Theme 3 – Inside The Neuron PDF
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Erasmus University Rotterdam
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This document appears to be lecture notes or study materials on the topic of neurons, focusing on concepts like resting potential, action potential, and transmission. It covers the stages of an action potential, and includes terms such as depolarization, hyperpolarization, and absolute refractory period. The document lists important concepts, and provides summaries of biological processes related to the transmission within nerves.
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Checklist Nerve impulse Resting potential and action potential All-or-none law Propagation of the action potential Different phases of the action potential Polarization Depolarization H...
Checklist Nerve impulse Resting potential and action potential All-or-none law Propagation of the action potential Different phases of the action potential Polarization Depolarization Hyperpolarization Absolute vs relative refractory period Membrane and neuron cell characteristics Ion channels Sodium-potassium pump Concentration gradient Myelin sheaths and nodes of ranvier Transmission at synapses Presynaptic neurons vs postsynaptic neurons Temporal vs spatial summation EPSPs and IPSPs Chemical transmission steps Ionotropic vs metabotropic receptors Neurotransmitters Synthesis Functions Types Storage Release - exocytosis Nerve impulse ◦ The axon periodically regenerates an impulse. ◦ All parts of a neuron are covered by a membrane that lets certain chemicals pass. ◦ When at rest, the membrane maintains anelectricalgradient, also known as polarization– a difference in electrical charge betweenthe inside and outside of the cell. ◦ The inside of the membrane has a slight negative charge compared to the outside. Theresting potentialis thenumericaldifferencein electrical charge, about -70 mV. ◦ The resting potential prepares the neuron to respond rapidly. Excitation of the neuron opens sodium channels, letting sodium enter the cell rapidly. Because the membrane did its work in advance by keeping so much sodium outside, the cell is prepared to respond vigorously to a stimulus. ◦ If we increase the negative charge inside a neuron, we can produce hyperpolarization(decreasing towards zero). ◦Depolarizationis reducing a neuron’s polarization(increasing from zero). ◦ When the membrane is depolarized enough to reach the cell’s threshold, sodium and potassium channels open. Sodium ions enter rapidly, reducing and reversing the charge across the membrane. This event is known as theaction potential. ◦ After the peak of the action potential, the membrane returns toward its original level of polarization because of the outflow of potassium ions. ◦ The action potential is regenerated at successive points along the axon as sodium ions flow through the core of the axon and stimulate the next point along the axon to its threshold. The action potential maintains a constant magnitude as it passes along the axon. Summary of the action potential ◦ When an area of the axon membrane reaches its thresh- old, sodium channels and potassium channels open. ◦ Opening sodium channels lets sodium ions rush into the axon. At first, opening the potassium channels produces little effect. ◦ Positive charge flows down the axon and opens voltage-gated sodium channels at the next point. ◦ At the peak of the action potential, the sodium gates snap shut. ◦ Because voltage-gated potassium channels remain open, potassium ions flow out of the axon, returning the membrane toward its original depolarization. ◦ A few milliseconds later, the voltage-dependent potassium channels close. ◦ Theall-or-none lawis that the amplitude and velocityof an action potential are independent of the intensity of the stimulus that initiated it, provided that the stimulus reaches the threshold. ◦ Therefore, to signal the difference between a weak stimulus and a strong stimulus, all that an axon can change is the frequency or timing of its action potentials. ◦ Thepropagation of the action potentialdescribesthe transmission of an action potential down an axon. ◦ During an action potential, sodium ions enter the axon. Temporarily, the spot where they enter is positively charged in comparison with neighboring areas along the axon. The positive charge flows to neighboring regions of the axon, where they slightly depolarize the next area of the membrane, causing it to reach its threshold and open its sodium channels. The membrane regenerates the action potential at that point. In this manner, the action potential travels along the axon. ◦ An action potential starts in an axon and propagates without loss from start to finish. However, at its start, it “back-propagates” into the cell body and dendrites. The cell body and dendrites do not conduct action potentials, but they passively register the electrical event that started in the nearby axon. This back-propagation is important: When an action potential back-propagates into a dendrite, the dendrite becomes more susceptible to the structural changes responsible for learning. Different phases of the action potential ◦ Polarization, depolarization, hyperpolarization. ◦ At the peak of the action potential, the sodium channels shut