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Chapter 4

Chapter 4 PSYC2410 Fall -Choleris

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PSYC 2410
Elena Choleris

PSYC 2410 – Chapter 4 Neural Conduction and Synaptic Transmission 4.1 Resting Membrane Potential  Cell Membrane: semi-permeable barrier o Made of double layer of phospholipids which have a polar hydrophilic head and a hydrophobic body (nonpolar). Nonpolar areas form a hydrophobic region between the hydrophilic head. At body temps the interior of the bilayer is fluid. o Cholesterol, give rigidity to cell membrane while remaining a fluid environment. Also have polar head and nonpolar tails. o Lipids:  Glycolipid: sugar groups attached to their heads point into the extracellular space.  Protective, insulators  Receptor binding  Recognition of self o Proteins:  Transmembrane or integral proteins: across the entire bilayer  Signal proteins: involved in communication b/w cells  Channel proteins: allows exchange of specific substances b/w inside and outside of the cell  Peripheral membrane proteins: either on the outside or inside, close association with the bilayer and with integral or Transmembrane proteins  They facilitate chemical reactions (usually enzymes)  Can help the function of Transmembrane proteins, open/close  Transmembrane traffic: lipids of membranes form a barrier to hydrophilic molecules, but need transportation across it o Diffusion: movement of substance (liquid or gas) along a concentration gradient (highlow). Lipid soluble, hydrophobic, molecules can move through the membrane (steroid hormones, ex: cortisol). o Electrostatic Pressure: charged particles ions (- or +). Same change  repel. Opp charge  attract o Facilitated Diffusion: diffusion through channels  Ion Channels: allow ions to diffuse across membranes when open, and not when closed. o Active Transport: requires E consumption (mitochondria), costly to the cell and body.  Charges Near the Cell Membrane: + - o Sodium, Na & Chloride, Cl are more concentrated OUTSIDE the cell o Potassium, K & Protein Ions are more concentrated INSIDE the cell o Overall charge: more negative inside than outside.  Membrane potential: difference in electrical charge between the inside and the outside of a cell  Neuronal resting potential: -70 mV  How is the potential across the membrane maintained?: cell membrane is not permeable to all ions o Impermeable to the electrically charged proteins (-‘ve charge) + o Not very permeable to sodium (Na ) ions + o Relatively permeable to potassium (K ) ions o Very permeable to chloride (Cl ) ions  Experiments by Alan Hodgkin and Andrew Huxley (1950): they calculated the electrostatic charge needed to keep the various ions in the location where, at rest, they are in greater concentration: o For Cl need 70 mV  70 mV – 70 mV = 0 + o For K need 90mV  90 mV – 70mV = 20 mV + o For Na 50 mV l 50 mV + 70 mV = 120 mV (+ sign because mostly outside the cell, takes a lot to keep them out). Chloride is easiest to maintain, for K there’s 20 mV left, which results in pressure to keep them. For Na it requires + + a pressure of 120 mV to maintain them. They showed that K ions ‘leak out’, Na ions get into the cell. Sodium ion PSYC 2410 – Chapter 4 are more concentrated outside and are positively charged, they will try to move down the gradient into the cell, and because they are positive they are attracted to the negative charge of the inside of the cell. o Sodium-Potassium Pump: an active co-transport mechanism. It uses energy provided by ATP (adenosine triphosphate) to transport 3 sodium ions OUT, and two potassium ions IN.  Phosphate binds to pump and provides energy for the pump  Binding of sodium ions to the pump causes it to change its shape and open to the outside  The sodium ions leave and potassium ions enter the pump  The phosphate group comes off, and the conformation changes back and the potassium ions are released inside the cell  Neuron’s resting potential: -70Mv, is polarized. o Synapses are found on dendritic spines or the cell body, axodendritic – from synapse on axon to dendrite on another cell, dendrodendritic – synapse from dendrite to dendrite , axosomatic – synapse from axon on cell body, axoaxonic – axon on axon. Synaptic neurotransmitters  changes in the potential of post-synaptic neurons o Move toward 0 is depolarization, increasing the