Neurotransmitters and You: The basics of how neurons work and are affected by drugs. - General

Neurotransmitters and You: The basics of how neurons work and are affected by drugs.

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This is the [I]quick[/I] guide to some of the basics behind how the brain communicates both chemically (which involves neurotransmitters) and electronically (action potentials and ionic charge). [B]What am I going to learn?[/B] Since neuropsychology is such a huge field and has the capability of being incredibly complicated, I'm going to restrict this to: 1) A brief summary explaining and labeling the parts of a neuron 2) How the neuron communicates via action potential and what an action potential is 3) How the neuron communicates via neurotransmitters and what parts of the cell is responsible 4) Drugs .....a) agonists and antagonists .....b) excitatory vs inhibitory .....c) competitive vs non-competitive .....d) How drugs can change the way it communicates (once you are done here you can go to wikipedia and under Pharmacology of the drug it explains exactly what it is and does like explained here) .....e) Cannabis (understanding how and why we get high) [B]Damn, this shit sounds hard. Do I have to know anything before reading?[/B] Well, a basic understanding of biology, chemistry, and physics would help, but I'm not going to blurt out things like electrostatic pressure without explaining it. A high school level of biology, physics, and chemistry would just make things easier to understand like the aforementioned property. Since I know there are some people who havent had those classes and/or are on the younger side, the guide should be fairly easy to understand since I learned from a professor that was very good at simplifying things to make them easier to understand and I dont mind explaining everything in detail. [B]Ok thats cool, but after I'm done reading this totally awesome lecture, what are we going to post?[/B] Anything pertaining to the brain whether it be neuropsychology, physiological psychology, biology, chemistry, or physical properties pertaining to brain function. My professor is currently involved in research on brain plasticity and has explained to the class ways of chemically controlling the brain by messing with ions and other material in the brain. That topic for example could be explained further with this new found knowledge you acquired in this thread. As I explain some of these topics in the original post, I might drift off for a little on these mini-topics that I've learned about in class, so if I do and you want to learn more post about it and I will get to it. -------------------------------------------------------------------- [B]The Neuron[/B] [img]http://employees.csbsju.edu/hjakubowski/classes/ch331/signaltrans/neuron3a.gif[/img] This is a multipolar neuron. The most important parts are the dendrites, the soma, the axon, and the terminal buttons. In this diagram the information would travel from left to right. Dendrites are where the neurotransmitters attach and the information goes from there, through the cell body (soma), down the axon and to the terminal buttons. The terminal buttons is where neurotransmitters are released, where another neuron or specialized cell will receive the information and continue on. Now at the ends of the terminal buttons you have the synapse which looks like this [img]http://employees.csbsju.edu/hjakubowski/classes/ch331/signaltrans/neuron3b.gif[/img] This is where neurotransmitter release happens. I will go into further detail of this later in the neurotransmitter section, but this is where the chemical aspect of communication happens. Now lets zoom in and look at the surface of a neuron's cell wall. [img]http://www.icagen.com/media/images/DrugTargets.jpg[/img] This is a intercalated protein, more specifically an ion channel. Intercalated proteins are holes in the cell wall that allow ions in and out of the cell. You have 3 types of these proteins: Ion channels: these allow ions into the cell such as sodium, potassium, chloride, and sometimes calcium (INTERESTING CONCEPT REGARDING WHAT Ca DOES) Transporters: these actively move ions and sometimes complex molecules in and out of the cell, however this requires energy Detectors: definition is in the name, they detect the presence of substances, for example hormones, on the outside of the neuron but does not typically allow movement of these substances into and out of the neuron These are found all over the cell, including the dendrites, soma, terminal buttons, and axon (unless its myelinated, ill get to this later). The most important one is the ion channel, I will mention transporters later, but ion channels is where the action happens. -------------------------------------------------------------------- [B]Action Potentials: The Electronic Aspect of Neuronal Communication[/B] Action potentials is how the neuron transfers information from the dendrites down to the terminal buttons. Let's start by explaining a huge discovery that was made not too long ago. Scientists always thought that the cell wall of neurons where impermeable, this means they thought the cell wall was a perfect seal and no ions or molecules could enter the cell without intercalated protein effort. They took an axon of a giant squid and put it into a petri dish. In the petri dish they radioactively labelled the liquid in the dish surrounding the axon. To make it easier to understand, imagine the radioactive liquid as being blue food coloring. If the axon turns blue on the inside by just sitting in the liquid with [B]no[/B] action potential, then that means the liquid seeped into the cell showing that the neuron's cell wall is not impermeable. This means the cell has to constantly pump in outside fluid in since the cell wall isnt perfect and inner contents sometimes leaks out. This is where transporters come in. They actively pump in and out ions to