2007 Wilson IB Biology

I decided to blog about cocaine. While doing some research, I learned that cocaine blocks the reabsorption of dopamine(Dopamine, a “reward” neurotransmitter that can be triggered by pleasurable activities like eating and sex, and by drugs ranging from alcohol and nicotine to marijuana and cocaine, is a primary player in addiction.) and noradrenalin at the synapse of the brain. This is bad because it helps in the increase of energy, alertness and talkativeness. Therefore, it gives a feeling of openness and extreme happiness.

Cocaine causes constrictions of blood vessels which delays the absorption of the dopamine and noradrenalin which causes the brain to be more pron to addiction and overdose problems.

Benzodiapenes are a sedative drug used to slow down the central nervous system. They generally have amnesic, anticonvulsant, and muscle relaxing qualities. They are also used as a means of “coming down” from a hallucinogenic attack. Benzodiapenes bind the the GABA receptors in the central nervous system. These receptors are some of the most inhibitory in the brain. When they bind to the GABA receptors, there tends to be a sedating or a hypnotic response depending on the section of the brain and the make-up of the receptors. These can also be inhibited by ligands that bind to the active sites of the receptors, thus not allowing the benzodiapenes to take effect.

As we all know, alcoholic beverages are harmful to our body, specifically our nervous system. It affects the brain by causing slurred speech, clumsiness, and delayed relaxes. Alcohol damages dendrites, which affects the nerve cells’ ability to send messages into the cell. Alcohol also affects the brain by altering levels of neurotransmitters. It increases the effects of the inhibitory neurotransmitter GABA in the brain. GABA causes the clumsiness and slurred speech that occurs . At the same time, alcohol inhibits the excitatory neurotransmitter glutamate. Suppressing this stimulant results in a similar type of physiological slowdown.

Alcohol affects the different regions of the brain listed below:

• Cerebral cortex: In this region, where thought processing and consciousness are centered, alcohol depresses the behavioral inhibitory centers, making the person less inhibited; it slows down the processing of information from the eyes, ears, mouth and other senses; and it inhibits the thought processes, making it difficult to think clearly.
• Cerebellum: Alcohol affects this center of movement and balance, resulting in the staggering, off-balance swagger we associate with the so-called “falling-down drunk.”
• Medulla: This area of the brain handles such automatic functions as breathing, consciousness and body temperature. By acting on the medulla, alcohol induces sleepiness. It can also slow breathing and lower body temperature, which can be life threatening.

In the short term, alcohol can cause blackouts — short-term memory lapses in which people forget what occurred over entire stretches of time. The long-term effects on the brain can be even more damaging.

 Moral of the story: DO NOT DRINK ALCOHOL!!!!!

We’ve all heard of the common antidepressent, Prozac [fluoxetine], released in 1987.  There are various neurotransmitters involved in depression.  Any changes out of the normal in the neurotransmitter serotonin, affect mood and behavior.  SRI’s seems to block the reuptake of the neurotransmitter by certain neurons.  This is a selective to serotonin.  Other drugs that a SRI’s include: Citalopram, Escitalopram, Fluoxetine, Paroxetine, and Sertraline.

  SRI’s are considered safer than other antidepressants.  Some of the side effects include: nausea, sexual dysfunction, diarrhea, nervousness, rash, agitation, restlesness, increased sweating, weight gain, drowsiness, and insomnia. These are general side effects to SRI’s but may vary for specific drugs.  It has also been reported that some symptoms of depression worsen, and there could be an increase in suicidal thoughts.  Ultimately, the most rare side effect would be known as Serotonin Syndrome.  Serotonin syndrome is characterized by high levels of serotonin in the brain.  This is caused by an interaction with other antidepressants (Monoamine Oxidase Inhibitors).  Some of the main symptonms of serotonin syndrome include: confusion, restlesness, hallucinations, extreme agitation, changes in blood pressure, an increase in heart rate, nausea (vomiting), fever and seizures. Serotonin Syndrome

 There are some safety concerns with SRI’s incluuding birthdefects in babies born from women who were taking Paxil.  Risk seem to increase after 20 weeks of pregnancy thus it is not suggested that pregnant womne take Paxil. Depression and Pregnancy 

Warning: Do not do this at home. Instead, do it with Carolyn…at a frat party.

Cocaine acts at synapses that use dopamine as a neurotransmitter.

 It binds to dopamine reuptake transpoters, which are membrane proteins that pump dopamine back into the pre-synaptic neuron. 

Because cocaine blocks these transporters, dopamine builds up in the synaptic cleft and the post-synaptic neuron is continuously excited.

Cocaine is therefore an excitatory psychoactive drug.

Synapses that use dopamine are part of what is known as the reward pathway that gives us pleasureable feelings during certain activities.

Cocaine gives its users feelings of euphoria that are unrelated to any particular activity.

This link gives animations of cocaine’s effect on the brain:

http://www.cerebromente.org.br/n08/doencas/drugs/anim1_i.htm

Benzodiaepenes are drugs that are used to treat many things including anxiety, insomnia, muscle spasms, and amnesia. Benzodiaepenes work by promoting and enhancing the neurotransmitter GABA.  GABA is an inhibitory neurotransmitter thus benzodiazepenes work to have a quieting effect on the brain, and work to slow the firing of neurons.

What is a Monoamine Oxidase Inhibitor?
  MAOIs are typically used to treat atypical depression. Certain variant forms of MAOIs serve to treat distinct phobias, anxiety and to assist people in quitting smoking.

