Community/Health

Cannabidiol…a possible replacement for medical marijuana?

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The topic of legalizing medicinal marijuana is a growing conversation in our society today as it is already legal in 17 states across our nation.  The article “Endocannabinoid system and psychiatry: in search of a neurobiological basis for detrimental and potential therapeutic effects” looks at how cannabis can be used medically to help aid in depression, anxiety and eating disorders and highlights the main negative effects of cannabis use.  Although scientists and psychologists have worked together to determine that cannabis can successfully help with depression, anxiety and eating disorders, is it really the best option for therapy?
 
While reading this article, the negative effects of cannabis use stuck out to me much more drastically than the positive effects.  The article described one side effect of cannabis use as being the development of schizophrenia.  Although scientists haven’t directly linked cannabis use to schizophrenia, there is proof that it can induce schizophrenia in users that are genetically predisposed to developing this disease and it works together with other risk factors to speed up the onset of the disorder.  This side-effect alone, without even considering the negative psychotropic effects of cannabis that are frowned upon by many, seems serious enough to wonder if cannabis is really a drug that should be used for treating any sort of mood disorder.
 
Another major piece of the article that stuck out to me while reading focused on the specific piece of cannabis called Cannabidiol (CBD). The writers briefly described the positive effects that CBD can have on treating anxiety and depression and stated that CBD doesn’t have the negative effects that cannabis has.  Immediately after reading about CBD, I wondered, could isolating this component of cannabis, CBD, be an alternative drug to medical marijuana?
 
Cannabidiol is the main non-psychotropic component of cannabis and exhibits many of the same therapeutic effects as marijuana.  The other main component of cannabis is tetrahydrocannabinol (THC).  THC is responsible for the psychotropic effects that many people think of when they think about marijuana.  All cannabis has a different ratio of THC and CBD as each strain of cannabis is different.  After noticing that different strains of marijuana were more or less successful in treating depression and anxiety, scientists explored the contents of cannabis and found that the strains with higher amounts of CBD worked much better for treating mood disorders.  This finding is responsible for the additional research that has been done to make CBD so popular as scientists look for a new possible drug that will exhibit the same therapeutic effects as marijuana without all of the negative side-effects that marijuana has. 

The understanding of Cannabidiol is a very intriguing aspect of cannabis, as it would be great to develop a new way to treat depression and anxiety without having the negative psychotropic effects.  This would make it much more socially acceptable for a patient to treat their depression or anxiety when they didn’t have to experience the “high” that is so commonly associated with marijuana.  After both human and animal testing, scientists have found a lot of promising evidence that CBD could be the new drug for treating many different disorders and ultimately eventually replace medical use of marijuana as a whole.  One of the main effects of CBD that scientists discovered is that with low doses, CBD is alerting and helps reduce depression, while at high doses it actually acts as a sedative and can reduce anxiety.  Scientists have also found that CBD can be used in many other medical ways, such as relieving convulsion, inflammation, nausea as well as inhibiting cancer growth.

After reading this article my eyes have been opened to the fact that it is very important that our society finds an alternative therapeutic drug rather than marijuana to help aid in the therapy of common mood disorders such as depression and anxiety.  I look forward to following the further research of Cannibidiol that must be done in order for it to become this alternative therapeutic drug that everyone is looking for.  After looking at what we know so far about CBD, it has definite potential to be a successful alternative to medical marijuana and even provide therapy in a wider array of patients than marijuana does today.
 
For more information, click on the link below, What is CBD?
What is CBD?

Health/Hot topics/Uncategorized

Marijuana: Oh the Possibilities

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So let’s not beat around the bush here: a significant number of people – not only in America but around the world – have tried or habitually done marijuana sometime in their lives, legally or illegally, for medicinal purposes or as a recreational drug. That being said, you would think that people would be clamoring to educate themselves and others on the risks and benefits associated with its use. I don’t know about the users, but there are plenty of scientists out there aiming to do just that, particularly in regard to the relation of cannabis and neuropsychiatric disorders. There are certainly therapeutic applications, but more research is needed to avoid some unwanted side effects.