keep the neuron in a special state. Another amazing discovery was made when they tested the electronic charge of a neuron compared to its surroundings. This is where the electronic aspect of communication comes in. The neuron at a resting state is actually [B]negatively charged[/B] (polarized) compared to the outside. Now lets look at this graph, probably one of the most important/famous graphs in physiology psychology and one you will always go back to. [img]http://hyperphysics.phy-astr.gsu.edu/hbase/biology/imgbio/actpot.gif[/img] Ok for those of you who may not be good at reading graphs I'm going to go real slow on this part. First lets look at the scaling aka how the graph is set up. On the left you have the [B]difference[/B] of voltage, comparing the charge of the inside of the neuron to the outside. The voltage difference is very tiny and is measured in millivolts (mV). This graph goes into the negative and positive values. The perfectly horizontal line at 0 means zero charge (that means at that value/point on the graph the charge between the inside and outside of the cell is none, no charge/neutral). When you go above that line you have a positive charge, meaning the inside of the cell is now positively charged. When you go below 0 charge into the negatives, that means the inside of the cell is negatively charged compared to the outside of the cell. [B]I want to make something clear, for some reason this graph is a little fucked up because the red line should be starting out from the -70 mV value[/B]. Keep that in mind. Ok, you see the red line starts at (what should be -70 mV), this is the neurons natural state. This is special, you would think it would want to be at 0 (neutral) charge since it would take less effort to stay that way. But this is the secret of how it communicates. So the cell actively stays at -70 mV as its resting state. Thats what the dotted line stands for, the resting state of a neuron. Now lets examine what is an action potential and how its caused. [img]http://hyperphysics.phy-astr.gsu.edu/hbase/biology/imgbio/actpot4.gif[/img] Ok for now ignore the ion part of the graph, I will get back to it later and repost this image so you dont have to keep scrolling up to reference to it. First lets define polarization. You can see depolarization and hyper polarization. Depolarization means the cell is losing its charge by getting closer to zero. Hyper polarization (hyper in the medical field means an excess of something) means the cell is even more polarized/has more negative charge than its resting state, so that would be below the dotted line. Repolarization as shown in this graph is when the cell is gaining its negative charge back, really it should be labelled as plain polarization since it is becoming more negatively charged as it returns to its resting state. Now we can see a little tiny dotted line at the beginning of the line labelled 'gate threshold'. This is the value that a stimulus must pass in order to create an action potential. What I mean is that that value shown in that graph (-55 mV) is the point of no return as it comes to creating an action potential. I got a little ahead of myself, the action potential is the spike in the graph and it is this wave that causes a chain reaction that happens along the cell wall using intercalated proteins to send the electrical signal down the neuron. Ok back to the threshold, what causes it, what is a 'stimulus'? Well a stimulus can either be caused by a neurotransmitter, this happens at the synapse, more specifically at the dendrite. Here neurotransmitters activate ion channels that start the chain reaction that allows ions into and out of the cell, what this does will be explained in the next section. So once the chain reaction starts this wave happens thousands of times along sections of the cell wall with the ion channels. The action potential activates the ion channel, when activated it opens up to ions that change the charge of the neuron, this change continues down the cell all the way to the axon. Ok now I have to move on to the next part, its hard to talk about this without teaching how ions play a role in this. [img]http://filesmelt.com/dl/diffusion_and_electrostatic.png[/img] Sorry if its a little large. This is the neuron's cell wall, but before i explain this we need to know a little bit of chemistry and physics. Ok what is an ion? It is an element that has either an extra electron (negatively charged) or is missing an electron (positively charged), they are labelled as cation (pronounced cat-ion) which is positively charged, and anion (an-ion) negatively charged. Now you have two properties of physics that play an important part to action potentials. You have [B]electrostatic pressure[/B] and [B]diffusion pressure[/B], these two properties of matter dictate the behavior of ions and what they do in space. First lets look at diffusion pressure. This is my professors way of describing it, and its pretty easy to remember. Imagine you and your friends are at a party in a crowded house, you guys will represent the ions. You have two areas the living room and the kitchen. Now the keg is in the kitchen, so everyone wants to get into the kitchen and get their share. With everyone trying to cram into the kitchen you figure you'll wait in the living room since the kitchen is so crowded. The high concentration area is the kitchen and you dont like/want to be in there because its so crowded so you and a few people move out of the kitchen and [I]diffuse[/I], aka spread out, into the living room. Then all the beer is gone and everyone moves into the living room, you realize its getting crowded in there so you and some people disperse into the living room to balance it out. Matter likes to be evenly spaced out from each other. Second is Electrostatic pressure. This is easier to understand if you know a little bit about magnets. As you know with magnets, same signs (negative ion to a