How does an MAOI work?
  MAOIs inhibit the effect of monoamine oxidase, an enzyme which is used to break down monoamine neurotransmitters (dopamine, seratonin, epinephrine, norepinephrin and melatonin. By disrupting the breakdown of these NTs, MAOIs prolong their effect within the nervous pathways, excitory effects which are converse in a person diagnosed with depression. MAOIs are able to permeate the brain blood barrier through a floride attachment and can remain there for a an ample amount of time. The danger with MAOIs is that may lead to hypertensive heart risks and possibility of stroke.

Today in class we finished up our discussion of neurons. As always, we discussed how the structure complements the different functions of the neuron. One specific example is that of the myelin sheath. The Schwann cells are comprised of liipids that are wound around the axon. These segments speeds up the action potential in the neuron. The myelin sheath alludes yet again to the electrical qualities of the human body, in that it acts as insulation from other neurons that may affect it. We also learned about the nodes of Ranvier. These are the segments of the axon that are not covered with the myelin sheath.

We also further affirmed our notions on how an action potential is generated. An influx of sodium ions, let in through voltage-gated channels, is let in when the neuron reaches its threshold. This creates a positive charge inside the normally negative membrane. The cell must then repolarize and potassium and sodium are let out though gated channels in order to maintain the charge of -70 millivolts. This reaction travels down the axon as seen in the picture below.

Today, we reviewed the action potential and the neuron.  In addition, it was established that the reason why the action potential was important was for the REPOLARIZATION post the action potential (for more information on the role of voltage-gated ion channel in the action potential go to p. 968 in the Campbell Biology book (5th edition) figure 48.7) .  We also established that the way to get the neuron to fire was if there was a lot of fast firing neurons (temporal summation) or to receive and input from many neurons.  Furthermore, it was introduced that not all receptor sites are excitatory, some are inhibitory.  In the brain, the cerebellum has a lot of inhibitory fibers which help keep balance, since the cerebellum has a lot of input from the mid ear. Similarly, inhibitory cells control excitatory activity to prevent epileptic attacks. 

 Here is a quick review on synaptic transmission:

 Messages travel through the neuron in the form of electrical impulses.  Neurons transmit messages through the synapse which is usually located at the end of the axon or attached to a receptor cell.  After traveling through the axon, the message arrives at the end. Once arriving at the end, a neurotransmitter [chemical substance] gets released.  The neurotransmitter substace is diffused across a gap to the next neuron.  This neurotransmitter propagates an electrical impulse.  While the electrical impulse travels down the neuron for the process to repeat, in the synaptic gap and enzyme breaks down the neurontransmitter.

Here is an example with more detail (from Allot, new edition):

First, a nerve impulse reaches the end of a ‘pre-synaptic’ neurons.  Then calcium diffuses through calcium channels.  Once the calcium diffuses, vesicles of neurotransmitter move to the membrane and release contents (exocytosis).  Neurotransmitters diffuse across the synaptic cleft and bind to a receptor.  Sodium channels enter ‘post-synaptic’ neuron and cause depolarization. This depolarization leads to an impulse set off in a ‘post-synaptic’ neuron. Then the neurotransmitter is broken down in the cleft and reabsorbed in the vesicles. 

FOR MORE INFORMATION ON SYNAPTIC TRANSMISSION YOU CAN GO TO THE ALLOT REVIEW BOOK: CHAPTER 24, PAGES 240-245 OR THE CAMPBEL BIOLOGY BOOK (5TH EDITION) CHAPTER 48 PAGES 960-989.   

 The rest of the class we devoted to the knee-jerk reflex.  Once the knee is jerked, the tendon (patella) below the knee, connect to the quadriceps (movement) of the thigh.  The ‘tap’ on the knee causes the muscle to stretch. This causes a stimulation in sensory neurons that send an impulse to the spinal cord (central nervous system).  Once in the spinal cord, motor neurons conduct an impulse to the quadriceps that make making the muscle contact (kick). At the same time, inhibitory interneurons, inhibit the contraction of the hamstring.   The knee-jerk reflex is also known as a monosynaptic reflex.

More on the reflexes

Remember there is a test on THURSDAY.  Chapter 30 (303-314) is specifically Neurobiology and Behavior.

If you have anything to add or correct, please comment.

The basic components you need to know for neural electrical properties are dendrites which receive input, the soma the body of the cell, and the axon which emits the output.

Na/K (Sodium/Potassium) Pump:

The sodium and potassium are a source of bio electric energy because their ions have charges. When there is a difference between the membranes of the sodium and potassium then there is an electromagnetic charge because of the diffusive force (ex. concentration of sodium rising on one side) and the electrical force (ex. pull of sodium to the more negative side). The diffusive force and the electrical force are both what powers the brain. When neurons get to a certain threshold, the active channels turn on and the gates open up for more sodium to come into the membrane. When the voltage is even higher, posstasium channels may open up and allow potassium to flow through.

In a neuronal transmission, an electrical signal is being sent down the neuron. Then during an action potential, a synaptic even will occur in which the synaptic termails will be activated to release neuro transmitters. The lease of neuro transmitters activates the ligand channels and binds to them to open the gates. The action potential is what proves the synpatic terminal to power up and function.

The dendrites are the part that recieves signals from many kinds of other neurons, in which the neuron uses all of the information and tries to compute answer as to either make an action potential or not.