With respect to communication among lateral line hair cells, these cells communicate via reveal synaptic communication which involves the use of Afferent neurons synapse. Communication is established between hair cells of a given polarity and the afferent neurons. A stimuli enters hair cells by passing directly through mechanically gated transduction channels on the stereocilia and subsequently permeates to the afferent neurons, but may be blocked when the mechanotransducing channels are closed.
The lateral line hair cells are said to interact with the neighboring cells such as the KINOCILIUM. The kinocilum is A special type of cilium on the apex of hair cells located in the sensory epithelium kinocilia are found on the apical surface of hair cells and are involved in both the morphogenesis of the hair bundle and mechanotransduction.. With respect to the communication between the hair cell and the kinocilium, the kinocilium is said to respond to Vibrations that cause displacement of the hair bundle, resulting in depolarization or hyperpolarization of the hair cell. The depolarization of the hair cells in both instances causes signal transduction via neurotransmitter release. This results in the movement of the entire hair bundle, which will cause will cause potassium channels on the stereocilia o the hair cell to open. This depolarization will open voltage gated calcium channels and the depolarization of the hair cell causes neurotransmitter to be released and an increase in firing frequency of cranial nerve VIII. Hence the communication process is complete.
The model organism is choose to study is the ZEBRAFISH.
What is a model organism?
Model organisms are those that useful data sets have been already gathered to describe basic biological processes. A model system is a simpler system that can be acquired and easily manipulated.The characteristics common to model organisms, include 1) rapid development with short life cycles, 2) small adult size, 3) ready availability, and 4) tractability. There are three advantages to using model organisms in teaching biology. Firstly in a laboratory setting, the model organism’s immediate response to the change of environment will generate observations. Secondly, it involves hands-on experience. Thirdly, by working with model organisms, students are able to explore scientific methods and concepts.
The cell I am researching from the Zebrafish are the LATERAL LINE HAIR CELLS
INTRODUCTION ON THE LATERAL LINE HAIR CELLS
Lateral Line hair cells are said to orginate in thickened sensory patches, where they are anchored in a pseudostratified epithelium, and are found distributed with supporting cells, which spread throughout the epithelium. The purpose of the lateral-line hair cell is to detect water movement and vibration and is important in detection of predators and prey. With respect to the aging of the these hair cells, they usually diminish in number due to cells being damaged. However, hair cells in the zebrafish lateral line regenerate rapidly and completely after damage. Damage to hair cells is result of with many factors, including exposure to various drugs, loud noise, and age-related degradation
STRUCTURE OF THE LATERAL LINE HAIR CELL.
Hair cells have a well-defined apicobasal polarity, with specialised cytoskeletal structures on their apical surfaces. These consist of a bundle of stereocilia, arranged in a stepped array, and a single kinocilium. Stereocilia and kinocilia are embedded in the otolithic membrane or a gelatinous cupula. Stereocilia vary in number and length, depending on the type of sensory patch. The location of the kinocilium relative to the stereocilia gives each hair cell a polarity in the plane of the epithelium. Hair cells synapse with afferent and efferent neurons are on their basal surfaces.
“Nerve agents.” http://www.pdhealth.mil. N.p., n.d. Web. 31 Mar. 2013. .
Nerve agents are weapons that are used in chemical warfare, such as tabun, sarin, soman and cyclosarin. There are usually volatile at room temperature and have greater density than air.
Nerve agents function by the inactivation of the enzyme/ phosphorylating acetylcholinesterase (AChE). The nerve agent binds to AchE and the chemical bond is formed resulting in the accumulation of acetylcholine (ACh) at receptors at nerve synapses, as well as receptors in the central nervous system (CNS). This leads to diarrhea, frequent urination, and salivation. Other symptoms include nausea, vomiting, eye pain, blurred vision, muscle pain, tremors, weakness, hypertension, headache, agitation, confusion, vertigo, decreasing consciousness, seizures, as well as coma. The combination of these effects can cause acute and fatal respiratory failure muscle paralysis, and CNS mediated depression of the respiratory drive.
The diagnosis of nerve agent exposure is done by drawing blood for red blood cell AChE activity. If this red blood cell AChE is reduced by 70%, the test is positive.
For treatment of nerve agent exposure, two antidotes are used 1) pralidoxime and 2) atropine. One is usually incubated and put under ventilation to control the airway, as there is usually muscle weakness, causing respiratory difficulty. Side effects of this antidotes include seizures and respiratory infection.
Recovery from nerve agent poisoning is the most crucial. There is a delayed response syndrome which is usually temporary but may also result in the re-initiation of respiratory incubation. Some usually experience muscle paralysis after recovery, as most of the nerve were damaged due to exposure to the nerve agent. As a result of nerve damage, blurry version occurs and in a worst case scenario blindness occurs.
Hamel, Jillan. “A Review of Acute Cyanide Poisoning With a Treatment Update .”
