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Local stimulus generates the interaction of ligand-gated channels within the cell membranes of dendrites in what is known as a graded potential (GP). It is referred to as ‘graded’ since its size and duration is equivalent to the stimulus that generates it and voltage potential associated with it is within the range of 1 to 50 mV (McCormick, 2014). GP is yielded by the flow of sodium ions into the fluid of the inner cell and this reduces the negative charges within until it reaches a specified threshold to cause local current flow at the point of stimulation. The voltage flow is however associated with leakage of sodium ions via capacitance and resistance of the membrane.
Action potential is not generated when the graded potentials do not have a specific threshold value of voltage. The GP therefore sum up to create a sufficient voltage for the creation of AP at the axon hillock. In other words, AP is created when a stimulus induces the cell membrane to depolarize beyond the threshold of excitation which compels the opening of all channels of sodium ion.
Depolarization is the decrease in the difference between the membrane potential of the inner neuron and the outer neuron. The resting membrane potential is due to the difference in the amount of sodium ions and potassium ions in the internal and external cells. Depolarization occurs when the nerve impulse forces sodium ions into the cell.
Action potential phase starts when there is sufficient strong depolarization occurring beyond a threshold excitation. Increased membrane potential makes depolarization to open up channels within the membrane to enable sodium ions to flow inside and potassium ions to flow outside of the axon. This short term change in the electric potential travelling along the cell can be described as follows;
Stimulus makes the targeted cell to depolarize from the resting potential up to the point of threshold of excitation. At the threshold of excitation, sodium ion paths opens up and the membrane becomes depolarized until it reaches the optimum level of the membrane potential. Channels of sodium ion then close at the peak of action potential. Repolarization ensues just after the peak action potential. Potassium ion channels then opens and potassium ions move out of the cell causing the membrane to be hyperpolarized. The resting potential is restored when the potassium ion no longer moves out of the cell membrane and the channels closes.
Neurotransmitters are required for the communication at chemical synapses. Pre and post synaptic membranes are usually gapped by a fluid filled space known as synaptic cleft. In the event that presynaptic membrane is depolarized, calcium ions enter the cell thus causing the synaptic vesicle to mix with membrane which in turn allows the molecule of neurotransmitter to be released into the synaptic cleft.
The fused neurotransmitter on the synaptic cleft then attaches itself on the channels of the postsynaptic membrane which leads to either a localized hyperpolarization or depolarization of the postsynaptic neuron. Calcium ion that gets in the cell therefore induces a signal of protein that has been attached to it, SNARE protein. Calcium bonded with the protein then associates with SNARE protein. The synaptic vesicle then fuses with the presynaptic axon terminal membrane and discharges calcium into the synaptic cleft via exocytosis (Webb and Adler, 2001).
Discuss Neurotransmitter Release by Motor Neuron
Neuromuscular junction is a chemical synapse link between the motor neuron and muscle fiber and for the nervous system to efficiently function, neurons must be able to send and receive signals. Signals are transmitted by neurons due neuromuscular junction and this enables contraction of the muscles. The signals transfers are possible since all neurons have charged cellular membranes. Charges on membrane shift with respect to the stimuli and neurotransmitter molecules discharged. In the event that AP reaches the neuromuscular junction, it initiates the freeing of acetylcholine within the particular synapse. The acetylcholine then attaches itself to the nicotinic receptors of the motor end plate which are specified of the post synaptic membrane.
Nerve impulses require neurotransmitters to move from one neuron to the next neuron. The nerve impulse arrives at the synapse at the neuron end where it initiates the neuron to release neurotransmitter that floats between the neurons. Synapses act as the link between the nervous system and the neurons. Neurotransmitter released in the synapse allows the neuron to send impulses between themselves in a single direction. The release of synapse is controlled by the voltage-dependent calcium membrane. Vesicles that are recreated by cells are also necessary for the transmission of nerve impulses. The transfer of electric impulse can either occur between a nerve and another nerve, or between a nerve and a muscle (Martini, 2018).