negative ion, or + to +) will retract or push away from each other, and that opposites (-+) attract. So lets say there is a space where for some reason there is a lot of positive ions near each other, they will spread out from each other because of this property. If there is a large concentration of them and they have nowhere to go, as soon as there is an opening to a more negative field, they will rush to that negative field to balance out the charge. In the keg party situation, imagine that it is the [I]want[/I] to go in and get a drink that attracts people into the kitchen. It wants the charge/beer. Now you may think that both of these properties would work together in reaching a homogeneous (balanced) state where the ions are happy. Problem is, this isnt the case. In fact both properties will often force the ions into a state that does not satisfy either physical property, and it is this phenomenon that the neuron manipulates to get information transferred through the cell. Let's look at the picture above. The bottom is the inside of the neuron and the top is the outside. We are going to ignore the A for now, since Na (sodium), Cl (chloride), and K (potassium) is way more used/important. Notice how the inside of the cell has a (-) signal showing negativity. Like I mentioned before it is negatively charged inside of a neuron. Also notice how the outside is positively charged as represented with a (+). This is important to remember so keep that in mind. Now K has a high concentration inside of the cell compared to the outside. This means according to the property of diffusion pressure, it wants to leave the cell into the lower concentrated potassium area. So you would think that K will want to leave the cell, however K is a cation (positively charged ion) so it WANTS to stay in with the negative field. This is just like what I mentioned before how both physical properties (electrostatic and diffusion) will fight each other to the point of neither of them being satisfied. In the graphic you can see this phenomenon being represented by the arrows next to the boxes. Notice how K has them going in opposite directions keeping K inside the cell in a higher concentration. Moving on to Na (sodium) you see something strange. Both arrows are point into the cell, meaning by BOTH electrostatic AND diffusion pressure Sodium wants to enter the cell. This is because a) Na is in higher concentration outside the cell wall, and b) it is a cation (positively charged) and wants to get into the negatively charged neuron. So, how does it do this? The only way for massive amounts of ions to get into the cell is by ion channels that are activated by action potentials and neurotransmitters. In this case we are going to talk about action potentials and the reaction they cause down the cell. Now remember how i mentioned that the cell wall isn't impermeable and does lose some ions and some seep in, well thats where transporters (the specified intercalated protein) comes in and keeps everything level. Since Cl is in the same situation as K, just on the outside wanting in, Im going to ignore it for now so we can move on to what actually happens during an action potential (finally). -------------------------------------------------------------------- [B]The Action of an Action Potential[/B] Action potentials are started by neurotransmitters at the synapse. The intercalated proteins at the synapse (on the dendritic surface) open up when activated and start the action potential by allowing floods of ions into and out of the neuron. Now because of all of these ions entering and leaving the cell, the cell's electrical charge changes and the neuron has to reset to its original charge by forcing some ions in and out. When the change in charge happens it activates ion channels along the cell wall which allows another flood of ions into and out of the cell; it is this chain reaction that I was talking about, and it keeps going all the way down the cell over and over again from each small section of ion channels to the other until it reaches the terminal buttons at the end of the neuron (which leads to neurotransmitter release or non-release). We need to look back at our graph from earlier, the one showing the ion flow during an action potential. You got the stimulus to go past the point of no return (gate threshold) and have activated the ion channels. The first thing to rush in is Na (sodium) because, as we learned before, it wants to enter the neuron both electrostatically and by diffusion. There are now tons and tons of positive ions entering the neuron, but the neuron wants to remain at -70 mV. All of this positive charge is making the neuron more positive as shown by the graph. The higher the line goes the more positively charged the inside of the cell becomes compared to the outside. In order to counteract this change, the ion channels for K open up so that it can release some of the positive charge (K is positive, by it leaving, it makes the cell more negative). Now it reaches a peak where the cell can be about 20-40 mV positive, thats when Na ion channels close and K keeps getting pumped out to bring the neuron back to -70 mV. (There is a slight difference between this graph and what i said, but this graph is different than the one i used in class so pay attention to more of what I say rather than that graph. This other picture with the cell wall and ions is from the powerpoint so that is current). So as the cell returns to normal it accidentally hyper-polarizes. Since the release of K was so much, it hasnt been able to leave the area around the cell. This makes the area more positive on the outside of the cell, making the difference more negative for the inside of the cell (remember the graph shows the [I]difference[/I] of charge between inside and outside). Once the potassium finally disperses everything goes back to normal. Its kinda like a party where you have a bunch of drunk people