Given its impact on our fight/flight response, and its generation of physical phenomena, such as sweating and tremor; it’s easy to understand why excesses in norepinephrine could trigger anxiety and panic.
It’s thought to go like this in a “normal” (dang, I hate that word) brain. Autoreceptors on a presynaptic neuron are responsible for receiving an assigned neurotransmitter from the neuron and releasing it in an effort to facilitate a synapse.
What’s known as an alpha-2 autoreceptor works exclusively with norepinephrine. As this autoreceptor is called-in for work, it actually slows down – brakes – the release of norepinephrine. And, naturally, when the braking stops, the secretion of norepinephrine cranks up again.
But wouldn’t you know it, our particular brains lean toward being anything but “normal,” so here’s how things may well go down with us.
An outpouring of norepinephrine occurs because its alpha-2 autoreceptor doesn’t hit the brakes. And that could be because it’s been antagonized, or blocked.
How does that happen? Well, it could be because of the introduction of what’s known as an alpha-2 autoreceptor antagonist, such as caffeine or yohimbine.
But what if one has a bunch of alpha-2 autoreceptors that are just plain acting silly, without the involvement of an antagonist, and levels of norepinephrine become excessive?
See, it happens; and scientists don’t know why. Well, the fix for this issue may be medicines known as alpha-2 autoreceptor agonists, which increase the flow of norepinephrine. This provides more neurotransmitter in the synapse, which results in a signal being sent to turn off the norepinephrine spigot, allowing anxiety to subside.
Alpha-2 autoreceptor agonists include the antihypertensives, clonidine (Catapres) and guanfacine (Tenex), and the beta-blocker, propranolol (Inderal).
Have I confused you enough? This stuff is tricky, but fascinating.
And there’s even more. Why don’t you come back and see us tomorrow?