Cannabis and the brain

Cannabis: Good or Bad?  The active ingredient in Marijuana is called THC which is short for delta-9-tetrahydrocannabinol.  This chemical closely resembles another naturally produced chemical in our bodies called cannabinoids, which like THC, bind to areas of the brain called cannabinoid receptors.  These receptors are located in many different areas of the brain including the hypothalamus, cerebral cortex, and the thalamus to name a few.  How the drug works is the THC is artificially responsible for causing increased amounts of the cannabinoid receptor to be stimulated.  This ultimately causes an overflow of feelings we would consider normal or naturally safe.  It’s because of these reasons why marijuana can be so useful in medical practices such as relieving pain/swelling and increasing appetites in cancer patients unable to enjoy food any longer.  However there are also many negative effects on the brain such as disruption of short term memory, altering the minds perception of time, and destroying natural levels of specific chemicals in your brain.  The question is does this drug have more pros then cons or is it as bad for you as your parents would have you believe.  This question cannot be completely yet due to the lack of long term evidence on the brain.  Until the long term effects of consuming THC are known, THC will continue to bind to medical patient’s receptors and illegally to the millions of recreational users throughout the world.

(http://io9.com/5794209/what-cannabis-actually-does-to-your-brain)

Stress: Good or Bad?

Everyone knows the feeling all too well, your cramped for time and you have so many things to do your head is spinning.  We call this mind boggling feeling stress.  Cortisol is the chemical found in the brain which is said to be responsible for managing stress levels.  While short term stress (less then 30 minutes) can be good for the brain and even incresase memory, attention span, and the immune system, long term stress takes our brains to the breaking point.  The article suggests that negative effects on the hippocampus may result from too much stress.  This happens when cortisol can no longer keep up with stress levels.  Long term exposure (greater than 30 minutes) may even result in the shrinking of the hippocampus with associated declines in memory, and cognitive function.  However, the article states that this damage may be reversed if the stressor is eliminated from the picture.    

(http://www.sharpbrains.com/blog/2008/02/05/stress-and-neural-wreckage-part-of-the-brain-plasticity-puzzle/)

lucid dreams

Imagine being able to control your dreams and do whatever you wanted while dreaming.  For some people this is possible and with training it may be possible for a majority of people.  A study conducted (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737577/pdf/aasm.32.9.1191.pdf) was able to obtain information from subjects able to produce lucid dreams in a lab.  Lucid dreaming can be described as dreaming however, you are aware that you are dreaming.  While dreaming the subject is able to recognize something isn’t right and realizes they are in fact dreaming.  A successful experiment was conducted in which subjects were asked to repeat a specific eye pattern (left horizontal movement, right horizontal movement, back to left, pause, then repeat) once they realized they were dreaming.  Further evidence was produced using electromyographic activity (EMG) in both periods of wakefulness and sleep.  They found that eye movements in REM sleep are significantly less distinct then the pattern the subjects were asked to repeat during lucid dreams.  Lucid dreaming can be thought of as a hybrid between REM sleep and being awake.  Graphical evidence supporting this statement shows the frequency averages of short, medium, and long-range coherences (in Hz) by measuring scalp potential, and current source density.  The graph depicts that lucid dreaming falls somewhere in between wakefulness and sleep.

Furthermore I have heard that it is possible to induce lucid dreaming by mentally preparing yourself before sleep to recognize strange things in dreams.  Im not sure if this is true either but if you lay perfectly still for 30-40 minutes without moving your brain begins to believe you are asleep and you are able to have out of body experiences such as lucid dreams.  

