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Noradrenergic cell groups

From Wikipedia, the free encyclopedia

Noradrenergic cell groups refers to collections of neurons in the central nervous system that have been demonstrated by histochemical fluorescence to contain the neurotransmitter norepinephrine (noradrenalin).[1] They are named

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  • Sympathetic Nervous System: Crash Course A&P #14
  • The Adrenergic Receptors
  • Nervous System: Acetylcholine (ACh) and Norepinephrine (NE) Receptors

Transcription

So you’re sound asleep, when your smoke alarm goes off. Before you even know what’s going on, you start to feel it. Those smoke alarms are loud -- for a good reason. Your heart starts to race, your breathing picks up, you become sweaty all over your body. You are stressed. And I’m not talking about the my-iPhone-just-died kind of stress. I’m talking about the I’m-afraid-I-might-die kind of stress. Even though it’s often seen as a dirty word, stress, like pain, isn’t all bad -- it’s actually very useful if you’re, y’know, trying to get out of a burning building. Your sympathetic nervous system is the part of your nervous system that responds to stress, and it does its job exceedingly well by focusing on what your body needs to do right now. Like, when you’re facing a life-or-death ordeal, you don’t need to be digesting that cashew cluster in your intestines, or producing reproductive cells, or fighting off an infection. That’s all stuff that you can deal with later, when you’re out of harm’s way. So your sympathetic nervous system sweeps these suddenly trivial functions aside to blast all of your energy to your brain and heart and muscles to deal with the threat at hand. So, this is where I tell you that you’re lucky to have a sympathetic nervous system. And that it keeps you alive. And that you would probably die in X Period of Time if you didn’t have one. All of which is true. But here’s the thing: the problem is, nowadays our bodies’ stress responses are triggered all the time, practically every day, even when we are not in mortal danger. I mean, worrying about paying your wireless bill or being late for an important meeting -- those things are terrible, but they will not kill you. But, good luck explaining that to your nervous system. Because your physiological responses to non-immediate stresses are largely the same as when you’re fighting for survival. So, if stress is, like, ruining your life, that’s why. And that’s part of the reason that should get to know how it works. Because by learning about your sympathetic nervous system, you come to understand one of the key players in the physiology of stress. You may recall from our tour of the anatomy of your autonomic nervous system, that in both your sympathetic and parasympathetic divisions, almost every signal has to cross two synapses. Each neuron travels from its root in the spinal cord to a ganglion, where it synapses -- and yes, that is a verb as well -- with another nerve fiber. And that one, in turn, leads to an effector organ, where it synapses again to create whatever response was signaled -- like sending more blood to your skeletal muscles, or making your heart pump faster. But you gotta wonder -- or at least I gotta wonder: how do these neurons and effectors actually communicate with each other? And how do all of those signals result in the high-octane sensations that we know as “stress”? By and large, the stress response includes two kinds of chemicals, both of which I’m sure you've heard of. The first, of course, are neurotransmitters. These are made and released from neurons themselves, and like we talked about in our lesson about synapses, they are what neurons use to communicate with each other -- or their effector organs -- across a synapse. The other chemicals involved in stress are hormones, which are secreted by your glands. There are at least 50 different hormones at work in your body right now, and they do everything from regulating your sleep cycles to making your body retain water so you’re not dying of dehydration all over the place. I’m telling you all of this now, up front, because hormones and neurotransmitters are 100% necessary for understanding how your sympathetic division ultimately works. BUT! When you trace a single sympathetic signal, from the initial stimulus to the final response, those chemicals can be kind of hard to keep track of. That’s because the very same substance can have different effects -- actually, sometimes, totally opposite effects -- depending on where it’s received in your body. And to make things even more fun, even though neurotransmitters are part of your nervous system, and hormones are products of your endocrine system, a compound can be considered either a neurotransmitter or a hormone -- even though it hasn’t changed one iota -- depending on where it happens to be operating in your body. So all of this can make understanding your stress responses pretty confusing! You might even say … stressful! All right, we’re going in. The smoke alarm wakes you up. You smell smoke. It is time to move muscles. Fast. Your brain sends action potentials down your spinal cord and preganglionic neuronal axons. Those signals flow all the way to their ganglia. When the signals reach the synapses inside the ganglia, the nerve fibers then release a neurotransmitter -- called acetylcholine, known to its friends as ACh. If you haven’t heard of acetylcholine yet, you’re gonna wanna remember that name. In addition to working in sympathetic ganglia like this, it’s also what the rest of your peripheral nervous system and lots of your central nervous system uses to communicate. So when it comes to nervous communication, ACh is really the coin of the realm. The premium currency. So, that acetylcholine crosses the synapse and, if there’s enough of it, it can stimulate action potentials in several neurons on the other end -- in the postganglionic fibers. That’s all it does, but it’s important. It’s basically a signal booster. Those postganglionic neurons then carry the action potential to the effector organs -- in this case, let’s say your leg muscles, which are going to need an influx of blood if they’re going to hustle you out of that house. And at the end of that second, postganglionic neuron, the fiber releases a different neurotransmitter. This one’s called norepinephrine. And it is always norepinephrine that’s released from postganglionic fibers in the sympathetic nervous system. It’s what crosses that final synapse and creates a response in the effector, like opening up blood vessels that lead to the leg muscles. So, the preganglionic fiber releases ACh, and the