunIntended). it's for that reason I cant stand benzos, atleast for recreational purpouses. BTW where can I find info on the effects of AMPA blockers, as far as I knew of they act as immobilizing agents in insects atleast, but that's about it.
 
Invertebrate neurotransmission is quite different to ours, even to the extent of some neurotransmitters having completely different modes of action and function than in vertebrates.

For instance GABA has a purely excitatory role in insects, playing a similar role in them to acetylcholine in mammals at the neuromuscular junction.

In vivo, an AMPA antagonist would most likely cause unconsciousness at sufficient doses.

AMPAr repetitive activation is required for opening of the NMDA receptor ion channel, which acts in a sense, as a detector of co-incidental activity on the parts of pre- and postsynaptic neurones, and which is required for longterm potentiation, a key part of synaptic plasticity, and its involved in the learning and memorising process in the hippocampus and entorhinal cortex especially.

AMPA antagonists have been investigated as neuroprotective agents and antiepileptic drugs, but given the key role of AMPAr type glutamate receptors in memory retention and learning they are going to take a humongous dump on your ability to memorise anything.

Look at what happens when they get burnt to a frazzle by AMPA-targeting excitotoxins such as domoic acid, the marine dinoflagellate toxin responsible for amnesic shellfish poisoning, one gets first seizure activity then permanent short term memory loss due to selective destruction of the hippocampi and amygdala.

An antagonist at AMPArs will have similar memory-impairing effects because it effectively shuts down excitatory activity and thus LTP in the hippocampus, although of course temporarily in a concentration-dependent manner.

That said, agonists at AMPA are really nasty and cause permanent brain damage if nothing worse, antagonists will cause temporary blockade of memory formation, although positive modulators (AMPAkines) show some very interesting potential as powerful nootropic agents augmenting wakefulness, attentiveness and memory formation, I'm looking forward to trying one (sunifiram) myself, I just have to wait until my next payday to get a few things still needed for the synthesis.

Could do with it too, my memory is absolutely buggered after a nasty love affair with barbs a few years ago.
 
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