Pair Bonding

Ever wonder what attracts you to your significant other and gives you a special bond with them?  A study done on monogamous voles may have surprising ties with humans.  The study (http://www.nature.com/neuro/journal/v7/n10/pdf/nn1327.pdf) has found that two chemicals found in voles (and in humans) Oxytocin (OT) and Arginine Vasopressin (AV), have found to be very important in pair bonding.  The chemical Oxytocin has been shown to be very important in both males and females however more so to females then males.  Males on the other hand, seem to be more effected by Arginine Vasopressin which leads them to be more aggressive, mark their territory and courtship.  This is interesting because both sexes show the same number of receptors for both Oxytocin and Arginine Vasopressin.  The study has been able to conclude that when Oxytocin is present in both sexes, pair bonding is increased even without mating.  If Oxytocin is blocked for any reason pair bonding is prevented and the animals do not show signs of courtship.  In addition, prenatal exposure of Oxytocin from mother to child is directly correlated with the probability that offspring will exhibit strong pair bonding later in adulthood.  Could this be true in humans as well?  Does a mother who is happily bonded to a father while pregnant give her child a greater chance of being happily bonded to an individual later in life?  Lactating females have been found to release large amounts of OT during nipple stimulation (breast feeding) which is part of the reason they are so close to their offspring.  The article finds that dopamine levels in the prefrontal cortex, nucleus accumbas and ventral palladium have been found to play an important role in pair bonding.  Is there a direct correlation between dopamine and pair bonding?  Evidence suggests that mating and pair bonding are directly correlated due to releases of Oxytocin, Arginine Vasopressin and dopamine.  In addition the specific smell of the partner stimulates the olfactory nerves which in turn, end up releasing dopamine which is why voles prefer to spend time where their partners smell is strongest.  This specific smell has also been shown to eventually release both chemicals associated with pair bonding furthering pair bonding between individuals.  The study has also found that sex releases OT and AV in both males and females with a higher level of AV being released in males and additionally a higher level of OT being released in females.  Although this specific of a study has not been conclusively done on humans, it is hypothesized that humans do in fact have similar correlations with pair bonding.

Neurological reasoning behind thrill seeking behavior

Ever wonder why some people partake in extremely risky behavior such as skydiving, gambling, driving fast, or other dangerous activities?  You may notice that they even seem to be addicted to these activities and go to extreme lengths to find new “fixes”.  A study conducted by the journal of neuroscience (http://teachhealthk-12.uthscsa.edu/curriculum/critical-appraisal/Thrill%20Seeking%20Module%20pdfs/Journal%20Article%20Thrill%20Seeking.pdf) has linked the neurotransmitter dopamine to these thrill seeking behaviors in both rats and humans.  The study was conducted on 34 subjects and found that persons who reported higher occurrences of thrill seeking behavior have fewer total number of dopamine receptors in their brain.  They were also able to conclude that the fewer dopamine receptors is inversely proportional to the amount of the neurotransmitter (dopamine).  As we know dopamine is responsible for that good feeling we get when something good or exciting happens.  The human brain is able to correlate the memory of the exciting event and the good feeling associated with it.  This correlation alone is enough to release dopamine and encourages the individual to recreate the excitement in order to attain the same feeling as before.  This may seem very similar to another group of individuals which we know to be drug abusers.  Drug use as we know is very addicting and it takes more and more of the drug to feel the same effects as the first time the drug was experienced.  This makes people who participate in risky behavior more inclined to drug use.  The feeling behind the event is responsible for the addictive properties in both cases.

The results of the experiment can be found graphically in figure 3 in the experiment.  It shows direct correlation between the dopamine receptor availability and the subjects thrill seeking score.

Visual hallucinations and the Visual Cortex

Thanks to a helpful tip I was able to find a very interesting article all about what hallucinations come from in the brain.  The article titled What Geometric Visual Hallucinations Tell Us about the Visual Cortex. Neural Computation by Bressloff, Cowan, Golubitsky, Thomas and Wiener (http://www.math.utah.edu/~bresslof/publications/01-3.pdf) is extremely useful information on where hallucinations originate within the brain.  Bressloff states that images are generally seen in both eyes and move with them, but maintain their relative positions in the visual field.  This leads him to believe that the above statement is evidence enforcing that hallucinations are generated in the brain.  Sited in the article is information stating that when subjects are instructed to inspect the fine details of their hallucination the fMRI of the V1 area of the brain shows increased activity.  Is it possible that it is coincidence, and does the fMRI show increased activity in areas of the brain responsible for creativity? Is there a possibility that connections between these areas of the brain are linked with areas of the brain responsible for rationalizing thoughts?  Could an error in communication between these areas be responsible for manifesting hallucinations?

What Geometric Visual Hallucinations Tell Us about the Visual Cortex answers this question by with this quote “a nonuniform retino-cortical magnification is generated by the nonuniform packing density of ganglion cells in the retina, whose axons in the optic nerve target neurons in the lateral geniculate nucleus (LGN), and in V1, that are much more uniformly packed.  The article then goes on to prove with using mathematics (which are way over my head) reinforcing that constants are generated in V1.  In addition, this article also gives significant evidence to suggest that iso-orientated patches located on a hypercolumn are the circuits in V1 responsible for detection of oriented edges and formation of contours commonly seen in hallucinations.  This is further evidence suggesting that the V1 area of the brain should in fact show higher levels of activity using fMRI when subjects reporting hallucinations are asked to describe the fine details of their hallucinations.