hanging around the house just after you end a party. This whole action potential happens in fractions of [B]milliseconds[/B] and can be repeated just as it returns to the rest potential line. So look at the graph, imagine several spikes, over and over again just as it gets back to the dotted line. I am going to leave out what happens at a mylinated axon when it comes to action potentials. If you want to know more about it, ask. But to keep this op as lean as possible I'm going to leave it out. -------------------------------------------------------------------- [B]Neurotransmitters: The Chemical Component of Neuronal Communication[/B] [img]http://i.imgur.com/KKeOo.png[/img] This is a terminal button (the top right figure), these are at the end of a neuron and are part of the synapse. These hang just above the synaptic gap and are responsible for the manufacturing of neurotransmitters and their release. The figure is pretty self explanatory. Inside the the terminal button is where neurotransmitters are created and they get packed into these small sacks called synaptic vesicles. These then attach to the cell wall and open up, releasing the neurotransmitters. The 'sack' that attached to the cell wall now becomes part of the cell wall. As more 'sacks' attach, they push older cell wall to the sides of the terminal button and are pinched into the cell, recycling the material. Neurotransmitters themselves are also recycled, after they are release and activate their designated ion channels they get sucked back into the terminal button via transporters. Neurotransmitter release is triggered by action potentials that send information down the cell to the terminal buttons. There you have parts of the cell like the Golgi Apparatus that create complex molecules used for neurotransmitters. [img]http://filesmelt.com/dl/neurotransmitter_binds.bmp[/img] This is the cell wall of the dendrite. The neurotransmitters connect to docks at the end of the intercalated protein which in turn opens or closes the channel. On the right we have a conventional neurotransmitter receptor. The transmitter will bind to the outside as seen above on the ring of the protein. Once it binds the channel will either open or close (depending on whether its an inhibitor or excitatory) for a very brief moment (fractions of milliseconds) and the neurotransmitter will unbind and either float around activating other intercalated proteins or be actively taken back up into the terminal button to be recycled. The figure on the left shows other kinds of 'docks' for the neurotransmitter to attach to. These are a little more complicated where they activate a G-protein that releases a chemical into the cell that [I]then[/I] binds to an intercalated protein to allow ions in. Even then it can go a step further and use an enzyme that creates a molecule called a "second messenger" and THAT then goes to the nucleus and other cell structures and changes your DNA. This change is whats linked to how we store memory and create personality, its groundbreaking stuff being researched right now at my university. My professor said how you can control what people can and cant remember by injecting certain chemicals that interfere with the second messenger, truly amazing and scary at the same time. Anyway, thats how neurotransmitters work on a basic level. Now FINALLY moving on to how drugs effect them and take their place. -------------------------------------------------------------------- [B]Drugs: What They Do To Neurons and Neurotransmitters[/B] Ok, this first bit may get a little confusing but is paramount in understanding what I mean when I say Agonist, Antagonist, excitatory, and inhibitory. This is the basis of understanding pharmacology and knowing this will allow you to understand the pharmacology section of a drug wiki page that will teach you what exactly the drug does. I am not going to go over every drug, only a few to use as examples to explain the different ways a drug effects neuronal communication. [B]Excitatory[/B]- Things that are excitatory send messages to make something happen. Excitatory does not mean sending message because you can have inhibitory messages. Neither does it mean depolarization, for the aforementioned reason. Moving your arm would be sending an excitatory message but keeping your arm from moving (for example you want to pick up somthing hot and you have to keep yourself from pulling back) will be inhibitory. [B]Inhibitory[/B]- These are messages made to stop actions. The example above is one where you inhibit your reflexive response of pulling your hand away from something hot. If you send enough inhibitory messages you should be able to pick up the hot object. There is a limit though. [B]Agonist[/B]- This is a drug that binds and triggers a response. The message it sends can be either excitatory or inhibitory. [B]Antagonist[/B]- Is a drug that binds and prevents an action from happening. This stops an action potential from happening, so it can stop an inhibitory or excitatory response. With that out of the way, its important to learn what kind of drugs their are and what they do at the binding sites. [img]http://filesmelt.com/dl/binding.png[/img] There is competitive binding and non-competitive binding. Competitive binding- when the drug takes the place of the neurotransmitter. This can either be an agonist by giving a better chance of activation or an antagonist by preventing activation. Non-competitive binding- when the drug falls in another site and allows for the natural neurotransmitter to also attach to the intercalated protein. [B]Notice[/B]- how agonists are opening the ion channel and antagonists are keeping the channel closed. Ok here we go, the basics of how drugs effect neuronal communication. This diagram is the bread and butter of getting it. [img]http://filesmelt.com/dl/ago.png[/img] I am going to break it up into two groups, Agonists and Antagonists. I will label the number for each box below in its proper category and you can then refer to the box in the diagram. This will build on what you know about agonists and antagonists. [B]Agonists[/B] 1) "Drug servers as a precursor" - this means that it promotes the creation of material used for making neurotransmitters and synaptic vesticles. [url=http://en.wikipedia.org/wiki/Nootropic]Nootropics[/url] are an example of this, where they aid the body by helping in the creation of enzymes, neuro-chemicals, etc. 4) "Drug stimulates release of T.S" - (transmitter substance is the material used for creating synaptic vesicles, the sacs that carry and release neurotransmitter) These drugs make the body produce and release more of these sacs, resulting in more neurotransmitter release. 