postganglionic releases norepinephrine. Boom. Congrats. Your life is on its way to being saved. But, your body has more than one mechanism for responding to things, especially things like a burning house. There’s another alternative for getting the message out. I mentioned those hormones, remember? In addition to nerve fibers that lead to ganglia and then your effectors, there’s also a set leaving the spinal cord that goes directly to your adrenal glands. Like all preganglionic fibers, these release acetylcholine, too. But here, the signal doesn’t end up in another neuron that triggers blood vessels to open or whatever. Instead, it triggers your adrenal medulla to release a flood of epinephrine and norepinephrine -- hormones that rush through your bloodstream toward your heart, lungs, and other organs. Now, hold up! Did you notice what I just said? Yeah, I said the adrenal glands release norepinephrine as a hormone. Whereas in that first scenario I said that norepinephrine was a neurotransmitter that sent the final signal to control blood flow to the leg muscle. Now, how can I say both of those things? Because they’re both true. Norepinephrine is BOTH a neurotransmitter and a hormone, and which one it is depends on how it’s being used. If it’s being released from a neuron and travelling across a synapse, we refer to a messenger chemical -- no matter what it is -- as a neurotransmitter. If it’s being secreted by a gland into the bloodstream for more widespread distribution, it’s a hormone. Even if it’s the same chemical. And to an effector, hormonal norepinephrine is just as good as neurotransmitter norepinephrine. But as scientists, we describe them differently, because they’re functioning differently. Now, the ways in which a neurotransmitter-slash- hormone like norepinephrine works, is a good example of another confusing aspect of your sympathetic nervous system. Because it works by both stimulating and inhibiting the same systems in your body at the same time! So, in our house-burning scenario, the norepinephrine your system releases causes an increase of blood flow in some parts of your body -- like your leg muscles -- while restricting blood flow in other places where it’s not urgently needed -- like your guts. How can the same chemical cause opposite responses? Well, it all depends on the particular kind of receptors that an effector has for receiving that chemical. In the case of norepinephrine, its effector is smooth muscle -- the muscle that controls all of your involuntary functions of hollow organs, like the stomach, and bladder, and also your blood vessels. On the smooth muscle cells controlling some blood vessels, there are receptors called alpha receptors -- when norepinephrine, or epinephrine, bind to those receptors, they make those smooth muscle cells contract, thereby restricting blood flow. But on smooth muscle cells that control other blood vessels, there are lots of beta receptors for epinephrine and norepinephrine, and when they are activated, they make the muscles relax, letting more blood flow through. So it makes sense that the smooth muscle around your blood vessels, which feed your skeletal muscles -- which you’ll need to get out of that smoky house -- are covered in beta receptors. Because you want those blood vessels to relax, and provide plenty of oxygen to the muscles in your arms and legs. And since running away is more important than digesting your dinner, the blood vessels leading to your stomach and intestines have lots of alpha receptors, which reduce blood flow to those areas, because that burrito can wait until you’re out of the house. So, there’s a lot going on in your sympathetic responses. And much of it can seem complicated, or even contradictory. But the thing is, all of these functions work together to create a full-body response, which is exactly what you need in an emergency. After all, it wouldn’t do you much good to speed up your heart without sending that blood to your muscles, where it’s needed. It’s up to those neurotransmitters and hormones, and the receptors on the corresponding effectors, to make sure that everyone is on the same page. So, the system works well. Really well. Sometimes, too well. Remember when I said at the beginning, how your body doesn’t know life-threatening stress from life-annoying stress? Since your body’s reaction tends to be a full-body response either way, it can become pretty taxing over time. I mean, we’re talking about throwing parts of your body into overdrive, while depriving others of blood and oxygen. That’s not something you want happening every morning. So the irony here? The real kick in the head? It’s that non-life-threatening stressors can actually end up endangering your life in the long run, because your body’s stress response is so effective. The frequent activation of your sympathetic nervous system, and the triggering the other part of your stress response -- the part that’s driven by hormones -- can have nasty consequences, like high blood pressure, digestive problems, and even the suppression of your immune system. So what your body needs to do is figure out how to relax. Rest and digest. Feed and breed. That is where your sympathetic system’s more mellow half-brother, the parasympathetic system comes in. And yeah, that’s what we’re gonna be talking about next time. For now you learned that your sympathetic nervous system controls your body’s stress response and how the signals in your sympathetic nervous system travel to an effector, using the neurotransmitters acetylcholine in the ganglion and norepinephrine at the effector. And you learned that other signals can go right to the adrenal glands, where norepinephrine and epinephrine are secreted as hormones. And you also learned that the same messenger chemical can evoke different responses depending on the receptors, with alpha receptors causing smooth muscles to constrict, for example, while beta receptors cause smooth muscle to relax. A big shoutout and thank you to our Headmaster of Learning, Thomas Frank, whose generous contribution on Patreon helps keep Crash Course alive and well for everyone. Thank you, Thomas. If you want to help us keep making great videos like this one, check out patreon.com/crashcourse This episode of Crash Course was co-sponsored by Harry Brisson, David Thompson, Jason Constam, and Tuseroni. Crash Course is filmed in the Doctor Cheryl C. Kinney Crash Course Studio. This episode was written by Kathleen Yale, edited by Blake de Pastino, and our consultant, is Dr. Brandon Jackson. Our director and script supervisor is Nicholas Jenkins, the editor is Nicole Sweeney, our sound designer is Michael Aranda, and the graphics team is Thought Café.

