Generating Graded Potentials - Essay Example

Biology 21 October Biology Questions How are graded potentials (for example, EPSPs and/or IPSPs) generated at dendrites and/or cell bodies of neurons? The brain comprises of two types of cells: neurons and glial cells. The neurons serve as the coordinators and recipients of information. Conversely, glial cells back the functions of the neurons. Information transmission occurs electrically along the neurons. This electrical information flow prompts nerve cells to produce two types of graded potentials, which are Action potentials and Graded potentials. The neurons transmit information to each other through the dendrites. Action potentials are however comparably large in size. They signal strength of stimulus by frequency and not by amplitude. Graded potentials on the other hand are generated in dendrites and sensory receptors. Graded potentials sometimes generate action potentials and thus referred to as generator potentials. In case of an incoming signal, a pre synaptic excitatory neuron fires releasing neurotransmitters to the synaptic cleft. Consequently, if the transmitter binds to the post synaptic dendritic membrane, it elicits a transient depolarization called Excitatory Post Synaptic Potential (EPSPs) (Akers and Denbow 214). Inhibitory neurons on the other hand, elicit partial hyper-polarizations known as Inhibitory Post Synaptic Potentials (IPSPs) (Akers and Denbow 214). Summarily, EPSPs and IPSPs are both graded potentials. Finally, a number of pre synaptic neurons maybe firing simultaneously, hence impacting on the level of activity of post synaptic neurons. Hence, the total potential in the post synaptic neuron; that is, Grand Post Synaptic Potential (GPSP) is a summation of all EPSPs and IPSPs occurring approximately simultaneously (Dowling 242). 2) What is the functional significance of spatial and temporal summation being performed by axon hillocks of neurons? Axon hillock is the most excitable portion of a neuron. It is the region at the beginning of an axon. Action potentials are generated in this region. The occurrence of an action potential at the axon hillock is by either temporal summation or spatial summation. Action potentials usually occur in three stages, namely Resting, Depolarization and Repolarization phases. (Brown, Miller and Eason 223).Temporal summation simply refers to addition of a number of EPSPs that manifest close together in time, as a result of a subsequent firing of a single presynaptic neuron. Conversely, spatial summation refers to addition of EPSPs originating at the same time from several pre-synaptic neurons (Sherwood 107). This implies that the position of a synapse on the neuron is significant in determining the generation of an action potential. Summarily, synapses closer to the axon hillock have higher level of activity than those further away. Furthermore, the central integrative state of a neuron is also determined by temporal and spatial summation (Beck 135). 3) How are action potentials generated at axon hillocks and propagated along unmyelinated axons? Action potential is propagated along unmyelinated axon by a mechanism known as continuous propagation. The membrane is considered as a sequence of adjacent segments. The action potential starts at the initial segment. In the first step, the transmembrane potential becomes briefly positive, rather than negative. In the second step, a local current develops due to the influx of sodium ions into the cytosol and extracellular fluid, and in step three and four, the local current spreads in all directions hence depolarizing adjacent segments of the membrane. Usually, the axon hillock like the rest of the cell body, cannot respond with action potential because it lacks gated ion channels. However, when the initial portion of the axon is depolarized to threshold, an action potential develops there. The process thus proceeds in a chain reaction until distant portions of cell are afflicted. Every time a local current occurs, action potential moves forward, and not backward, since the previous segment of membrane is in a refractory period (Martini et al. 305). 4) How are action potentials generated at axon hillocks and propagated along myelinated axons? Action potential in myelinated axons is transferred by a mechanism known as salutatory propagation. The axolemma of myelinated axons is covered with a myelin sheath. In contrast, continuous propagation does not occur in myelinated axons, since the myelin sheath prevents the flow of ions across the membrane except at the nodes; hence, only nodes are responsive to depolarizing stimulus. In case an action potential occurs at the first segment of a myelinated axon, the regional current bypasses the internodes and depolarizes the closest node to the threshold. Therefore, instead of the action potential moving along the axon, it basically leaps from one node to another. The speed of action potential propagation is greatly increased by myelin sheath. Furthermore, the axon diameter also affects the propagation speeds although the effects are much lower. The axon diameter is important in relation to the movement of ions in the cytoplasm of axon since the cytoplasm offers resistance to movement of ions within it (Martini et al. 305). 