6) "Drug stimulates postsynaptic receptors" - this is what we discussed earlier regarding competitive and non competitive binding. The drug attaches to the ion channel and activates or prevents an action potential. 9) "Drug blocks autoreceptors; increases synthesis/release of T.S" - Remember autoreceptors' job is to retrieve the stray neurotransmitters after they have activated a ion channel. By disabling them, you keep more neurotransmitters out in the synaptic gap and reactivate ion channels. This one also states that it is releasing more synaptic vesicles, which in tern is releasing more neurotransmitters. 10) "Drug blocks reuptake" - this is the same as the one before except it blocks transporters that take back in neurotransmitters. As you can see above cocaine blocks these transporter channels and keeps more dopamine in the synaptic gap. 11) "Drug inactivates acetylcholinesterase" - AChE for short, is an enzyme that breaks down acetylcholine which is mainly an excitatory neurotransmitter. By deactivating the enzyme, the neurotransmitter doesnt get destroyed and keeps sending excitatory messages. [B]Antagonists[/B] 2) "Drug inactivates synthetic enzyme; inhibits synthesis of T.S" - Basically stops the materials needed for synaptic vesicles from being put together. 3) "Drug prevents storage of T.S in vesicles" - The terminal button can no longer keep synaptic vesicles in preparation for future neurotransmitter release. 5) "Drug inhibits release of T.S" - Keeps synaptic vesicles from being released, thus stopping new neurotransmitters from being released. 7) "Drug blocks postsynaptic receptors" - This was mentioned before as the competitive neurotransmitters which take the place of natural neurotransmitters. 8) "Drug stimulates autoreceptors; inhibits synthesis/release of T.S" - By stimulating the autoreceptors you take in more neurotransmitters from the synaptic gap and keep them from re-activating ion channels. Since I feel like the Drug section is a little short compared to everything and this [I]is[/I] durg discussion, I'm going to include one extra subject. -------------------------------------------------------------------- [B]Cannabis: What Makes You High and How[/B] I know marijuana is the most popular recreational drug, but despite there being a lot of new research and knowledge that can easily be found on the web I still see people trying to explain what's in it and how the chemicals work, when in reality they have no fucking idea what they are talking about. The point of this section is to compile some of the more basic information from wikipedia. "Thats fucking dumb why would you just copy pasta shit from wikipedia, i can just go on there and read it myself, NNNNNNRRRRRRUUUUGHGHH" I'm not going to just copy info from them, but rather put it in easier terms for people to understand, because lets be honest once wikipedia gets into medicine and other scientific subjects it doesnt even try explaining the concepts and you are stuck in a never ending loop of wiki pages trying to figure out what one word means and you forget what you were trying to figure out in the first place. Along with clarifying facts people usually get wrong, I want to explain the true benefits and harms of use on the brain and the two paramount chemicals responsible for them. [B]Cannabinoid Receptors in the Brain[/B] I want to start here because I am sick and tired of people saying, "hurrr our brains were made to smoke weed because we have cannabis receptors in our brains". No, these cannabinoid receptors have been there for hundreds of thousands or millions of years. In fact, "Cannabidiol has [B]no affinity[/B] for CB1 and CB2 receptors but acts as an indirect antagonist of cannabinoid agonists" (wikipedia). Anyway, cannabinoid receptors serve an important function in the brain as being responsible for appetite, pain-sensation, mood, and memory. Cannabinoid receptors are also considered neuromodulators, which means they can communicate with other cells in the brain by releasing an excess or neurotransmitters that travel beyond the synaptic gap and activate other parts of the brain. This is why cannabinoid receptors have such a wide range of function. So after a lot of digging, I was able to find out how these receptors link to the rest of the brain and where it alters normal function. Just to make it easier to understand, I'm going to separate the two major chemicals from cannabis and explain their pharmacology. [B]THC aka Tetrahydrocannabinol[/B] THC is best known for its psychoactive properties as well as pain suppression and increased taste sensation. For pain it alters neurotransmitter communication in the dorsal root ganglion and the Periaqueductal gray. The dorsal root ganglion is a collection of neurons that act as a information highway for sensory articles like vibration, fine touch, and proprioception (knowing where your body parts are in space), so by suppressing this area you stop the info from being perceived. As for the periaqueductal gray or PG or short, it is very complicated in the sense there is a lot of "it activates this, then this activates those, and those inhibits that" so in short when stimulated it will