But… withdrawal looks like so much fun…

Cannabis (marijuana) has two main active ingredients: tetrahydrocannabinol (THC) and cannabidiol (CBD). These two compounds interact with the brain via the endocannabinoid (eCB) system, activating ligand-binding cannabinoid receptors (CB1 and CB2). It’s through these two receptors that most of the action happens, whether ultimately beneficial or detrimental. THC is the addictive, psychoactive, and “munchies”-inducing contributor to cannabis that has also been suggested to cause anxiety. CBD is attributed with many therapeutic effects, which includes treatment of spasticity in multiple sclerosis patients, inhibiting cancer growth (most notably in breast cancer), and being an antipsychotic for treating schizophrenia. It interacts with the eCB system as an antagonist to the two receptors in low doses, and increases CB1 expression in high doses.

The eCB system has been shown to be extremely influential in neuropsychiatric disorders such as anxiety, depression, and schizophrenia. Its effects, however, are both positive and negative. For example, the CB1 receptor is involved with inducing anxiety when it’s expressed on one type of neuron (glutamate) and relieves anxiety when expressed on another (GABA). You can see why things can get a little messy.

Seems pretty straightforward…

Here’s an overview of the results linking the eCB system with these disorders:

  • CB1 expressed with GABA relieves anxiety
  • CB1 expression likely helps avoid depression (deletion enhances depression)
  • CB2 overexpression relieves anxiety
  • CB2 likely decreases vulnerability toward depression
  • Presence of  CB2  seemingly reduces the risk of developing schizophrenia
  • CB1 expressed with glutamate induces anxiety
  • Prolonged activation of receptors increases the risk of developing schizophrenia

The negative aspects seem to tap into the subtle complexities of the eCB system and neurological signaling in general – pathways are often very convoluted and activation or inhibition often have multiple different effects, influencing many different pathways. One particular pattern I’ve noticed is that dose and frequency of use play a significant part in the ultimate effects due to receptor activation. For example, low doses of cannabis seem to give a calming, anxiety-relieving effect, but high doses actually lead to anxiety, paranoia, and psychosis. Also, it seems that activation of the CB2 receptor is necessary to decrease one’s risk of developing schizophrenia, whereas prolonged activation of the eCB system increases this risk. Most confusing of all, testing for these neuropsychiatric disorders with eCB agonists and antagonists with the same receptor expression gave different results across groups. All of this says one thing to me: we have quite a long way to go to characterize exactly what’s going on with the eCB system and these disorders.
There seems to be a strong basis of hope for cannabis-related drugs in the treatment of many different illnesses. Cannabidiol itself has fantastic applications for the treatment of multiple sclerosis and cancer, among many other things, and has been shown to positively affect people with neuropsychiatric disorders, relieving anxiety, acting as an antidepressant, and protecting against psychotic reactions and symptoms. However, cannabis does not look like the answer, due to its adverse effects from THC (anxiety-inducing, addictiveness, etc). There is great potential in the study of cannabis and cannabinoid substances in medicine, but cannabidiol seems to have a lot more promise than cannabis. In either case, before cannabinoids are highly implemented in medicine there should be greater definition of the mechanisms through which they work, so as to define safe dosage and ensure that the pros really outweigh the cons. Like that withdrawal party…

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Cannabis, Depression, and You

