Dr. leigh on the pharmacology of marijuana

August 10, 2009

HAHAHAHAHAHHAHHA! Okay dope fans….go beat up on the new doc in town for awhile….

CB1 receptors affect the function of the presynaptic terminal. When CB1 receptors are activated, they signal through G proteins to close calcium channels, preventing entry of calcium into the terminal. Calcium is needed for vesicles to fuse with the membrane and release inhibitory neurotransmitters into the synapse. So CB1 signaling stops inhibitory neurotransmitters from being released to the postsynaptic neuron. CB1 receptor activation also results in opening of potassium channels. In a resting neuron, these channels are closed. Outflow of positively charged potassium ions leads to increases in the net negative charge across the membrane. This is called hyperpolarization, the opposite of depolarization. As you might imagine, since depolarization causes neurons to fire, hyperpolarization keeps a neuron from firing. This further decreases the chances that neurotransmitter will be released from the presynaptic terminal. There are some other effects too, which I won’t detail here.

Now let us see, do you think this closing bit is a tad optimistic?

I hope that this helps to make the effects of marijuana make more sense. For the record, I am not interested in discussing policy or the legal status of the drug. I am just here writing about how it works.

No Responses Yet to “Dr. leigh on the pharmacology of marijuana”

  1. leigh Says:

    a zillion hits via stumbleupon, but crickets chirping from the drug policy mouth-foamers. heh.


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