Critical Care Nurse. http://ccn.aacnjournals.org/content/31/1/72.full (accessed March 31, 2013).
Acute Cyanide Poisoning With a Treatment update
Cyanide can be found in many household item, such as wool and which contain carbon and nitrogen and may release cyanide gas when exposed to high temperatures. Constant exposure to cyanide gases, result in increase in cyanide concentration within the blood and hence causing cyanide poisoning, Cyanide can also be used in the industry for the use of electroplating of metals. These cyanide salts the produce hydrogen cyanide gas with the presence of acids, hence resulting in cyanide poisoning. . Left untreated, it can result in illness and death.
Cyanide is poisonous as it diffuse into the tissues and connects to target site immediately and symptoms occur quickly. One of the most common sources of cyanide poisoning, is from smoke inhalation from structural fires. Cyanide poisoning occurs from improper functioning of the cyanide metabolism, causing an accumulation of thiocyanate. The accumulation of thiocyanate is due to the fact that the enzyme rhodanese, from the liver, does not catalyze all the cyanide to thiocyanate. The thiocyanate then gathers in the kidney causing impaired renal function, due to the high toxicity, hence the body is unable to excrete thiocyanata at the proper rate, resulting in cyanide poisoning.
Upon inhalation of cyanide gas one can develop anxiety, headaches and lack of focus. Further progression of cyanide poisoning one may experience skin ashening, rapid and deep respirations. It also affects the cardiovascular system such as vasodilatation , hypotension, increase in arrhythmias, bradycardia, heart block and cardiac arrest.
For treatment of cyanide poisoning one must determine the cause of exposure of cyanide gas to be given to proper antidote. A person health status is also a factor in determining the correct antidote. These antidotes include 1) cyanide antidote kit and 2) hydroxocobalamin.
The cyanide antidote kite contains 3 medications given together for their combined effect. When it is administered, great attention is paid to the patient as vasodilatation and hypotension may occur. Basically, the cyanide antidote kit, restores the proper functioning of the enzyme rhodanese. However, Hydroxocobalamin detoxifies cyanide by combining with it to form, nontoxic cyanocobalamin. Cyanocobalamin diffuses cyanide at a rate that is adequate enough to permit the enzyme rhodanese to detoxify the cyanide in the liver. Hence they both convert cyanide.
Based on what u have u learned on this topic you should be able to answer the following question. Good luck!!!!
1)Which of these enzyme reactions is not irreversible in glycolysis?
c) phosphoglycerate kinase
e) Pyruvate kinase
2)Select the correct multiple answer using ONE of the keys A, B, C, D or E as follows:
a) 1, 3 and 4 are correct
b) 1 and 3 are correct
c) 2 and 4 are correct
d) only 4 is correct
e) all are correct
Which of the following enzymes are involved in the prepartory phase of gylcolysis:
Glycolysis is the conversion of glucose to pyruvate. It is universal meaning is its a process done by bacteria, yeast and humans. It involves two stages 1) Energy investment stage and 2) Energy generation stage, each of which involves 5 enzyme reactions, Giving a total of 10 enzyme reactions
overall the net gain is 2ATP AND 2NADH
THE FATE OF PYRUVATE
Metabolism of Fructose
1)in the adipose tissue, muscle and kidney – hexokinase can phosphorylate fructose to fructose-6-phosphate that the enters glycolsis.
2)in liver – glucokinase enzyme is presnt instead of hexokinase and doesn’t phosphorylate fructose. fructose is metabolized by frcutose-1-phosphate pathway
metabolism of Galactose
Below are some questions bases on what we have learned on Enzymes good luck!!!
1)All of the following are characteristic of enzymes expect :
a)very specific ie catalyze one type of reaction
c)enzyme catalyzed reactions are irreversible
d)lower the activation energy of a reaction
e)enzyme is left unchanged after the reaction
2)Select the correct multiple answer using ONE of the keys A, B, C, D or E as follows:
A. 1, 3 and 4 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. only 1 is correct
E. all are correct
Which of the following can affect enzyme activity
Inhibition of Enzymes
any substance that can diminish the velocity of an enzyme catalyzed reaction is called an inhibitor. Irreversible inhibitors bind to the enzymes through covalent bonds. Reversible inhibitors bind to the enzyme through non-covalent bonds.
Types of inhibition
occurs when the inhibitor binds reversibly to the same site that the substrate would normally occupy and therefore, competes with the substrate for that site.
Non- competitive inhibition
This type of inhibition is recognized by its characteristics effect on Vmax. Occurs when the inhibitor and the substrate bind at different sites on the enzymes.
the inhibitor binds only to the enzyme substrate complex, at separate site from the substrate active site and not with the free enzyme.
when inhibition binds at a separate site from the substrate active site, to either the free enzyme or the enzyme-substrate complex. It resembles the non-competitive inhibition.