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Depression is a serious psychological disorder that affects millions of Americans. I am one of those millions. Around the time I entered second grade, a psychologist diagnosed me with depression and put me on medication; Wellbutrin to be specific. Although this drug seemed to do the trick with me essentially spinning my life in a 180-degree turn, it may not work for everyone. Wellbutrin acts upon the body by increasing dopamine concentrations in the brain which in the end helps us feel “happier”. A certain person may not have the same feeling after taking this drug though, so then what do we do? Simply put, we find a different drug that works in a different way. One area of drugs that is getting a lot of attention for treatment of major depression is cannabinoids. Cannabinoids, specifically tetrahydrocannabinol (THC) and cannabidiol, are key components to the well-known drug marijuana. These two molecules act upon the endocannabinoid system in our body which is a key regulator in mood function such as anxiety and depression
In the article “Endocannabinoid system and psychiatry: in search of a neurobiological basis for detrimental and potential therapeutic effects” the researchers were looking at this exact topic. After reading through the article, I can communicate some of the main ideas. First, when the endocannabinoid system was activated through cannabis use, subjects were more likely to feel happy and less stressed. This is hardly news to us though as we are all familiar through the media’s interpretation of marijuana as making us laugh and lose all the cares in the world; don’t worry, be happy. Although this is a good thing, other research has shown that with chronic cannabis usage, the rate of depression and anxiety increases. So at this point, there really isn’t an end all answer to this question. Second, as with every drug, there are side effects. With cannabis use, the main side effect (and a nasty one at that) is that if you using cannabis to treat your disorders, you also put yourself at risk of developing schizophrenia with continued use. This side effect has a very small chance of occurring though, and is really only a problem with a genetic predisposition to schizophrenia. With this side effect, I personally believe that cannabis in the form of marijuana should not be used to cure mood disorders, but if a patient is well aware of the risks and still wants to use it, they should be able to. Personally, I see more potential in researching the two components of cannabis (THC and cannabidiol) more to see if they can help without having to “light one up”.
As stated above, cannabis and the endocannabinoid system have a seemingly promising future in curing these mood disorders we all have come to know. There are still a few kinks to work out, and a lot more research to be done, but if the research proves to be useful, this could be a very promising drug to look at for some people with depression.
For anyone who would like more information on this topic, feel free to visit http://www.drugabuse.gov/publications/drugfacts/marijuana to learn more about medical marijuana.

Community/Disease/Health/Hot topics

Smoking Marijuana Causes…Schizophrenia?

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When you hear marijuana what do you think of? For me, I don’t think much of it other than a waste of money to cause you to feel a little loopy and give you the munchies. Marijuana has many uses however medicinally as it can help manage pain and appetite. Recent studies however, have shown a link between marijuana use and schizophrenia. How can that be? To understand this, we must know a few things about both marijuana and schizophrenia.
What is marijuana?
Cannabis sativa, commonly known as marijuana, is one of the most frequently abused illegal drugs in western culture. The active ingredients in cannabis are delta-9-tetrahydrocannabinol (THC) and cannabidiol. THC is the compound responsible for the addictive and psychoactive properties of cannabis while cannabidiol is often the compound which is attributed to the medicinal effects. Cannabis is illegal for recreational use in the US but is permitted medicinally in 17 states (including Alaska, California, Michigan, and Montana) plus DC. Cannabis works on the endocannabinoid system in the brain which regulates neurotransmission in brain regions associated with the regulation of pain, emotion, motivation and cognition.
What is schizophrenia?
The term schizophrenia means ‘split mind’. It is a psychotic disorder which is characterized by disturbances in perception, behavior, and communication. There are three types of schizophrenia: paranoid, disorganized and catatonic. A person is classified in a certain category depending on the specific set of symptoms they exhibit. General symptoms include (but are not limited to) hallucinations, delusions, lack of attention, memory impairment, impaired information processing, loss of interest and loss of ability to experience pleasure. Schizophrenia often presents itself in young adulthood but a good percentage of people with the disease report psychotic symptoms starting as early as age 11. Researchers are not sure of the exact causes of schizophrenia but there are many hypotheses about possible contributing causes. The most common hypothesized cause is that there is an imbalance of brain chemicals or other sort of brain abnormality.
So how can marijuana use be linked to schizophrenia?
Well the truth is, A LOT of things have been linked to schizophrenia. Although, as stated earlier, marijuana works to change brain chemistry which is also thought to be a cause of schizophrenia; it is not as if we can say that smoking marijuana CAUSES schizophrenia rather researchers say at this point that cannabis use presents an ‘increased risk’ for developing the disease. However, the list of things which are found in the population of people with schizophrenia as possible ‘risk factors’ is quite extensive and, if you ask me, some of them are just absurd.
Here is a list of some known ‘risk factors’ for the development of schizophrenia:

