Wednesday, September 4, 2019
Inhibitory Or Excitatory Potential Changes :: Biology Biological Papers
Inhibitory Or Excitatory Potential Changes Graded potentials can be either hyperpolarizations (inhibitory) or depolarizations (excitatory). Inhibitory postsynaptic potential, also referred to as IPSP, is the temporary hyperpolarization of a membrane. An inhibitory postsynaptic potential occurs when synaptic input selectively opens the gates for potassium ions to exit the cell (carrying a positive charge with them) or for the chloride ions to enter the cell (carrying a negative charge with them). Inhibition is not just the absence of excitation, it is an active brake that is able to suppress the excitatory responses from occurring (Kalat, 2004). Excitatory postsynaptic potential, also known as EPSP, is a graded depolarization. As a result of sodium ions enter the cell, excitatory postsynaptic potential occurs. As a result of the synaptic activation, the sodium gates open, allowing an increase in the flow of sodium ions crossing the membrane. Excitatory postsynaptic potential is a subthreshold event that decays over space and time, meaning its magnitude decreases as it travels along the membrane (Kalat, 2004). Lithium has both inhibitory and excitatory features. Evidence has shown that lithium alters sodium transportation (http://www.mentalhealth.com). In the extracelluar fluid lithium may replace sodium. During the process of depolarization lithium has an extremely rapid intracellular influx. Although, it is not effectively removed by the sodium-potassium pump. According to Kalat (2004) the sodium-potassium pump, "[is] a protein complex that repeatedly transports three sodium ions out of the cell while drawing two potassium ions into the cell" (p. 41). As a result, it prevents the cellular reentry of potassium. This interferes with the electrolyte distribution across the neuronal membrane, resulting in a decrease in the membrane potential, changes in conduction and neuronal excitability. As measured by cortical evoked potential, for humans lithium alters the excitability of the central nervous system (http://www.mentalhealth.com). Lithium enhances the uptake of norepinephrine and serotonin into the synaptosomes, thus reducing their action. Lithium also reduces the release of norepinephrine from synaptic vesicles and inhibits production of cAMP. "Lithium inhibits the synthesis of cAMP by the adenylyl cyclase in many brain regions, including the cerebral cortex, caudate, and hippocampus, but not the brain stem or cerebellum" (Feldman, Meyer & Quenzer, 1997). "The inhibitory action of lithium on NE-sensitive adenylyl cyclase is a consistent finding, but lithium clearly has distinctive effects on the adenylyl cyclase that is coupled with receptors
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