Batrachotoxin Case Study

A voltage-gated sodium ion channel opens when there is a change in the voltage of the membrane and allows sodium ions to flow across its electrochemical gradient. These voltage-gated channels are made up of amino acids and they aid in generating and moving an action potential down a membrane or axon (Brooker, Robert, 106).

This stage is called repolarisation. The K+ channels then close, the sodium-potassium pump restarts, restoring the normal distribution of ions either side of the cell surface membrane and thus restoring the resting potential. In response to this the Na+ channels in that area would open up, allowing Na+ ions to flood into the cell and thus reducing the resting potential of the cells. If the resting potential of the cell drops to the threshold level, then an action potential has been generated and an impulse will be fired.

Increasing the extracellular potassium reduces the concentration gradient, and less potassium diffuses out of the neuron and into the cell.

Both electrical and chemical forces combine to determine the resting membrane potential of the cell. Although the resting membrane potential of most cells is normally negative, the selective permeability of the membrane allows certain ions in and out, causing the neuronal membrane voltage to become depolarized (more positive), or hyperpolarized (more negative). Key ions involved in muscle membrane potential are sodium, potassium, and chloride, which move via passive or active diffusion through ion channels and transporter pumps (Baierlein et al. 2011). The Nernst equation predicts the membrane voltage based on the assumption that the membrane is only permeable to one type of ion. In this investigation, we are seeking to understand the basis for how different ions interact to produce the membrane potential of DEM, DEL1, and DEL2 crayfish muscle

Voltage gated channels are necessary components of life processes, in many organisms. One in particular, is the calcium voltage gated ion channel. Often lodged within the phospholipid bilayer, the imbalance of the calcium, or, the inside vs outside concentration, creates a gradient. The channel proteins often undergo conformations, states that which allow or block calcium ions from passing through. As ions move inside the cell, this creates a depolarization, or surge in the voltage. Clinically, this is associated with the heart and how it allows the heart to contract, which can be read in the

Barbiturate brands included Amobarbital,Pentobarbital and has the street name of Downers, blue heavens, blue velvet, blue devils,Nembies, yellow jackets, abbots, Mexican yellows.Barbiturate is a class of drugs derived from barbituric acid that act as depressants to the central nervous system,which cause it to decease hart beats,respiration, blood pressure. It can dissolves easily in fat,and it already has access to the brain because they can cross the blood brain barrier easily. Barbiturates dissolves into body fat, they can accumulate and enter the blood stream later. Different barbiturates clear out of the blood stream at different rates.When is binds to the receptor for the neurotransmitter called GABA it increase the flowing of chloride ions across the neuronal membrane and causes the action potential to occur less frequently.

They are classified according to the trigger that opens the channel for such ions, either a voltage change or a binding of a substance to the ligand-gated sodium channels. Sodium channels consist of a large α subunit that associates with other proteins, such as β subunits. An α subunit forms the core of the channel and is functional on its own. When the α subunit protein is expressed by a cell, it is able to form channels that conduct Na+ in a voltage-gated way, even if β subunits or other known modulating proteins are not expressed. When accessory proteins assemble with α subunits, the resulting complex can display altered voltage dependence and cellular localization. Binding of natural brevetoxins to voltage-sensitive sodium channels (VSSC) results in a cadre of four distinct effects: a shifting of the activation potential to more negative values; prolonged channel open times; inhibition of inactivation; and induction of subconductance states. Individual brevetoxins exhibit differential sodium channel binding affinities and potencies. Differences in affinity of the natural toxins have been attributed to variations in lipophilicity, topographic features relative to the binding site, and differential toxicities based on affinity governed by specific molecular or structural differences of each toxin. Regardless of affinity, all toxins affect

When a membrane is excited depolarization begins. When the membrane depolarizes the resting membrane potential of -70 mV becomes less negative. When the membrane potential reaches 0 mV, indicating there is no charge difference across the membrane. the sodium ion channels start to close and potassium ion channels open. By the time the sodium ion channels finally close. The membrane potential has reached +35 mV. The opening of the potassium channels allows K+ to flow out of the cell down its electrochemical gradient ( ion of like charge are repelled from each other). The flow of K+ out of the cell causes the membrane potential to move in a negative direction. This is referred to as repolarization. ( Marieb & Mitchell, 2009). As the transmembrane potential comes back down towards its resting potential level and the potassium channels begins to close, the trasmembrane potential level goes just below -90mV, causing a brief period of hyperpolarization (Martini, Nath & Bartholomew, 2012). Finally, as the potassium channels close, the membrane turns back to its resting potential until it is excited or inhibited again.