  • Occurs twice as often in unmarried/divorced people as in married or widowed populations
  • Left handed people have significantly higher instances
  • A significant number of schizophrenics have OCD 
  • People with schizophrenia often have excessive shyness or minor physical/motor-control problems in childhood
  • Some studies show that a person whose father was older when they were born have greater chance of schizophrenia
  • A family history of epilepsy increases chance for schizophrenia
  • 10% risk if one immediate family member has disease
  • 40% if both parents or identical twin have disease
  • Winter/ spring births pose a 5-8% higher possibly of developing schizophrenia because of prevalence of colds/viruses in infancy
  • People from large families with multiple children in short intervals because of exposure to infection early in infancy
  • Child born if pregnant mother had exposure to viruses such as rubella, measles, or chickenpox while infant is in the womb have been associate with higher risk

As you can see, not only can use of marijuana be linked to schizophrenia but so can a range of things from infections in early infancy to being left handed.
So, no, smoking marijuana cannot lead to development of schizophrenia. It may however, put you at a higher risk in conjunction with other risk factors for developing the disease.

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Capstone Closing Comments

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This semester has been full of information that would make most people’s heads spin! Some of the material could be so dense at times that reading it three times and going through the words with a dictionary sometimes still didn’t give you a specific answer. This makes the course frustrating because you want to know but getting a headache while trying to read/understand is not on your to-do list. But your quest for knowledge outweighs the frustration you feel while reading the material (this is my case). This course brought forth so many different topics to study and learn more about. The topics covered ranged from addiction to aging and a large variety in between.
The range of topics really made the class more interesting because you weren’t talking about the same things over and over again. Every week it was a different subject and different discussions that brought up good points and brought new light on some things that some of us hadn’t thought about. Learning this information in a small group setting really helped us learn it better and it actually made us want to do our homework and study. The type of environment we were in really made it easy to learn. It wasn’t a class where the professor did all the talking and the students simply sat there and took notes. This course was a fully student run course where the professor was more of a student and learned the information right along with us.
The part of this course that really caught my attention was that no matter what subject we talked about, they were all connected by one part of the brain or another even if they were complete opposites of each other. And knowing this is a scary thought because you know that if you were to damage one specific area of your brain there is a chance that you could lose multiple abilities. Doesn’t that scare you? Cause it scares me…but it’s so hard not to pursue more information because the complexity, mystery, and danger of the brain is so fascinating and we are a society that needs to have answers to everything.
This class was a fantastic class and I really enjoyed it. Even though the material at times was hard to understand and it could be a lot at times the class was still worth every second and I would recommend it to any student that asked about it.

