1. The following are 8 factors that can influence the potential on the postsynaptic membrane:
(a) Excitatory Postsynaptic Potentials (EPSPs): EPSPs increase the postsynaptic neuron’s likelihood to generate an action potential by generating a local depolarization. EPSPs result from excitatory stimuli, such as an excitatory neurotransmitter (Glutamate) released by the presynaptic neuron. Excitatory stimuli will bind and open ligand-gated Na+ channels, allowing Na+ ions to move inside a cell down their concentration gradient. The influx of Na+ ions will cause a local depolarization at the postsynaptic membrane, which if summated can reach threshold and fire an action potential.
(b) Inhibitory Postsynaptic Potentials (IPSPs): EPSPs decrease the postsynaptic neuron’s likelihood to generate an action potential by generating a local hyperpolarization. EPSPs result from inhibitory stimuli such as an inhibitory neurotransmitter (GABA) released by the presynaptic neuron. Inhibitory stimuli can bind and open ligand-gated K+ channels and Cl- channels, allowing K+ ions to move out of a cell and allowing Cl- ions to move into a cell down their concentration gradient. The influx of Cl- ions and the outflux of K+ ions causes a local hyperpolarization at the postsynaptic membrane, which reduces the postsynaptic neuron’s probability to firing an action potential.
(c) Temporal Summation: The presynaptic neuron can influence the postsynaptic neuron by changing the frequency of the stimulus.
If the frequency of action potentials in the excitatory presynaptic cell increases than the number of action potentials in the postsynaptic cell will increase as well. This is due to temporal summation of EPSP at very frequent times. This causes the postsynaptic cell to produce many action potential in succession.
1. Exceeding the threshold depolarization at the trigger zone DECREASES the likelihood of generation of action potential.
Inhibitory transmission is the process of producing hyperPolerpolarizin which makes presynapse transmission band synaptic invasion less likley.
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.
Once a presynaptic neuron is passive, an electrical current is spread along the length of the axon (Schiff, 2012). This is known as action potential (Pinel, 2011). Action potential happens once an abundant amount of depolarisation reaches the limit through the entry of sodium, by means of voltage gated sodium channels
B ) (1) neurotransmitter released (2) diffused across the synaptic cleft to a receptor protein (3) binding of the transmitter opens pores in the ion channels and negative ions move in.
Increasing the extracellular potassium reduces the concentration gradient, and less potassium diffuses out of the neuron and into the cell.
-It is harder to generate a second action potential during the relative refractory period because a greater stimulus is required because voltage-gated K+ channels that oppose depolarization are open during this time.
In a normal and healthy nervous system, many electrical signals are received and sent through neurons. The arrival of those signals at the end of the neuron triggers the release of many chemicals, in specific, neurotransmitters (Brooker, 2011). These chemicals travel into a gap between the presynaptic (end of one neuron) and the beginning of he postsynaptic (next neuron). This gap is named a synapse (Brooker, 2011). Neurotransmitters are then released into the synapse and then bind to the ibid (post -synaptic neuron). When this
When neurons in the body are stimulated they send signals, in the form of action potentials, to the brain relaying messages. These tell the body how to respond. This is why, for example, the body recognises a feeling of pain when it is wounded. During this stimulation, there occurs an opening of activation gates of voltage-sensitive sodium channels. This allows sodium to enter the cell, reducing the cell’s negative charge. When a full action potential is generated, there
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.
Depolarization in membrane potential triggers an action potential because nearby axonal membranes will be depolarized to values near or above threshold voltage.
The communication between neurons advances through a series of steps. First, the presynaptic neuron delivers an action potential down its axon until it loses its myelin sheath and divides into many branches called buttons or synaptic knobs. (Zillmer, 2008, p. 105) Between the two neurons is a space called the synaptic cleft. This is the space where neurotransmitters are sent before being received by the postsynaptic neuron.
The rhodopsin is a protein found within rod cells. As rhodopsin absorbs the light (photon), it causes metarhodopsin II to be produced. This ends up activating a protein called transducin by switching GDP with GTP on this protein. At this point, transducin is activated, and it ends up activating phosphodiesterase, which causes cyclic GMP to decrease, which in turn causes Na+ channels to close. As a result of this, hyperpolarization occurs, and nerve impulse is sent to the brain.
Most neurons do not make direct connections with surrounding neurons, signals (molecules) must make the transition from the presynaptic (upstream) neuron to the postsynaptic (downstream) neuron. This transition space is called the synaptic cleft. The exchange of information from the pre- to postsynaptic neuron is called a synapse.