Meth in Drosophila

The authors of Fruit flies on meth (http://www.sciencedaily.com/releases/2011/04/110420184431.htm) were able to identify the effects of meth on molecular pathways using Drosophila as test subjects.  A barrage of pathways affected by meth such as energy generation, sugar metabolism and hormones have been identified using fly's of all things.  Manfredo Seufferheld (co-author) found evidence that indicates that meth mirrors rapidly growing cancer cells by altering the metabolism of the user.  Both meth and cancer cells use a process known as glycolysis  to provide the energy needed to maintain homeostasis in both humans and flys.  This is different from oxygen respiration which is the process normal cells use while in the presence of oxygen.  This is also known as the Warburg effect.  In this study they were also able to determine that fly's like humans, crave drinks containing large amounts of sugar which is thought to be related to reducing the toxicity of meth.

Although Im no meth expert, a sugary drink seems a bit weak in combating the worlds worst drug and all the negative effects that go along with it.  

Hallucinations

My most recent article titled Visual Hallucinations Clinical Occurrence and Use in Differential Diagnosis which can be found (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1307180/pdf/westjmed00149-0042.pdf). The article defines visual hallucinations as a visual sensory perception without external stimulation, or operationally, as a behavioral syndrome in which a patient claims to see something or behaves as if he or she sees something that an observer cannot see.  One common form of hallucinations are from optic nerve disease which can be characterized by bright light in conditions where bright light is absent such as low light scenarios and closed eyelids.  This is usually stimulated by horizontal movement of the eye.  For whatever reason, the optic nerve is enflamed which causes the hallucinations.  Narcolepsy has also been found to cause hallucinations in cases of hypnagogic (falling asleep) of which 15-50% of subjects report experiencing hallucinations often occurring during sleep paralysis in which REM is interrupted.  Hypnopompic (waking up) subjects did not have a set % of occurrences.  Toxic or metabolic disorders often manifest different hallucinations due to low or high levels of chemicals affecting activity of optical nerves. 

The article also touches on area 17 or the primary occipital striate cortex.  This area of the brain is more likely to produce more unformed hallucinations or hallucinations that are noticeable but not clear.  In addition, area 18 or the area of the brain known as the peristriate visual association area has been found to produce patterned hallucinations such as swirls or checkered boxes.  Higher areas of visual association (area 19) produce complex hallucinations such as people and animals or larger more detailed hallucinations.

I also found it very interesting that children are much more likely than adults to have hallucinations such as imaginary friends or play objects as well as the ability to recall previously seen images as hallucinations.  Finally if anyone knows a great spot for more information on how LSD effects the brain let me know!

A clinical study of type 1 neurofibromatosis in

The article titled A clinical study of type 1 neurofibromatosis in north west England (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1734324/pdf/v036p00197.pdf) includes a study in NW England about Neurofibromatosis type 1 (NF1).  They found that in this particular region about 1 in 3000 to 1 in 4000 people have inherited this disorder which can be found as a mutation on chromosome 17.  The authors studied characteristics of NF1 and found Café au lait spots, Axillary freckling, Groin freckling, cutaneous NF as well as subcutaneous NF to be common symptoms associated with NF1.  The most common of outcomes due to these symptoms included optic nerve gliomas and Malignant nerve sheath tumors (MNST). The authors used a “time until an event” system from date of diagnosis to date of birth to determine percent’s of individuals and severity of symptoms and age comparison.  Out of the 523 persons affected by NF1, 327 of which were found to have a first degree relative showing symptoms of NF1 as well.  There was no evidence to show preference over male to females born to mothers known to have NF1.  Table 2 (found in article) demonstrates that younger persons tend to have higher numbers of expressed symptoms in comparison with persons of age.  This could be due to a higher death rate in cases with more severe symptoms or a greater number of symptoms expressed.  Of the reported tumors Plexiform tumors followed by Malignant nerve sheath tumors were found to have to highest percent rate of risk.  The necessary information was not available in regards to previous-existing plexiform neurofibromas. 

I am more interested in MNST and if anyone knows of a better study or any idea as to where to look, please share.  I am looking forward to learning more about MNST and will probably be writing another blog solely about them.  Thanks for your help!

