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Chapter 4

Chapter 4 Notes.docx

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PSYC 271
Richard Beninger

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Cindy Zhu, PSYC271 Fall 2011 Page 1 of7 Chapter 4: Neural Conduction and Synaptic Transmission 4.1 Resting Membrane Potential • Fine microelectrodes (tips < 1/1000 of a millimetre) are placed inside neuron, and another electrode is placed outside. • Resting potential is -70 millivolts (mV), making the neural membrane polarized • Resting potential due to ratio of negative to positive charges (ions) being greater inside neuron than outside. • Homogenizing effects o Random motion: move down concentration gradient when in constant motion o Electrostatic pressure: accumulation of charges tends to be dispersed due to repulsion and attraction • Greater outside neuron: Na and Cl ; greater inside neuron: K + • Why unequal distribution? Calculating electrostatic pressure (Cl = 70mV, K = 90mV, Na = 120mV) shows sodium is still being driven in against gradients. o Differential permeability of ions - K and Cl pass readily but Na and negative protein ions do not pass at all. Instead must use specialized ion channels. This is passive. o Sodium-potassium pump: an active energy-consuming transporter that exchanges 3 Na out of cell for transporting 2 K ions into cell. 4.2 Generation and Conduction of Postsynaptic Potentials • Neurotransmitters released from terminal buttons diffuse across synaptic clefts and interact with specialized receptor molecules on the receptive membranes of the next neuron. • The transmitter can cause a depolarizing effect (increase membrane potential from -70mV to -60mV, for example) o a hyperpolarizing effect (decrease from -70mV to -75mV). • Postsynaptic depolarizations are excitatory postsynaptic potentials (EPSPs), while hyperpolarizations are inhibitory postsynaptic potentials (IPSPs). Both are graded responses, with amplitudes of the PSPs being proportional to intensity of the signals that elicit them. • These PSPs are rapid travelling quickly from sites of generation (dendrite or soma), and are decremental, decreasing in amplitude as they travel through the neuron. 4.3 Integration of PSPs, Generation of Action Potentials • Whether a neuron fires or not depends on balance between excitatory and inhibitory signals it receives. Action potentials are not generated at the axon hillock, but adjacent to the axon. • To depolarize a neuron, the sum of PSPs at the axon hillock must reach the threshold of excitation (-65mV) to generate an action potential. Cindy Zhu, PSYC271 Fall 2011 Page 2 of7 • The action potential depolarizes to +50mV, and lasts for only 1 millisecond. It is not graded like PSPs, but an all-or-none response. • Summing the individual PSP signals into one overall signal is integration, and can happen by: o Spatial summation: local PSPs produced simultaneously on different parts of receptive membrane sum together. o Temporal summation: PSPs produced in rapid succession at same synapse sum. Signals can add together over time because the PSPs last for a while and take time to dissipate. o Each neuron continuously integrates signals over both time and space. 4.4 Conduction of Action Potentials • Action potentials are produced and conducted due to voltage- activated ion channels. • The number of ions that flow through membrane during an action potential is very small in relation to the total number of ions inside and outside the cell: the action potential involves only those ions right next to the membrane. • Absolute refractory period: 1- 2 milliseconds after initiation of action potential during which it is impossible to illicit a second one. After this, during the relative refractory period it is possible to fire the neuron again but only by applying higher-than-normal levels of stimulation. o Explains: action potential can only travel in one direction down axon (previous sections are in refractory period, cannot fire again in reverse direction) and rate of neural firing is related to intensity of stimulation (high level of stimulation causes high frequency of firing). • Conduction of AP is nondecremental, not growing weaker down axon; APs slower than PSPs. o AP is active – the first AP travels passively to the adjacent sodium channels, then once that channel opens actively a new full-blown AP is generated again. Slower because each channel has to be reset through refractory period until it can fire again. o Analogy of domino of mouse traps. • Antidromic conduction: when a stimulation of sufficient intensity is applied to the axon, an AP generated at axon and ravelling back to cell body. Normal AP is orthodromic conduction. • In myelinated neurons, ions can pass through the membrane only at the nodes of Ranvier – the signal is conducted passively along the segments between the nodes (still strong enough to open the next channel) – and increases speed of conduction. This is salutatory conduction. Cindy Zhu, PSYC271 Fall 2011 Page 3 of7 • Conduction is faster in larger-diameter axons and in myelinated axons. Mammalian motor neurons (large, myelinated) can conduct at 100 m/s, in humans maximum is about 60 m/s. • Conduction in interneurons (small or no axons) is passive and decremental. • Hodgkin-Huxley Model (1950s) was important but does not represent all the variety, complexity, and plasticity of neurons and neural conduction. o Neurons can fire continually without input. Some axons can conduct both graded signals and action potentials. Action potentials of different classes of neurons vary greatly in duration, amplitude, and frequency. Many neurons have no axons and do not display action potentials. Dendrites of some axons can actively conduct action potentials. 4.5 Synaptic Transmission: Chemical Transmission Structure of Synapses • Axodendritic synapses: synapses of axon terminal buttons on dendrites; axosomatic synapses: synapses of terminal buttons on somas (cell bodies). • There are also dendrodendritic synapses (capable of transmission in both directions) and axoaxonic synapses which can mediate presynaptic facilitation and inhibition. • Axoaxonic inhibition: synapse partially depolarizes the terminal button, leading to less calcium entry into terminal when action potential arrives, and therefore less NT release. • Axoaxonic facilitation: increased calcium transmission • Directed synapses: synapses at which the site of neurotransmitter release and the site of neurotransmitter reception are in close proximity. Nondirected synapses have a distance in between, such as where transmitters are released from varicosities along the axon (en passant synapses) and are widely dispersed to surrounding targets (string-of-beads synapses). This is called volume transmission. Synthesis, Packaging, and Transport of NTs • Small NTs are synthesized in the cytoplasm of the terminal button, and packaged in synaptic vesicles by the Golgi complex. Once filled with NT, the vesicles are stored in clusters next to the presynaptic neuron membrane. • Neuropeptides are large NTs, and are chains of 3-36 amino acids. They are assembled in ribosomes before being packaged by the Golgi complex and transported by microtubules to the terminal buttons, at a rate of about 40cm/day. • Coexistence: a neuron can contain (synthesize and release) more than one NT. Release of Neurotransmitters Cindy Zhu, PSYC271 Fall 2011 Page 4 of 7 • Exocytosis: synaptic vesicles containing NTs congregate near presynaptic membrane regions rich in voltage-gated calcium channels; when an action potential reaches the area, these channels open and the influx of Ca ions causes synaptic vesicles to fuse with the membrane and empty the NTs into the synaptic cleft. • Snare complex due to interaction of proteins on surface of vesicle and membrane (docking), then calcium triggers conformational change that causes lipid bilayer fusion and release of vesicle contents. • Small NTs are released in a pulse each time an action potential triggers an influx of calcium; neuropeptides are released gradually in response to general increase in intracellular calcium level. Activation of Receptors by NTs • NTs cross the synaptic cleft to bind to receptors in the postsynaptic membrane – receptors are proteins with specific binding sites for particular NTs (which are the ligands). Most NTs bind to several different types of receptors – receptor subtypes can be located in various brain areas and respond to the NT in different ways. • Ionotropic receptors: associated with ligand-activated ion channels. When the NT binds, the associated ion channel change
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