Diazinon is a synthetic OP acaricide and insecticide widely used for veterinary and agricul-tural purposes; its animal and human exposure leads to nephrotoxicity (Pizzurro et al., 2014). Normally, chemical impulses are transmitted from the end of one nerve cell to the beginning of another in a synaptic cleft; one of the chemical transmitters used in animal nervous systems is called acetylcholine (ACh). After transmitting the nerve impulse, acetylcholine is destroyed by an enzyme called acetylcholinesterase (AChE); this helping to clear the way for another trans-mission. Organophosphates attach to AChE and prevent it from destroying acetylcholine, causing overstimulation of the nerves (Ware, 2000). Abdel-Daim (2014) confirmed that, DZN functions as an acetylcholinesterase (AChE) inhibitor. This enzyme breaks down the neurotransmitter acetylcholine (ACh) into choline and an acetate group. The inhibition of the AChE causes an ab-normal accumulation of ACh in the synaptic cleft.

Every organism has thousands of these junctions that control the movements of the body and cause the heart to beat. The neuromuscular junction is a chemical synapse consisting of the point of contact, between the axe on terminals of a motor neuron and the motor endplate other skeletal muscle fiber. The events at the neuromuscular occur in seven coordinated steps. 1. The action potential arrives at the axon terminal. 2. Voltage-regulated calcium channels open allowing calcium ions to enter the axon terminal. 3. Presence of calcium ions in the axon terminal cause synaptic vesicles to fuse with the membrane. 4. Acetylcholine is released into the synaptic cleft and calcium ions are pumped out of the axon terminal. 5. Acetylcholine binds to receptor sites on the motor end plate, causing an influx of sodium ions and a small efflux of potassium ions, which results in a local depolarization of the motor end plate. 6. An action potential is generated which propagates along the sarcolemma in all directions and down the T tubules. 7. The action potential causes the release of calcium ions from the terminal cisternae into the

The human body has various systems of how it is able to transmit signals across various tissues. One of the most important systems the body uses for this signaling is ion channels. Ion channels are found in every part of the body, and are specifically used to transmit ions across gradients. In skeletal muscle, these ion channels are used for muscle contractions that are coupled with action potentials and are initiated by depolarization of cellular membranes. In skeletal muscle this occurs by a single nerve impulse that travels through neuromuscular junction (NMJ) and along the surface of the sarcolemma membrane. The signal then enters radially inward along the transverse tubules which causes a conformational change of the calcium channels and releases Ca2+ from the sarcoplasmic reticulum, inducing a muscle contraction. In certain disorders caused by mutations of ion channels downstream of the NMJ, altered muscle contractions or muscle weakness may occur.

Ion channels only allow certain ions in and out of the cell and can open or close depending on input received from other neurons. When positively charged information (excitatory) is received from other neurons it is called the action potential, during this phase sodium is allowed through the ion

Anesthetics inhibits nerve conduction by blocking sodium channels (prevent increase of membrane permeability to sodium ions) so the raising phase of action potential is inhibited, hence no action potential is generated and no nerve impulses are conducted to the central nervous system. Nerve cells are selectively permeable to ions. During rest, potassium channels are open in nerve cells and sodium channels are closed. If a nerve cell is excited, the membrane opens due to its permeability to sodium ions. A positive charge is gained, and the propagated action potential is passed along. The opening of more potassium leak channels means that more potassium ions will flow out of the cell, consequently resulting in the hyperpolarization of the cell.

The GABA receptor is a ligand –gated chloride channel. The binding of GABA increases the influx of chloride ions into the postsynaptic cell raising its membrane potential. This is extremely fast response only taking a

Saxitoxin (STX) is a neurotoxin that blocks neural transmission by binding to the voltage-gated Na+ channel. When bound to the voltage-gated Na+ channel, STX inhibits the permeability of Na+ ions, which are responsible for depolarizing the membrane. Since STX keeps the membrane from depolarizing, the resting membrane potential would remain the same.