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Alcohol Withdrawals

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Some people don’t consider alcohol a drug because it doesn’t give a person the same symptoms as say cocaine or heroin would. But this is not the case. Alcohol is as much a drug as any other because it causes impairments and can be highly addictive just like actual drugs. Just because alcohol is a social item and millions of people drink it during social occasions does not mean it is any different.
Our article on the topic of ethanol focused on the intracellular signaling pathways that are thought to regulate behavioral responses with the consumption of ethanol. In the article, evidence shows that alcohol “modulates” the functions of specific cascades within the brain that include cAMP, PKA, PKC, the tyrosine kinase Fyn, cyclic adenosine 3′, and PLD. With their experiments, they found that some of the cascades mediated the effects of ethanol while others modified the response to ethanol. The authors stated that the studies they looked at found that the specific effects of alcohol on signaling appeared to be only in certain parts of the brain due to the restricted distribution of the proteins during their experiment.
The article talks about the neurological aspects of ethanol behavior but it doesn’t talk about what the actual behaviors are and what they can lead to. The behaviors that come with alcoholism include frequent intoxication, an established pattern of heavy drinking and drinking in dangerous situations, such as when driving. Other early signs of alcoholism include black-out drinking or a drastic change in demeanor while drinking, such as consistently becoming angry or violent. The main symptom of alcohol abuse occurs when someone continues to drink after their drinking reaches a level that causes recurrent problems. Continuing to drink after it causes someone to miss work, drive drunk, avoid responsibilities or get in trouble with the law is considered alcohol abuse. For someone who is alcoholic or alcohol dependent, the symptoms include all of those associated with alcohol abuse. But alcoholics also continue to drink in spite of all the problems it has caused in their lives. When alcohol abuse reaches the alcohol dependence stage, the person also experiences at least three of seven other symptoms, including neglect of other activities, excessive use of alcohol, impaired control of alcohol consumption, persistence of alcohol use, large amounts of time spent in alcohol-related activities, withdrawal symptoms and tolerance of alcohol.
The topic that interest me is the event of alcohol withdrawals. Do alcohol withdrawals actually happen or is that simply something that happens with narcotics? The answer is yes they actually happen and they can be equally as bad as the symptoms of drug withdrawals. Alcohol withdrawal symptoms usually occur within 5 – 10 hours after the last drink, but can occur days later. Symptoms get worse in 48 – 72 hours, and may persist for weeks. Common symptoms include:

  • Anxiety or nervousness
  • Depression
  • Not thinking clearly
  • Fatigue
  • Irritability
  • Jumpiness or shakiness
  • Mood swings
  • Nightmares
  • Clammy skin
  • Enlarged (dilated) pupils
  • Headache
  • Insomnia (sleeping difficulty)
  • Loss of appetite
  • Nausea and vomiting
  • Pallor
  • Rapid heart rate
  • Sweating
  • Tremor of the hands or other body parts

A severe form of alcohol withdrawal called delirium tremens can cause:

  • Agitation
  • Severe confusion
  • Seeing or feeling things that aren’t there (hallucinations)
  • Fever
  • Seizures

Looking at all of these symptoms and the way people can act during intoxication being an alcoholic does not seem anywhere close to fun but as of June 2011 almost 18 million people have alcohol addictions…that’s one in 12 adults! This is an outrageous number and it only seems to get higher every year. Prevention of alcoholism is being studied but specific treatments are still to be found. Right now they are using treatments that make the person physically ill and the other treatments make the person want to drink less but it does not get rid of their cravings completely. Going back to the article, could it be possible to treat alcoholism using the intracellular signalling pathway cascades talked about in the article? Time will only tell what we can use within the body to help treat this ever growing disease.
http://alcoholism.about.com/od/about/a/symptoms.htm
http://www.bettermedicine.com/article/alcoholism-1/symptoms
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001769/

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Neurochemistry vs. Student Teaching

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You could say I am lucky enough to have the experience of two capstones for my undergraduate degree. Officially as a chemistry education major student teaching is my capstone, but neurochemistry sounded so good I couldn’t pass it up. It is nice to have student teaching count as a capstone for teachers because our majors are filled to the brim. Yet I feel that for secondary education majors, it is a great benefit for them to take the capstone of the field. I think neurochemistry is able to show the true relevance of chemistry in the world today. There are infinite doors that can be unlocked by the understanding of neurochemistry. I am glad that I have gotten a foundational knowledge in neurochemistry. I feel that in the next few years the field will explode, it will be interesting to see the discoveries that are made and the debates they will fuel.
I am also excited to see how I can incorporate what I have learned and bring it to my own students. I mean I know I can’t get down to the individual pathways with them (which is okay because I am sure I won’t remember most of them), but I am hoping that I can use the foundational knowledge that I have acquired and use it to show my students just how important chemistry is in this world. I think neurochemistry can truly show students just how far a knowledge of chemistry can take them. And this is truly one of my goals in life, I believe that it is possible to get any high school student to be interested in chemistry, you just have to show them the right information in the right way. So many high school students are board out of there mind in chemistry class, and by no means is it their fault. I have watched too many teachers talk on and on and on about this subject without giving any rational to why the students should learn the subject. For every lesson plan teachers Teachers are suppose to create a rational that they can explain why students need to know the topic. Yet so many teachers are focusing on that specific topic, or on state standards that they forget to give the rational for their entire coarse. As a future teacher I find this so concerning, I plan to take the first two days off from chemistry content. The first day I want to talk the rational of getting an education with my students, because I believe so many of them are just as caught up in the systems rut as the teachers are. The second day would be a rational for chemistry, I want to create a very discussion based class period in which I can hopefully open there eyes to what chemistry can do for them. And I can promise that neurochemistry will be part of that disscussion.