tightly and remain tightly shut for approximately the next millisecond. This is theabsolute refractory period, the time when the membrane can’t produce anaction potential regardless of the stimulation. ◦ After that millisecond, the sodium channels relax a bit, but the rapid departure of potassium ions has driven the membrane potential farther into negative territory than usual. This is therelative refractory period, whena stronger-than-usual stimulus is necessary to initiate an action potential. ◦ The refractory period depends on two facts: The sodium channels are closed and potassium is flowing out of the cell. Membrane and neuron cell characteristics ◦ If charged ions could flow freely across the membrane, enough positive ions would enter to depolarize the membrane. However, the membrane is selectively permeable. ◦ When the membrane is at rest, the sodium and potassium channels are closed, permitting almost no flow of sodium and only a small flow of potassium. Stimulation can open these channels, permitting freer flow. ◦The sodium–potassium pumprepeatedly transportsthree sodium ions out of the cell while drawing two potassium ions in. Because of this pump,sodiumions are more concentratedoutsideandpotassiumions are moreconcentratedinside. ◦ The sodium–potassium pump is effective only because the selective permeability of the membrane prevents the sodium ions that were pumped out from leaking back in. ◦ However, some of the potassium in the neuron slowly leaks out, carrying a positive charge. This leakage increases the electrical gradient across the membrane. ◦ When the neuron is at rest, two forces tend to push sodium into the cell: 1. The electrical gradient – Sodium is positively charged and the inside of the cell is negatively charged. Opposite electrical charges attract, so the electrical gradient attracts sodium into the cell. 2. The concentration gradientis the difference in distributionof ions across the membrane. Sodium is more concentrated outside than inside, so it’s more likely to enter the cell than to leave. Sodium would enter rapidly if it could, but the sodium channels are closed. ◦ Potassium is positively charged and the inside of the cell is negatively charged, so the electrical gradient tends to attract potassium into the cell. However, potassium is more concentrated inside the cell than outside, so the concentration gradient tends to drive it out. ◦ The potassium channels, almost completely closed, permit a small amount of potassium flow (more outward than inward) but the sodium–potassium pump continues pulling potassium back into the cell. ◦ To increase the speed of the action potential, axons evolved a special mechanism: sheaths of myelin, an insulating material composed of fats and proteins. ◦ The myelin sheath is interrupted periodically by short sections called nodes of Ranvier. In myelinated axons, the action potential starts at the first node of Ranvier. ◦ The action potential can’t regenerate along the membrane between nodes because the axon has few if any sodium channels between nodes. ◦ After an action potential occurs at a node, sodium ions enter the axon and diffuse, pushing a chain of positive charge along the axon to the next node, where they quickly regenerate the action potential. ◦ The jumping of action potentials from node to node is referred to assaltatory conduction. ◦ In addition to providing rapid conduction of impulses, saltatory conduction conserves energy – instead of admitting sodium ions at every point along the axon and pumping them out, a myelinated axon admits sodium only at its nodes. Transmission at synapses Summation ◦Temporal summationis the phenomenon that repeatedstimuli within a brief time combine their effects. A light pinch of the dog’s foot didn’t evoke a reflex, but a few rapidly repeated pinches did. ◦ The neuron delivering transmission is thepresynapticneuronand the one receiving it is thepostsynaptic neuron. ◦ Although a single subthreshold excitation in the postsynaptic neuron decays over time, it combines with a second excitation that follows quickly. With a rapid succession of excitations, each adds its effect to what remained from the previous ones, until the combination exceeds the threshold of the postsynaptic neuron, producing an action potential. ◦Spatial summationis the summation of potentialsfrom different locations. A combination of excitations exceeds the threshold to produce an action potential. ◦ Temporal summation and spatial summation occur together when a neuron receives input from several axons in succession. EPSPs and IPSPs ◦ Unlike action potentials, which are always depolarizations,graded potentialsmay be either depolarizations (excitatory) or hyperpolarizations (inhibitory), and they decay over both time and distance. ◦ A graded depolarization is anexcitatory postsynapticpotential (EPSP), which results from sodium ions entering the neuron. A graded hyperpolarization is an inhibitory postsynaptic potential (IPSP), producedby the flow of negatively charged chloride ions into the cell. ◦ Temporal and spatial summation also occurs with EPSPs. ◦ A dog raising one leg needs to extend the other legs to maintain balance. A pinch on the foot sends a message along a sensory neuron to an interneuron in the spinal cord that excites the motor neurons