Motor neurons release acetylcholine that penetrates through the synaptic cleft and sticks on nicotinic acetylcholine receptors in the motor end plate. Motor end plate is the terminal formation where axon of the motor neuron creates a synaptic link with bands of muscle fiber. Neurotransmitter is released when an AP moves to the axon of the motor neuron and this causes a change in the permeability of the synaptic terminal membrane that allows in calcium ions. Calcium ion then allows binding of synaptic vesicles with neuron’s presynaptic membrane. Neurotransmitters act as the binding sites. Binding at neurotransmitter causes opening of the ion channels where sodium ion gets in the cell to cause polarization and depolarization on the outer side. Neurotransmitter binding to its receptor can be reversed and it continues to impact membrane potential provided it is attached to the post synaptic receptor.
Discuss how the Neurotransmitter Causes Muscle Stimulation
Motor neurons that are responsible for relaying signals have their synapse ends on muscle fiber at the neuromuscular junction (NMJ). The signal from the brain is received by the motor neuron which then excites impulse on its axon to the NMJ; within NMJ motor neuron releases acetylcholine neurotransmitter over the muscle fiber. Calcium pores on the muscle fiber therefore opens their pores. Calcium ion then fills the fiber thus causing contraction. The acetylcholine is then released and drawn by the motor neuron. Absorption of acetylcholine by motor neuron causes muscle fiber to release calcium and the same time making muscle to relax.
Adenosine triphosphate (ATP) is the biochemical energy that is utilized to power the motion of contraction within muscles. According to Dharani, ATP is however not kept largely within the cells but only released with respect to the movement of the muscles. ATP has three main uses within the muscle fiber contraction, that is;
i. It activates myosin head so that it attach itself to it,
ii. Once it attaches to myosin, it causes release of whatever was attached on actin,
iii. It provides the energy that powers the transportation of calcium ion.
ATP attaches to myosin which then raises its energy and then it removes the myosin head from actin. ATP then again attaches to myosin to allow the beginning of another cycle which promotes further muscle contraction.
The two common ions which are monitored here with respect to cell membrane are potassium and sodium. The sodium ion concentration is highest in fluids outside the cell of neurons while potassium ions are at a high concentration inside. Signals can then be passed through the membrane since the membrane potential can be shifted by opening and closing the ion channels of potassium and sodium.
Usually, the resting membrane potential is at -70 mV while the threshold of excitation of the membrane where ions can exchange is at about -55 mV (Martini, 2018). The inner part of the membrane amasses more anions due to the presence of cations of sodium and potassium and its preferential permeability to these anions. Since the plasms membrane is easily penetrated with potassium than sodium, the transmission rate of sodium to potassium is in the ratio of 3 to 2 so as to conserve the resting potential between the anions and cations (Johns, 2014).
Muscles have myosin and actin filaments of proteins. Contraction of muscles happens when myosin and actin successively slide over each. Impulse or command is first sent to down to the neurons that connects to the muscle, motor neuron. The first step starts by ATP attaching itself to the myosin thus elevating its energy potential. The enzyme ATPase then causes the ATP to be decomposed through hydrolysis into ADP, inorganic phosphate, and energy. The energy released then transforms the myosin head in a tilted position for binding to actin at free sites. This causes the lighter actin filament to slide on top of the myosin filament and contraction occurs.
Dharani, Krishnangopal,‘The Biology of Thought,’ 2015.
Johns, Paul, ‘Chapter 6-Electrical Signaling in Neurons’ 2014, pp.71-80 https://doi.org/10.1016/B978-0-443-10321-6.00006-0 Accessed 13 November 2018
Martini, Frederick, et al Visual Anatomy & Physiology. Pearson, 2018
McCormick, David, A. Membrane Potential and Action Potential from Molecules to Networks, 2014, pp. 351-376
Webb, Wanda & Adler, Richard, Neurology for the Speech-Language Pathologist, (6th
Edition), 2001, ISBN-13: 978-0323100274
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