5) What are the mechanisms underlying/mediating the release of neurotransmitters by axon terminals? Neurotransmitters are stored in the cytoplasm of an axon terminal inside secretory vesicles known as synaptic vesicles. Exocytosis is the process by which an axon releases neurotransmitters on arrival of an action potential at the terminal. Neurotransmitter molecules are released into the synaptic cleft once the secretory vesicles fuse with the presynaptic membrane. Release of synaptic vesicles is dependent on voltage-gated Ca2+ channels in axon terminal plasma membrane (Russell, Hertz and McMillan 863). Hence Ca2+ ions are consistently pumped outside the cell membrane, thus maintaining their higher concentration outside than within. As the action potential arrives, changes in membrane potential trigger Ca2+ channel gates in axon terminal to open. This allows Ca2+ to influx back into the cytoplasm. The apparent rise of Ca2+ causes proteins in the membrane of synaptic vesicles to bind to the plasma membrane. Consequently, neurotransmitters are released into synaptic cleft. Each action potential arrival at a synapse causes roughly a similar number of synaptic vesicles to release their neurotransmitters. Action potentials are no longer produced in the absence of a stimulus. Hence in such a scenario, a series of events prevent continued signal transmission (Russell, Hertz and McMillan 863). Once action potentials cease arriving at axon terminals, the voltage-gated Ca2+ axon terminal channels close and the Ca2+ions in axon cytoplasm are rapidly pumped outside. This low level of cytoplasmic Ca2+ ions stops secretory vesicles from fusing with the presynaptic membrane and thus no neurotransmitters are released. Excess neurotransmitters in the cytoplasm diffuse away or undergo enzymatic breakdown or are pumped back to the axon terminal or glial cells through a process of active transport (Russell, Hertz and McMillan 863). 6) What are the mechanisms by which the gate-control theory modulates nociceptive/noxious signals? Gate-control theory was postulated in by Wall and Melzack. The theory operates on a spinal cord level and proposes a gating mechanism. It specifically focuses on the dorsal horn of the spinal cord; which only allows a single sensation at a time to pass through the brain. This process manifests in substantia glatinosa. In this region, large fibers (A?) responsible for the transmission of non-painful stimuli inhibit activity of smaller nerve fibres (A? and C) that transmit pain. There are four different types of pain; Neuropathic pain, nociceptive pain, psychological pain and pain mediated by the sympathetic system. Nociception basically refers to the patient’s sensation of pain. In addition, it can be defined as the process involved in modulating and signaling of noxious stimuli. Nociceptive signals undergo four distinct processes before they manifest as pain perception. The four processes include transduction, transmission, modulation, and perception (Goldman, Hain and Liben 195). 7) What are the mechanisms by which the endogenous analgesia systems modulate nociceptive (or noxious) signals? Three levels of nociceptive signal modulation are present in the central nervous system. The levels are summarized as: (a) Spinal mechanisms: local analgesia. It was postulated by Wall and Melzack. In this theory, the nociceptive signal is modulated as it enters the spinal cord. A local analgesia is produced as a result of the activation of non nociceptive A? fibers, which in turn causes recruitment of inhibitory neurons of posterior spinal cord. (b)Descending inhibitory mechanisms (Diffuse inhibition). Reynolds’s in 1969 showed that stimulation of Periaqueductal Grey (PAG) and Nucleus Raphe Magnus (NMG) leads to strong inhibition of pain. LeBars and colleagues later in the 1970’s postulated the diffuse noxious inhibitory controls theory. This theory postulates that a localized nociceptive stimulation causes an analgesic effect on the rest of the body. Some medical conditions like fibromyalgya are related to low levels of endogenous inhibition. (c)Superior control centers: These centers modulate pain in diverse ways. Modulation is either by reinterpreting nociceptive signal hence changing perception of pain, or modulating descending mechanisms (Goldman, Hain and Liben 195). Works Cited Akers, R. Michael D. and Michael Denbow. Anatomy and Physiology of Domestic Animals. Oxford: Blackwell Publishing Ltd., 2008. Print. Beck, Randy W. Functional Neurology for Practitioners of Manual Medicine. 2nd ed. Edinburgh: Churchill Livingstone Elsevier, 2011. Print. Brown, Stanley P. Wayne C. Miller, and Jane M. Eason. Exercise Physiology: Basis of Human Movement in Health and Disease. Philadelphia: Lippincott Williams & Wilkins, 2006. Print. Dowling, John E. The Retina: An Approachable Part of the Brain. Cambridge: Belknap Press of Harvard University Press, 1987. Print. Goldman, Ann, Richard Hain and Stephen Liben. Oxford Textbook Palliative Care for Children. 2nd Ed. New York: Oxford University Press, 2012. Print. Martini, Frederic et al. Anatomy and Physiology’ 2007 Ed. Jurong: person Education South Asia Pte. Ltd, 2007. Print. Russell, Peter J., Paul E. Hertz and Beverly McMillan. Biology: The dynamic science, Volume 1. 2nd Ed. Belmont: Brooks/Cole Cengage Learning, 2011. Print. Sherwood, Lauralee. Human Physiology: From Cells to Systems. 8th ed. Belmont: Brooks/ Cole Cengage Learning, 2011. Print Read More