connected to the flexor muscles of that leg and the extensor muscles of the other legs. The interneuron also sends messages to inhibit the extensor muscles in that leg and the flexor muscles of the three other legs. ◦ At inhibitory synapses, input from an axon hyperpolarizes the postsynaptic cell, moving the cell’s charge farther from the threshold and decreasing the probability of an action potential. ◦ Most neurons have aspontaneous firing rate, a periodicproduction of action potentials even without synaptic input. ◦ In such cases, the EPSPs increase the frequency of action potentials above the spontaneous rate, whereas IPSPs decrease it. Chemical transmission steps 1. The neuron synthesizes chemicals that serve as neurotransmitters, either in the cell body or at the end of the axon. 2. Action potentials travel down the axon. At the presynaptic terminal, the depolarization enables calcium to enter the cell. Calcium releases neurotransmitters from the terminals and into thesynaptic cleft, the space between the presynaptic and postsynaptic neurons. 3. The released molecules diffuse across the narrow cleft, attach to receptors and alter the activity of the postsynaptic neuron. 4. The neurotransmitter molecules separate from their receptors. 5. The neurotransmitter molecules may be taken back into the presynaptic neuron for recycling, or they may diffuse away. 6. Some postsynaptic cells send reverse messages to control the further release of neurotransmitters by presynaptic cells. Neurotransmitters ◦ The chemicals that a neuron releases at a synapse areneurotransmitters, or neuromodulators. Types Functions ◦ Many neurons releasenitric oxidewhen they arestimulated. In addition to influencing other neurons, nitric oxide dilates the nearby blood vessels, thereby increasing blood flow to that brain area. ◦ Your serotonin levels rise after you eat foods rich in the amino acidtryptophan. Synthesis ◦ Neurons synthesize nearly all neurotransmitters from amino acids, which the body obtains from proteins in the diet. ◦ Note the relationship among epinephrine, norepinephrine and dopamine – compounds known as catecholamines. Storage ◦ Most neurotransmitters are synthesized in the presynaptic terminal, near the point of release. The presynaptic terminal stores high concentrations of neurotransmitter molecules invesicles, tiny nearly spherical packets. ◦ However, neurons release nitric oxide as soon as they form it instead of storing it. Release ◦ An action potential by itself does not release the neurotransmitter at the end of the axon. Rather, depolarization opens voltage-dependent calcium channels in the presynaptic terminal. The calcium entry causesexocytosis,a release of neurotransmitters from the presynaptic neuron. ◦ The released neurotransmitter diffuses across the synaptic cleft to the postsynaptic membrane, where it attaches to a receptor. ◦ Most neurons release a combination of two or more transmitters. The result could be immediate brief excitation followed by slower inhibition, or other complex messages. Some neurons simultaneously release an excitatory transmitter and an inhibitory transmitter, the equivalent of saying “yes” and “no” at the same time. Ionotropic vs metabotropic receptors ◦ The effect of a neurotransmitter depends on how it affects its receptor. When the neurotransmitter attaches to its receptor, the receptor may open a channel, exerting an ionotropic effect, or it may produce a slower but longer metabotropic effect. ◦ When the neurotransmitter binds to anionotropicreceptor, it twists the receptor just enough to open its central channel to let one type of ion pass through. ◦ The channels controlled by a neurotransmitter aretransmitter-gatedor ligand-gated. A ligand is a chemical that binds tosomething. ◦ Ionotropic effects begin and decay quickly. ◦ Glutamate is usually the neurotransmitter used to elicit anexcitatoryionotropic effect, which opens sodium channels (positively charged) and facilitates the depolarization of the neuron cell. On the other hand, the neurotransmitter GABA is usually used to elicit aninhibitoryionotropic effect,which opens chloride ions channels (negatively charged), provoking an further polarization of the neuron cell. ◦ Other receptors controlmetabotropic effectsbyinitiating a sequence of metabolic reactions that start more slowly but last longer than ionotropic effects. ◦ Metabotropic synapses use many chemicals. ◦ When a neurotransmitter attaches to a metabotropic receptor, it bends the receptor protein that goes through the membrane of the cell. The other side of that receptor is attached to aG protein, a protein coupled to GTP,an energy-storing molecule. Bending the receptor protein detaches that G protein, which is then free to take its energy elsewhere in the cell. ◦ An ionotropic synapse has effects localized to one point on the membrane, whereas a metabotropic synapse influences activity in much or all of the cell and over a longer time. ◦ For vision and hearing, the brain needs immediate, brief information, the kind that ionotropic synapses bring. Metabotropic synapses are suited for more enduring effects such as taste and pain. Metabotropic effects are also important for arousal, attention, hunger, thirst, and emotion – functions that arise slowly and last longer than a sensation.
