Do we have THC receptors in our brain or not? If so, it would seem a pity to waste them?

Question

Are they there? There seems to be some dispute, from what I've read. Or is it down to the old dopamine?

http://www.druglibrary.org/schaffer/hemp/BRAIN.HTM

Answer 1

memory loss ....
well actualy thats just to do with being vaige so we loose our edge !

so not being sharp is where the memory loss okers

not bothering is why totaly man
its the attitude not a direct problem
to loose is to vague
so it goes we dont remember as much
and dident work also making the memory refreash less likely

Answer 2

No a receptor is a protein on the cell membrane or within the cytoplasm or cell nucleus that binds to a specific molecule (a ligand), such as a neurotransmitter, hormone, or other substance, and initiates the cellular response to the ligand. Ligand-induced changes in the behavior of receptor proteins result in physiological changes that constitute the biological actions of the ligands.The THC receptors act like a keyhole, and are the binding sites for various brain chemicals (neurotransmitters). When neurotransmitters are attached to the receptors they instruct brain cells (neurons) to activate and regulate various brain and body functions.

Dopamine is one such neurotransmitter. It originates in the ventral tegmental area of the brain, and is associated with the feeling of pleasurable sensations (being high)

Answer 3

Anandamides inhibit binding to the
muscarinic acetylcholine receptor
by
Lagalwar S, Bordayo EZ, Hoffmann KL,
Fawcett JR, Frey WH 2nd
Department of Neurology,
Alzheimer's Research Center,
HealthPartners, Regions Hospital,
St. Paul, MN 55101-2595, USA.
J Mol Neurosci 1999 Aug-Oct; 13(1-2):55-61

ABSTRACT
Loss of memory and cholinergic transmission are associated with both Alzheimer's disease (AD) and marijuana use. The human brain muscarinic acetylcholine receptor (mAChR), which is involved in memory function and is inhibited by arachidonic acid, is also inhibited by anandamides. Two agonists of the cannabinoid receptor derived from arachidonic acid, anandamide (AEA) and R-methanandamide, inhibit ligand binding to the mAChR. Binding of the mAChR antagonist [3H]quinuclidinyl benzilate ([3H]QNB) is inhibited up to 89% by AEA (half-maximal inhibition at 50 microM). Binding of the more polar antagonist [N-methyl-3H]scopolamine ([3H]NMS) is inhibited by AEA up to 76% (half-maximal inhibition at 44 microM). R-methanandamide inhibits more than 90% of both [3H]QNB binding (I50 = 34 microM) and [3H]NMS binding (I50 = 15 microM) to the mAChR. Both AEA and R-methanandamide stimulate mAChR binding of the agonist [3H]oxotremorine-M at low concentrations (25-75 microM), but significantly inhibit agonist binding at higher concentrations (I50 = 150 microM). The cannabinoid antagonist SR141716A did not alter AEA or R-methanandamide inhibition of [3H]NMS binding to the mAChR, even at concentrations as high as 1 microM. Further, the cannabinoid agonist WIN 55212-2 does not alter antagonist binding to the mAChR. This demonstrates that mAChR inhibition by the anandamides is not mediated by the cannabinoid receptor. Since AEA and R-methanandamide are structurally similar to arachidonic acid, they may interact with the mAChR in a similar manner to inhibit receptor function.

Answer 4

We probably have receptors, but THC receptors I don't know.I will have to smoke and ponder this question some more.

Answer 5

Yes.

Answer 6

Its all about the dopamine.

Answer 7

Lemme' check.


*pfffffffffffffft*















what was the question?

Answer 8

put that bong down!!!!