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Autism vs. Asperger's Syndrome

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One of the articles we read had the main topic of autism and the environmental and genetic factors that can cause it. In the article it talks about the redox/methylation hypothesis and how it leads to the development of autism. The hypothesis states that genetic factors and environmental factors bot lead to impaired sulfur metabolism in the body which leads to oxidative stress which scientist believe not only leads to autism but also can lead to cancer and Alzheimer’s disease. In terms of autism, the oxidative stress leads to a decrease in methionine synthase activity. The hypothesis then states that this decrease will lead  to both a decrease in the methylation of DNA and also a decrease dopamine receptor phospholipid methylation. The decrease of both of these lead to decreases in attention, cognition and development, which are a few of the main symptoms in autistic individuals. One question that some want to know is if this mechanism causes the other autism spectrum disorder (ASD) and how truly different are classic autism and Asperger’s.
We know that autism is a developmental disorder that affects the communication, social and development skills of those affected by it. They usually have a difficult time with speech and gesturing, communication, socializing with others and they are know to have very repetitive qualities such as continuously clapping their hands or they can  also repeat sounds or movements. Echolalia or repeating of the words someone has just said to you, is another symptom of classic autism. Also, some individuals with autism can have tantrums, physical tics, they sometimes do not like physical contact such as cuddling or hugs but this is usually pertains to people outside of their immediate family, they can sometimes have difficulty understanding other people’s emotions,Signs that a child might have autism include: doesn’t babble or coo by 12 months, doesn’t gesture — such as point or wave — by 12 months, doesn’t say single words by 16 months, doesn’t say two-word phrases by 24 months, or loses previously acquired language or social skills at any age.
Asperger’s syndrome is a developmental disorder that affects a person’s ability to socialize and communicate effectively with others. Children with Asperger’s syndrome typically exhibit social awkwardness and an all-absorbing interest in specific topics. Asperger’s syndrome symptoms include: engaging in one-sided, long-winded conversations, without noticing if the listener is listening or trying to change the subject, displaying unusual nonverbal communication, such as lack of eye contact, few facial expressions, or awkward body postures and gestures, showing an intense obsession with one or two specific, narrow subjects, such as baseball statistics, train schedules, weather or snakes, appearing not to understand, empathize with or be sensitive to others’ feelings, having a hard time “reading” other people or understanding humor, speaking in a voice that is monotonous, rigid or unusually fast, and moving clumsily, with poor coordination. Unlike children with more-severe forms of autism spectrum disorders, those with Asperger’s syndrome usually don’t have delays in the development of language skills. However, children with Asperger’s syndrome may have difficulties holding normal conversations. Their conversations may feel awkward and lack the usual give and take of normal social interactions. Toddlers and school-age children with Asperger’s syndrome may not show an interest in friendships. Those with Asperger’s often have developmental delays in their motor skills, such as walking, catching a ball or playing on playground equipment. In early childhood, kids with Asperger’s may be quite active. By young adulthood, people with Asperger’s syndrome may experience depression or anxiety. If an elementary schoolchild has frequent problems in school or seems unable to make friends, a doctor should be consulted.
So looking at both of these disorders there doesn’t seem to be a big difference between them and in all actuality there isn’t. But the big difference is how children with Asperger’s develop and the communication skills they have. Children with autism develop very poor speech  if any at all and those with Asperger’s usually have a very extensive vocabulary. Autistic children usually do not attend public schools, those with Asperger’s are more than capable of attending school it’s just that they will have a difficult time holding conversations and making friends. These two disorders are so similar and yet so different. But in the end I believe that the mechanism described in the paper for autism also plays a big part in the development of Asperger’s.
http://www.mayoclinic.com/health/aspergers-syndrome/DS00551
http://www.mayoclinic.com/health/autism/DS00348

