I agree that it DOES improve hearing. Consider what hearing actually is. It is the process by which waves emanating from a given source reach the ear, then get processed in the brain. Let's not disregard the latter arguably crucial part of this process.
I have yet to know the precise means by which it works. One possible avenue is acetylcholinesterase inhibition. Another could be direct cannabinoid receptor agonism. However it is of course the sum total of the cannabinoid actions at all relevant receptors that causes the subjective hearing enhancement.
What I have noticed: if I take harmala alkaloids then part of the pleasure is there, however it is not very close to marijuana at all. Then if I take cacao with an MAO-B inhibitor (Kava Kava), I experience an intensification of pleasure experienced with music. I am not normally the type of person to jump out of my seat at music and actively press play although I do LOVE music like many. Yet after a day of kava + cacao and then followed by a good dose of b. caapi the next day, I experience a sense of ecstasy just hearing music; the same kind of ecstatic anticipation and consumatory pleasure that you get from eating a really sour chewing gum type sweet; how every second of it is like a hot ember of juicy soury taste which seems to never stop; the sound is ecstatic in its own aural taste. That combination is great for both participatory and anticipatory anhedonia, I can attest to that much.
Cacao contains anandamide and phenethylamine which are two crucial endogenous chemicals of interest here, as they are heavily related to the endocannabinoid & reward pathways. Perhaps picamilon or phenibut may reproduce the phenethylamine aspect of it but as for the endocannabinoid stimulation I know of no natural way other than either cacao or cannabis itself. And I am not quite sure if anandamide in cacao permeates through the blood brain barrier either. Regardless, the subjective enhancement is very real and very much like cannabis.
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Cannabinoids inhibit sensory gating -
http://eprints.notti...ipt_revised.pdf"Direct numerical simulations of this model suggest that the basic mechanism for this effect can be traced to the suppression of inhibition of slow GABA
B synapses. Furthermore, by working with a simpler mathematical firing rate model we are able to show the robustness of this mechanism for the abolition of sensory gating."
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Associate Professor Fredrik Ullen believes his findings could help explain why.
He looked at the brain's dopamine (D2) receptor genes which experts believe govern divergent thought.
He found highly creative people who did well on tests of divergent thought had a lower than expected density of D2 receptors in the thalamus - as do people with schizophrenia.
The thalamus serves as a relay centre, filtering information before it reaches areas of the cortex, which is responsible, amongst other things, for cognition and reasoning.
"Fewer D2 receptors in the thalamus probably means a lower degree of signal filtering, and thus a higher flow of information from the thalamus," said Professor Ullen.
http://www.bbc.co.uk/news/10154775=====
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Our data indicate that activation of CB1 receptors interferes with neuronal network oscillations and impairs sensory gating function in the limbic circuitry, further supporting the connection between cannabis abuse and increased susceptibility of developing schizophrenia spectrum disorders.
Activation of cannabinoid-1 receptors disrupts sensory gating and neuronal oscillation: relevance to schizophrenia.=====
I think we need to get someone to hook themselves up to an EEG headset and smoke like cheech and chong, any takers? Rest assured this is an absolute smorgasbord of different receptors working in synergy.
Edited by BLimitless, 14 January 2013 - 05:51 PM.