eventually release opioid neurotransmitters that inhibit Substance P, which is what creates the sensation of pain. After further researching the structure, I found out it is also responsible for defensive behavior like mammalian freezing, running, jumping, tachycardia, and increases in blood pressure and muscle tonus. So judging by that, it may be the reason your blood pressure and heart rate spikes when smoking sativas. However, i doubt THC would cause couch lock since most people report couch lock after smoking a strong indica, which is a lot lower in THC but has a higher ratio of CBD. As for taste, it effects CB1 receptors in the hypothalamus, responsible for hunger. It not only reduces the feeling of fullness (you eat until you are sick, it slows the signals from the stomach saying its full) but it also increases the palatability of food. Palatability is the reward feeling of food, and is based in the nucleus accumbens (structure that releases dopamine whenever you do/consume something you like sex, water, food, smoke). When you havent eaten for a while, the food you eat feels more rewarding than if you have already eaten and are full. So by affecting the CB1 receptors in the area eating food feels really good and you dont want to stop. [B]CBD aka Cannabidiol[/B] CBD is just as important as THC in terms of the high and health. I am sick of people not knowing that there are other cannabinoids, especially this one since in comparison to THC its the part of weed that is 'good' for you, in a sense. CBD in the medical field can help anxiety disorders, schizophrenia, dystonia, certain cancers, depression, and combat the adverse effects of THC. Yes, THC is bad for you, especially if you only smoke very strong sativas and hash. They have a high ratio of THC to CBD so there isnt enough CBD to counteract side effects like memory loss, susceptibility to schizophrenia, and heart abnormalities; I will elaborate on this later. Here is a quick pic of how much CBD does compared to the other cannabinoids [url]http://upload.wikimedia.org/wikipedia/commons/2/20/Health_Effects_of_cannabinoids.png[/url] . Anyway CBD when it comes to the high, CBD has an antagonist property where THC has a partial agonist one, so it helps keep the anxiety, that THC causes, down. Since CBD activates the same receptors as THC, you still get munchies, feelings of euphoria etc, you only have less of a mind high because you cancel out the agonistic effect from THC. [B]The Research of Cannabis: Debunking the Bullshit[/B] This is the final section and one that I really want people to know, because it is important to know what research is legitimate and what is biased bullshit. Now, remember that scientists get payed to make findings, and despite the null hypothesis practice used in statistics and research, scientists still go into experiments biased trying to find a breakthrough. So expect both sides (pro and anti marijuana) to release incomplete, rigged, or exaggerated results. THC can act as a "constellation factor" leading to schizophrenia. Im just going to quote the cross examination since it was done by a research professional, "[I]Results On an individual level, cannabis use confers an overall twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis. Conclusions Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Research is needed to understand the mechanisms by which cannabis causes psychosis.[/I]" So there is a slim chance that cannabis will add to your psychosis IF you have other factors that can cause you to develop schizophrenia. As for other research you come across, try to read the procedures section carefully. This is VERY important, I cant stress it enough. Im just going to jump to it, cannabis research doesnt always use weed to test. Some will use pure injections of THC only, or only use very strong sativas or hash with loads of THC and no CBD. This increases the possibility of mental illness, memory loss, and heart problems as mentioned before. This is probably done to get around the issue of growing for the lab, but this means its not really weed being tested, just pure THC. And as we all know, THC in huge quantities without its counterpart CBD is very bad for you. I've seen a lot of studies where they do this and its very frustrating since they get these harmful results and label it as being from all kinds of weed. It would be like saying that drinking a whole bottle of everclear has the same effects as drinking a beer. As for studies about the lungs, expect them to use very inefficient or carcinogenic ways of smoking like joints without filters or loads of papers with lots of tobacco. We already know breathing in smoke from anything burned is bad for you, which is why edibles and vaporizers are the healthiest way of consuming. And remember [B]"Correlation does not equal Causation.[/B] To really find out if something is a causation, you need a longitudinal study with a control group, showing with significance that the group introduced to the controlled variable, was affected in a certain way. Thank you for reading, I hope this has expanded your knowledge of drugs and how they work. If there are any broken links let me know immediately. If you have any questions, or want me to elaborate on something that I touched on in the op post it here so we can keep the thread alive and discuss how the brain functions. Note that this is only knowledge accumulated through a few years of studying psychology in college (from 300 lvl classes like Cognition, Neuropsychology, Adolescent Development, Infant and Child Development, Physiological Psychology, Statistics in Psychology, Sociology of Mental Health, Conditioning and Learning, and Social Psychology) so information may be oversimplified, slightly inaccurate, or maybe even outdated as new research comes out. Im going to be taking Sensation and Perception and Health psychology next semester so maybe i will add a ton more to the thread. Enjoy.