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Ethanol and Knockouts… Mice, that is

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One of the articles we focused on was a review on the signaling caused by ethanol (commonly known as alcohol). Ethanol has various cellular effects that result in dependence, preference, and seeking behaviors. One of the main pathways is where ethanol stimulates the synthesis of the second messenger cAMP through activating the enzyme adenylyl cyclase. Formation of cAMP is also reinforced by inhibiting ENT1, which leads to the accumulation of adenosine outside of the cell.
Another mechanism of ethanol reward reinforcement is the activation or inhibition of NMDA receptors. NMDA is a glutamate receptor that is important in the reward pathway. Ethanol binds to a complex, Fyn, that regulates NMDAR activity.Fyn dissociates from the receptor. NMDARs are also affected by a molecule called DARP-32, which when phosphorylated, keeps NMDARs active. DARP-32 receives a phosphate from an enzyme called PKA which is regulated by cAMP. With ethanol, there is more cAMP which increases the active DARP-32. These mechanisms encourage reward signaling.
Many pathways are characterized using knockout mice. Knockout can also refer to transgenic or genetically modified. A specific gene has been interrupted in mice (also yeast, bacteria, plants. . . just about anything), by a piece of DNA. The genetic expression of the mouse will be affected; hopefully the absence of a protein product will tell researchers what that gene is used to produce.
Knockout mice were used in many of the cited studies in the ethanol paper. For instance, mice without the ENT1 gene showed lower responses to ethanol. The ethanol didn’t affect them as much, indicating ethanol interacts with the ENT1 receptor. One important transgenic mouse was the Fyn kinase deficient mice. These guys (or girls) did not produce any Fyn product. The results showed that NMDA receptors were not phosphorylated. Based on this, the conclusion is that Fyn is the enzyme that acts on the NMDA receptor.
Transgenic organisms can be used to study gene sequences that are known but the function remains unknown. They are a useful tool for elucidating the signaling pathways, not only in the nervous system, but the rest of body as well. A drawback of transgenic mice is that there is a possibility the cells are somehow compensating for the lost gene product. The organism is a messy system, but taking it step-by-step, one knockout at a time, we may be able to figure out the mechanisms that drive life.

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Final Thoughts on Neurochemistry

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Neurochemistry was a unique science course, different from any of my other courses throughout my college career. We read articles, focusing on understanding them, and then discussing the scientific concepts along with how they pertain to everyday life. The latter aspect is one of the most important lessons I took away from the semester. The research performed by scientists impacts everyday life. It leads to the development of new drugs and a greater understanding of the mechanisms behind the brain and disorders. But another thing that is just as important as the discovery is the communication of results, not only to the science community but the general public as well. I have realized that many people outside of science disciplines are interested in research. I looked forward to reading or hearing about comments left by other AreaVoices readers.
This course has improved my skills at reading and interpreting scientific papers. In addition, I have developed my ability to communicate findings to both my peers and others. The blog was a beneficial and fun aspect of the class. I believe this is what made Neurochemistry so unique. None of my previous courses have emphasized the importance of communicating to the general public. It was all about academic audiences. Although I did not do my best at maintaining my blog entries (I have never been good with journals either), I feel this is something I would like to continue, especially during my graduate studies. Overall, the Neurochemistry course had a completely different set-up than others but it was a beneficial class that encouraged the Concordia motto: becoming responsibly engaged in the world.

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