Quote (TheMagicFlightBox @ Sep 19 2014 10:20pm)

Any alterations in motor learning pattern? example would be trying to learn guitar while stoned versus sober.

Quote (ViviLOL @ Sep 19 2014 10:18pm)

That would be pretty sick, still don't believe you live in West Virginia with the way you speak 

Quote (Balla @ Sep 19 2014 06:25pm)

Yeah they've shown inhibition of learning motor tasks too.. aka it indeed affects the cerebellum as well. I don't think it's robust or anything, but noteworthy.



Haha I'm hoping to leave this shithole as soon as I can.

Quote (Balla @ Sep 19 2014 10:02pm)

Just general constant CB1/CB2 mediated transduction events. The problem w/ the constant activation is as it inhibits cAMP signaling events, it will generally inhibit CREB, which is integral for long-term memory and may induce LTD. It can also, via activating COX-2, cause AMPA receptor internalization, further opposing memory formation. Even use everyday SHOULD be fine (idiosyncrasies always govern, remember), assuming it's only some, say, once a night.. a bowl pack maybe. Then the effects cannot manifest so robustly. Further long term changes, though generally only seen with chronic & heavy use, would be shifts in PFC DA as well as alpha wave power, manifesting as quasi-ADHD symptoms while not under the influence.

As for the use at night, if you ARE going to use at night to sleep, make absolutely certain you use melatonin. It can inhibit the NE mediated melatonin synthesis in the pineal.. so supplementing melatonin helps ensure full REM.
I generally use every single night for quite some time now and I've suffered no hinderence, anecdotally. I think it may also help "unclog" my synapses via LTD induced synaptic pruning of the weakly formed synapses (ie memories I place no merit or salience on remembering are forgotten). I have actually noticed with some things such as names, I've gotten worse at recalling and I think that may be the cause. I truly do not care or place any salience on it, thus the synapses are weakly formed, and cannabis can come through and whipe it out, luckily. If done right, you should generally only notice true memory impairment while actually high, and that's mostly manifest in working memory and not full on long-term storage. That's because the CB1 receptors are located presynaptically, so it's a unique form of LTD, whereby it inhibits transmitter release (and decreases vesicular pool recycling), but given a robust enough stimulus & transmitter firing, LTP in the postsynaptic spine will still ensue just fine.
While on the subject, I wrote that previous post on the last page while high and heavily sleep deprived and hardly remember even writing it lolol. I'm surprised it was coherent at all.

Quote (ViviLOL @ Sep 19 2014 10:26pm)

Come to cali, there are so many sloots here.


annnnd

SUPER DANK WESTCOAST NUGZ!

Quote (Balla @ Sep 19 2014 06:50pm)

Prob applying to med schools mostly along the east coast or east in general
ie Duke, UK, VT, WVU, etc

Quote (noob_whacker @ Sep 19 2014 10:49pm)

to the uneducated majority here, it was hard to understand lol

Quote (ViviLOL @ Sep 19 2014 10:52pm)

You should apply to some UC's in california, they're pretty gg too.

Quote (Balla @ Sep 19 2014 10:54pm)

Just know.. I know most of this stuff in quite a lot of detail. If you want me to dumb it down or want specific clarification, just ask and I'll remove jargon for you.



Maybe. I'm really not sure. Taking MCAT this Jan, so in feb I'll know where I stand and where I even should apply lol

Quote (Balla @ Sep 20 2014 12:02pm)

Just general constant CB1/CB2 mediated transduction events. The problem w/ the constant activation is as it inhibits cAMP signaling events, it will generally inhibit CREB, which is integral for long-term memory and may induce LTD. It can also, via activating COX-2, cause AMPA receptor internalization, further opposing memory formation. Even use everyday SHOULD be fine (idiosyncrasies always govern, remember), assuming it's only some, say, once a night.. a bowl pack maybe. Then the effects cannot manifest so robustly. Further long term changes, though generally only seen with chronic & heavy use, would be shifts in PFC DA as well as alpha wave power, manifesting as quasi-ADHD symptoms while not under the influence.

As for the use at night, if you ARE going to use at night to sleep, make absolutely certain you use melatonin. It can inhibit the NE mediated melatonin synthesis in the pineal.. so supplementing melatonin helps ensure full REM.
I generally use every single night for quite some time now and I've suffered no hinderence, anecdotally. I think it may also help "unclog" my synapses via LTD induced synaptic pruning of the weakly formed synapses (ie memories I place no merit or salience on remembering are forgotten). I have actually noticed with some things such as names, I've gotten worse at recalling and I think that may be the cause. I truly do not care or place any salience on it, thus the synapses are weakly formed, and cannabis can come through and whipe it out, luckily. If done right, you should generally only notice true memory impairment while actually high, and that's mostly manifest in working memory and not full on long-term storage. That's because the CB1 receptors are located presynaptically, so it's a unique form of LTD, whereby it inhibits transmitter release (and decreases vesicular pool recycling), but given a robust enough stimulus & transmitter firing, LTP in the postsynaptic spine will still ensue just fine.
While on the subject, I wrote that previous post on the last page while high and heavily sleep deprived and hardly remember even writing it lolol. I'm surprised it was coherent at all.

Quote (FrozenWater @ Sep 20 2014 03:57am)

how do you know that you wouldnt 'prune' any weakly formed synapses that are formed from studying?

Quote (et3rnal @ Sep 19 2014 07:11am)

smoke then work out. that's fun, and keeping your mind off food is the hardest part lol