Alcohol and Nuerotransmitter Interactions

I found an interesting article titled Alcohol and Neurotransmitter Interactions (http://pubs.niaaa.nih.gov/publications/arh21-2/144.pdf). The article states that alcohol disrupts the sensitive balance between inhibitory and excitatory neurotransmitters (NT) which can be thought of as a sort of scale such as a titer totter. Short term use of alcohol or binge drinking causes inhibitory neurotransmitters to become more heavily weighted on this scale which the article states decreases responsiveness of other neurons to further stimuli. Long term use of alcohol has just the opposite effect and the brain tries to equilibrate this unbalanced scale and thus increases the amount of excitatory neurotransmitters. Alcohol affectively increases receptors of glycine which acts as an inhibitory NT in the spinal cord as well as the brain stems causing the behavioral changes associated with alcohol consumption. The main inhibitory NT is called Gamma-aminobutyre (GABA) which is also responsible for behavioral changes. Increased amounts of GABA (in short term use or binge drinking) due to the effects of alcohol on Purkinje cells also affects the activation of neuroepinefrin which controls the NTs. Neuromodulators such as adenosine are increased which leads to the sedative effect of alcohol. Chemicals such as caffeine and theophylline found in coffee and energy drinks have the opposite affect and inhibits adenosine which is why it is very dangerous to mix alcohol with beverages containing caffeine. The main excitatory NTs are known as N-methel-D-aspartate (NMDA) and when these excitatory receptors show activity, increase changes in calcium levels of the nerve cells. GABA and NMDA are thought to work together and ultimately change the voltage-sensitive calcium channels, which in turn, are responsible for the electrical currents created in the neurons. In addition, short term use of alcohol increases GABA and inhibits the calcium flow which is vary dangerous because in large quantities can cause death through sedation of breathing and heart rate. In contrast, long term use decreases GABA which decreases the sensitivity to NTs.

I am still a little confused and would greatly appreciate any feedback to hopefully clarify this study. It was also hard to state the authors findings in a better way, simply said, they said it best!

Synesthesia

After listening to guest speaker David Eagleman talk about Synesthesia during a recent lecture I became extremely curious as to what it would be like to experience this condition. I did some goggling and found an interesting article which explains a little more about this condition. The article can be found here (http://www.lurj.org/article.php/vol2n1/synesthesia.xml).

Synesthesia is a condition in which someone’s bodily senses are associated with completely different senses as well as that particular sense. Such as being not only able to hear sounds but also see the colors of different specific sounds and be able to tell the difference in sounds by the color they see alone. There are many different examples of how synesthesia could be perceived such as hearing colors or smelling sound or even tasting the shape or different objects. Neurologists have concluded that persons with this condition are not able to control it and automatically done. They have also been able to conclude that different synesthetic events happen at different locations outside the body. An example we discussed in class was how the different days of the week had completely separate locations outside the body and can be recalled by locating the position. Having more than one way to remember a sound or read a word vastly improves people with synesthesia ability to remember extremely large quantities of information. For example the words of this blog would all appear as different colors (with the exception of identical words). Ramachandran and Hubbard were able to determine that synesthesia is a perceived effect after the organized a test in which they sporadically placed 2's and 5's (which look similar) onto a sheet or paper or other similar area and found that people with the synesthesia effect of seeing numbers as colors were immediately able to pick out the 2's from the 5's while people without this condition had to look at each individual number to pick out the 2's. This experiment only works with association of numbers with colors however. There is an example on the webpage which helps understand what it would really be like to have this condition.

The authors were also able to determine different areas of the brain (V1-V5) which are responsible for different visual processing abilities. They found that different areas of the V series could be activated through cross activation without the stimuli of that particular V series being present. They also found that when subjects view color their specific V series number which is responsible for color may not be stimulated.

Apparently there are drugs which can cause these effects such as LSD and Mescalin which could possibly be used to further study this condition. Another interesting stat noted is that this condition is found in a ratio of 6 women to every 1 man. I am very curious as to what would happen if you showed a person with association of color to numbers a number in an opposite or complementary color they see that number as. In addition I’m curious as to what would happen if you showed the reverse of areas associated with things such as days of the week to people with this condition. If anyone has any thoughts as to what might happen please share!