holy shit

holy shit son. gonna read this when i'm blazing soon.

holy mother of god, just started its gonna take a while.

It's about a 15 minute read. I found it to be pretty informative, and it affirmed my suspicions that my pot use may somehow be related to my level of psychosis (which has never been very high, but seems to get noticeable at times). This is mostly assumed to be because the craze in my area is pure sativas and hash, and indica [which I love] is immensely hard to come by.

[QUOTE=Cactusman;35876537]holy mother of god, just started its gonna take a while.[/QUOTE] really? to be honest when i posted it i thought it looked a little short lol

[QUOTE=Cpn Crunch21;35877625]really? to be honest when i posted it i thought it looked a little short lol[/QUOTE]It's merely concise, not short.

the part on cannabinoids is interesting, especially this image [img]http://upload.wikimedia.org/wikipedia/commons/2/20/Health_Effects_of_cannabinoids.png[/img]

brb finding my brain

[QUOTE=TamTamJam;35879158]the part on cannabinoids is interesting, especially this image [img]http://upload.wikimedia.org/wikipedia/commons/2/20/Health_Effects_of_cannabinoids.png[/img][/QUOTE] There are some dispensaries that find ways of measuring percentage of certain cannabinoids like CBD and THC since you want to make it clear to customers as to which strains are rich in what, and what will help them with what they need.

Yay finally it's out! Good read man!

i always found neurology/chemistry very interesting but it was hard to get into, great thread dude.

[QUOTE=lotusking;35881275]i always found neurology/chemistry very interesting but it was hard to get into, great thread dude.[/QUOTE] before i took physiological psychology, i had the same attitude and didnt really want to get into the biology of brain function. However, this professor was so great a generating interest and referencing to important concepts that it really made me take interest and find a new field to be interested in. He would occasionally go off on a tangent and talk about research in the field and its amazing to think that right now at my university they are working on ways of altering how we think and learn by chemically tweaking things in the brain. I mentioned in the op a thing about plasticity and learning. Just to keep things short, in class we discussed how the brain is constantly changing as you get older on a physical level, so for example you get a lesion, your brain will try to compensate the damage by repairing it as much as possible and by having other parts of the brain incorporate some of the lost function so that way you gain back what you lost. Also, learning creates physical change by not only adding connections between neurons but by altering DNA in your cells. Thats right, your DNA changes over time the more you learn, possibly explaining evolutionary things like imprinting as those behaviors are passed on through generations of a species (bird songs for example). Now things like appearance doesnt really change but this is probably how long term memory works, havent learned enough on this subject though. Anyway, regarding chemical control of the brain, their are certain chemicals that you can inject into the brain and prevent certain types of learning. I can condition you to be afraid of a red light and have you not remember the training, yet you will still jump in your chair when you see it. The effect can even be reciprocated by injecting chemical in specific cranial structures. Its wild stuff.

