10.2.07

Neurotransmitters Pt. 2~ Chemical Transmission-A Bit Of History

This my second post on Neurotransmitters. I found, as I reread my last post on this subject, that there were several parts I had to read twice (or more) to get them into my head even though this is a book I've read before. I seem to always find new things in books I reread. I don't know if this is because I don't pay enough attention the first time or if the author is just that clever. Maybe it's just that I hadn't had enough caffeine to put my brain in drive. Regardless, I think I'm going to try to make the text a little more plain just so that I can understand it better and I hope that anyone else who reads this might understand it better. It's very important to me for things to be understandable. I've read some books in school and on my own in which I thought the author was being paid by the word, just because the text was so wordy and the words so uber-scientific. I just think things should be said in the most uncomplicated way possible. I hope y'all don't mind. I'm not trying to "dumb it down" or anything. Like I said before, assimilation is everything when it comes to understanding things. Everyone assimilates information in a different way because we are all unique individuals. Thank God.

So, on with it then. Yes?

Chemical Transmission
The origins our our modern understanding of chemical transmission in the brain can be traced to the middle 1800s, in France. Explorers, long before, had brought back from South America an arrow poison called curare, which natives smeared on their blowgun darts to paralyze prey. Claude Barnard, the founder of the science of pharmacology, used frogs to study how curare paralyzes. When he applied a mild electric shock to a nerve in the frog's leg, the leg muscle contracted; but if he had first injected the frog with curare, it did not. So, either the electrical stimulus was not reaching the muscle, or the muscle itself was not responding to it. Bernard didn't know which of these guesses were true, so he soaked the nerve in a curare solution without exposing the muscle to the poison. No paralysis resulted; so it seemed that curare must paralyze the muscle directly. To his great surprise, however, when he soaked the muscle (but not the nerve)in curare and then shocked the muscle directly (not through the nerve), it contracted normally, even though it would not respond to nerve stimulation. Bernard was forced to conclude that curare acted neither on nerve nor on muscle tissue.

In 1909 in England, at the University of Cambridge, J.N. Langley discovered that nicotine, applied directly to the neuromuscular junction(Wikipedia's deinfinition of the neuromuscular junction), made the muscle contract; and remarkably, this action of nicotine could be prevented by curare. No nerves were needed; even if they were destroyed, nicotine made the muscle contract, and curare prevented the nicotine action. The fact that curare could also block nerve impulses, as Bernard had shown years before, suggested to Langley that a nerve might normally stimulate a muscle by releasing a chemical like nicotine, which would act on the neuromuscular junction and make the muscle contract. Since various other substances he had tried did not do this, he also had to suppose that the neuromuscular junction contained some kind of specialized material which nicotine, as well as the postulated (guesstimated) substance released by the nerves, would act. Langley called this hypothetical material receptive substance, a name later shortened to receptor.

Shortly after, in London, H.H. Dale discovered that visceral smooth muscles (like the intestine, bladder, or pupil of the eye) behaved very differently from the skeletal muscles studied by Bernard and Langley. Nicotine did not stimulate them to contract, but a mushroom poison called muscarine did. Curare did not prevent the action of muscarine, but a plant poison called atropine did. So, the receptors on the smooth muscle, which responded to muscarine and were blocked by atropine, were called muscaranic receptors. Dale's experiments first showed clearly that receptors were specific; nicotine and curare acted only on nicotinic receptors, muscarine and atropine only on muscaranic receptors.

It was not until the 1930s that the hypothetical substances released from nerve endings by nerve impulses which caused different types of muscles to contract were discovered. It was proved, in a famous experiment conducted by the Austrian pharmacologist Otto Loewi, that nerves actually did transmit their messages by means of neurotrasmitters released from nerve endings. This was shown by using a frog heart, with its nerve intact, placed in a small container of salt solution; it continued to beat. In another container there was placed a second heart. Fluid from the first container, when it was transferred to the second container, had no effect. Loewi slowed the beating of the first heart by stimulating its nerve electrically, then transferred the bath fluid to the second container. Remarkably, the second heart slowed, even though its nerve had not been stimulated. This proved conclusively that some substance released by the nerve onto the first heart had slowed it; and that the same substance, transferred with the bath fluid to the second heart, had slowed it, too. (Dale and Loewi shared the Nobel Prize in 1936 for their discoveries about chemical transmission.)

A few years later, the substance released by nerves in these experiments was found to be acetylcholine, the first of many neurotransmitters to be recognized. Langley's nicotinic receptors and Dale's muscaranic receptors were actually two types of acetylcholine receptor-the nicotinic one on skeletal muscle, the muscarinic one on visceral smooth muscle and heart.

Acetylcholine turned out to be responsible not only for neurotransmission from nerve to muscle, but also from nerve to nerve, as in the brain. The junction (called a synapse)where the ending of one nerve contacts another is-like the neuromuscular junction-a microscopically tiny gap. A neurotransmitter released into this gap from the ending of one neuron can cross over to one of the nearby processes (called dendrites [Miriam Webster Online's definition of dendrites] on another neuron, and there it can stimulate a specific receptor. In this way, a "message" is transmitted across the synapse to the second neuron. Sometimes, if the right receptor is present on the nerve ending, a neurotransmitter can act back on the same nerve cell from which it was released, in a kind of feedback loop.

Nicotinic and muscarinic acetylcholine receptors are found in many regions of the brain, and acetylcholine is one of the brain's most abundant neurotransmitters. Nicotine, when delivered to the brain in a smoker's blood, combines with certain nicotinic receptors, mimicking the actions of acetylcholine.


That's how addiction starts: whichever addictive drug is introduced into the body mimicks the action of acetylcholine or another neurotransmitter, preventing that neurotransmitter from "locking" into its specific "keyhole". As more and more of the drug is introduced into the body, the body will make less and less of that specific neurotransmitter for that specific function of the body because of the drug's mimicking action.


I never really liked History as a subject when I had to take in high school and I hated it when I took it in college. So, I hope this wasn't too boring. I just wanted to give a bit a background info about the main people responsible for originally studying neurotransmitters and chemical transmission in the hopes that it will later blend in, or complete, the rest of the info.


Text taken from: Addiction:From Biology to Drug Policy; Avram Goldstein, M.D. author; pp 21-24



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