Anomalies in Neuronal Migration

I am still very curious about exactly how neurons develop and upon further investigation I found an interesting article that dictates how neuronal development can be considered abnormal. The article titled MR of Neuronal Migration Anomalies can be found here (http://www.ajronline.org/content/150/1/179.full.pdf+html).

In this study 13 patients with abnormal migratory neurons of all severities were observed using Magnetic Resonance (MR) to image the patients due to its high contrast between grey and white matter. Correct neural migration occurs from developing brains to all parts of the body during weeks 8 through 16 of pregnancy. Continual development also occurs until week 25 of pregnancy. However its during weeks 8-16 when the authors concentrate their study. Any injury to the brain during weeks 8-16 alters the migratory pathway of the neuron resulting in abnormalities such as seizures, mental retardation, and developmental delay to identify a few. The researchers also hypothesize that there is a possibility of genetics that plays a key role in the development of neuronal pathways.

The article states that at a specific area in the brain called the cell-sparse layer is most likely where a diversion of normal growth takes place. They believe that necrosis occurs in this area and further hinders the patient because the axons and places of dendritic connection which have already been established are also affected by the necrosis of the cell-sparse layer of the brain. They are able to determine that the axonal and dendritic connections of the white matter have been diminished due to the necrosis in the cell-sparse layer of the brain. This is called "syndromes with lissencephaly" and is still debated between professionals.

There is still much more to this article that explains in greater detail exactly how and why they believe the things mentioned above. I think it is very interesting how they have determined the information and I would really like to learn even more about other anomalies in neuronal migration
.

what happens during a seizure

While attending the U of M football game against New Mexico State I suddenly became intrigued as to what happens and what causes a seizure when U of M head coach Jerry Kill collapsed and had a seizure following a controversial call with 20 seconds left in a close game during a hot Saturday afternoon. The article (http://seizures.nicheinfo.info/Seizures_What_Causes_Them.php) seizures: what causes them, was just the info I needed to come to my conclusion. After reading this article I learned that what needs to happen in order for a seizure to occur is an irregular discharge of electrical impulses. With even a single irregular discharge the net of neurons connected to that single irregular impulse would also be affected. Although on medications for seizures Jerry Kill was dehydrated and most likely yelling after the blown call which was enough to trigger the seizure that followed. The article states that a lack of oxygen or any metabolic irregularities such as a change in chemical levels can be causes of a seizure. The dehydration would be enough to turn his blood slightly acidic and changed the amount of chemicals entering his brain and the blown call on top of that was enough to cause that sudden irregular impulse in his brain leading to the cascading effect of a seizure.

Second Impact Syndrome

During the season of my senior year of football I suffered two concussions within the same week. After hearing more about concussions (on multiple doctor visits) I became interested as to just what makes them so dangerous. When two concussions occur within a short amount of time there is a possibility of Second Impact Syndrome (SIS) which generally leads to death or being reduced to a vegetative state. I found an interesting article (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672291/ ) which explains why SIS is so dangerous

The article states that after a primary concussion the body tries to auto regulate the amount of damage to the brain by reducing the amount of blood flow to the brain. This is obviously problematic due to the fact that we know the brain needs plenty of oxygen and other essential items as well as getting rid of the waste products in order for the brain to operate at maximum performance. With an already limited amount of blood flow to the brain this makes the second concussion even more dangerous now that the brain has lost its ability to auto regulate. The article then states that even a non-lethal blow to the head after the initial concussion is sufficient to hinder the brains ability to manage intracranial pressure which leads to a subdural hematoma resulting in death. This can happen in a matter of minutes following the second impact!

I find it very interesting as to how the brains limits blood flow in order to try and minimize the amount of damage. Then again I can’t think of a better way to try and keep the amount of swelling down.

Migration of neurons

I found an intregging artical regaurding how nuerons "know" where to migrate to.  The article is titled Do neurons in the vertibrate CNS migrate on laminin.  Neurons connect to glical cells using a glycoprotein (specificly the glycoprotein laminin) to direct neural migration.  The authors used the brains of rat embryos to test limiting the amount of laminin to determine if it did or didnot affect the migration of neurons in the growing brain.  After the use of anti-laminin antibodies, "pockets" of laminin were found near radial glial fibers.  This provides evidence that this link between the laminin and the radial glial fibers (which provide a pathway for neuron migration) is somehow needed in order govern the role of glial fibers and the migration of neurons.  I found this article to be somewhat helpful but it is still unclear as to how exactly neurons migrate.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC554319/pdf/emboj00270-0085.pdf