About time.

long term memory stored in dna that's pretty fuckin crazy man.

Holy shit you finally posted it. I've seen you tinkering on that for over a month.

Very nice read, thanks for putting the effort into creating this. Neurology/Biology/Chemistry always interested me so much and how certain substances interacted with the human brain/body.

[QUOTE=Cpn Crunch21;35881209]There are some dispensaries that find ways of measuring percentage of certain cannabinoids like CBD and THC since you want to make it clear to customers as to which strains are rich in what, and what will help them with what they need.[/QUOTE] Dispensaries are ten steps ahead with this shit. I have never been to a coffeeshop that has listed both THC and CBD or any of the other cannabinoids.

re-read it all and now it makes more sense than it did a year ago nice edit: aint gonna let your baby die

[QUOTE=Cpn Crunch21;35881557]before i took physiological psychology, i had the same attitude and didnt really want to get into the biology of brain function. However, this professor was so great a generating interest and referencing to important concepts that it really made me take interest and find a new field to be interested in. He would occasionally go off on a tangent and talk about research in the field and its amazing to think that right now at my university they are working on ways of altering how we think and learn by chemically tweaking things in the brain. I mentioned in the op a thing about plasticity and learning. Just to keep things short, in class we discussed how the brain is constantly changing as you get older on a physical level, so for example you get a lesion, your brain will try to compensate the damage by repairing it as much as possible and by having other parts of the brain incorporate some of the lost function so that way you gain back what you lost. Also, learning creates physical change by not only adding connections between neurons but by altering DNA in your cells. [B]Thats right, your DNA changes over time the more you learn, possibly explaining evolutionary things like imprinting as those behaviors are passed on through generations of a species (bird songs for example). Now things like appearance doesnt really change but this is probably how long term memory works, havent learned enough on this subject though. [/B]Anyway, regarding chemical control of the brain, their are certain chemicals that you can inject into the brain and prevent certain types of learning. I can condition you to be afraid of a red light and have you not remember the training, yet you will still jump in your chair when you see it. The effect can even be reciprocated by injecting chemical in specific cranial structures. Its wild stuff.[/QUOTE] What? Your DNA has very little to do with your long-term memory, long-term memory is made up of different proteins on the nerve cells and the connections between the cells, eh? It's not even proven that DNA changes over time has any impact on your memory or is used as some kind of storage mechanism in the brain, most like it is just random mutations triggered by the electrical activity in the cells. But even if these changes actually affect long-term memory it does not mean we have genetic memory. It doesn't matter how mutated our nerve cells become, it is the sperm/egg cells that determine the DNA that will be passed on to your offspring, and they are in no way connected to the nerve cells. Surely someone who is educated in neural biology should know this.

yeah youre right, i got a little ahead of myself there about the bird song example. however my professor did mention that the neurons themselves change during the life time but as it was one of his side notes he did not continue a full explanation on it.

hey look it's psychology class all over again :v:

[QUOTE=Cpn Crunch21;35942019]yeah youre right, i got a little ahead of myself there about the bird song example. however my professor did mention that the neurons themselves change during the life time but as it was one of his side notes he did not continue a full explanation on it.[/QUOTE] While it may be so, it does not prove that DNA is used as a memory mechanism, but rather points to, as I already said, random mutations over time. We have found nothing in the structure of the neurons that points to capabilities for controlled mutation of the DNA structure in the form of long term memory. [editline]13th May 2012[/editline] However, I should not only be so negative. The post as a whole was a good read (with the exception of a few details like the DNA-memory thing), even though I already knew most if not all of it :)

[QUOTE=Mindtwistah;35942288]While it may be so, it does not prove that DNA is used as a memory mechanism, but rather points to, as I already said, random mutations over time. We have found nothing in the structure of the neurons that points to capabilities for controlled mutation of the DNA structure in the form of long term memory. [editline]13th May 2012[/editline] However, I should not only be so negative. The post as a whole was a good read (with the exception of a few details like the DNA-memory thing), even though I already knew most if not all of it :)[/QUOTE] out of curiosity and to help keep this thread alive, i was hoping you can share some of your knowledge on neurology or physio psych. It can be about anything, but to maybe start a discussion lets make it about idk, brain plasticity or maybe the substantia nigra and how it is effected by drugs maybe. Im excited to hear from someone more familiar in the field.

Finally got around to reading this, pretty enlightening. Thanks Cpn.

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