See also

References

  1. ^ Fuxe K, Hoekfelt T, Ungerstedt U (1970). "Morphological and functional aspects of central monoamine neurons". International Review of Neurobiology. 13: 93–126. doi:10.1016/S0074-7742(08)60167-1. ISBN 9780123668134.
  2. ^ Smeets WJAJ, Reiner A (1994). "20:Catecholamines in the CNS of vertebrates: current concepts of evolution and functional significance". In Smeets WJ, Reiner A (eds.). Phylogeny and Development of Catecholamine Systems in the CNS of Vertebrates. Cambridge, England: University Press. OCLC 29952121.
  3. ^ German DC, Bowden DM (1975). "Locus ceruleus in rhesus monkey (Macaca mulatta): a combined histochemical fluorescence, Nissl and silver study". J Comp Neurol. 161 (1): 19–29. doi:10.1002/cne.901610104. PMID 48520. S2CID 1022935.
  4. ^ Felten DL, Sladek JR Jr (1983). "Monoamine distribution in primate brain V. Monoaminergic nuclei: anatomy, pathways and local organization". Brain Research Bulletin. 10 (2): 171–284. doi:10.1016/0361-9230(83)90045-x. PMID 6839182. S2CID 13176814.

External links


This page was last edited on 2 November 2022, at 10:27
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