chance that the cell fires o Making the cell more negative, you are increasing the polarity and you’re hyperpolarizing the cell, inhibiting the cell, making it less likely to fire. o Depolarization: excitatory postsynaptic potentials o Hyperpolarization: inhibitory postsynaptic potentials o ESPS: excitatory postsynaptic potentials o IPSP: inhibitory postsynaptic potentials. Usually caused by opening of potassium channels, potassium rushes out 4.2 Generation and Conduction of Post Synaptic Potentials  Post Synaptic Potentials o Graded responses: stimulate strongly, big wave, stimulate a little, small wave PSYC 2410 – Chapter 4 o Travel very rapidly: because its electrical o Decremental conduction: signal gets weaker and weaker as it goes along the axon because it is passive, signals die off. However, there are some systems where this is not the case; Dendritic Signals Amplification. o Post synaptic potentials add together (Integration)  Spatial summation: at the same time in different locations, diff axons on one cell body and add together, so if you have an IPSP and an EPSE they can cancel out  Temporal summation: in rapid succession at the same synapse, they can sum to produce a large EPSP/IPSP 4.3 Integration of Postsynaptic Potentials and Generation of Action Potentials  Action Potential: a massive rapid (1 millisecond) reversal of the membrane potential from -70mV to +50mV. ALL OR NONE. o summation  threshold of excitation (~ -65 mV)  depolarization (sodium rushes in)  neuron fires o action potential happens in the axon’s membrane adjacent to the axonal hillock 1. threshold is reached (~ -65mV): see a bit of an EPSP 2. Na channels open + 3. Massive influx of Na ions 4. The cell membrane starts depolarizing 5. Depolarization opens K channels (“voltage gated”) + 6. K ions exit the cell following their concentration gradient 7. Full depolarization of the cell membrane (+50mV) + 8. Na channels close 9. K ions still exit the cell because of electrostatic pressure (inside of cell has become positive) 10. Cell membrane starts Repolarizing + 11. K channels close gradually: cell becomes hyper-polarized because they don’t all close at once, overcompensate 12. Temporary hyperpolarization 13. Refractory period: can’t fire no matter how strongly you stimulate the cell, recovering 14. Ready to start over  Refractory Periods o Absolute Refractory Period: can’t fire at all, the cell is recovering o Relative Refractory Period: coming out of the hyper-polarization, but you need a much stronger stimulation than normal. Allows you to do things in a graded manner and have different frequencies. o Thanks to the Refractory Periods:  Neuronal firing rate is related to Stimulus Intensity  High intensity  firing rate set by absolute refractory period  Low intensity  firing rate set by refractory period  Action potentials cannot travel backwards within the axon under natural conditions, because of absolute refractory period  Orthodromic conduction: normal direction, from axon hillock towards axon terminal  Antidromic conduction: opposite direction, from axon terminal towards axon hillock 4.4 Conduction of Action Potentials  Conduction of Action Potentials: * there are some action potentials that travel backward through soma and dendrites, function unknown o Post Synaptic Potentials (EPSP, IPSP)  Close to the synapses  Very fast  Decremental  Passive o Action Potentials PSYC 2410 – Chapter 4  Along the axon  Slower  Nondecremental, signal does not degrade over time  Active  Action potential is a step by step process, active step (sodium channels opening), ion flow (passive), effect on the neighbouring channel is the passive step  Axonal Conduction: single wave, actively spreading  Conduction in Myelinated Axons: saltatory conduction (saltare = jump) o Action potential is regenerated at Nodes of Ranvier o Decremental conduction under myelin sheath because myelin covers the axon and it has limited access to extracellular fluid and thus ions. Slow  very fast (EPSP)  slow  very fast (EPSP) thus under the myelin it is an EPSP conduction which is faster than an action potential. 4.5 Synaptic Transmission: Chemical Transmission of Signals among Neurons  Synaptic transmission: transmission of signal from one neuron to another  Types of Synapses: o Axodendritic Synapses: axon – dendrites (most common) o Axosomatic Synapses: axon – cell body o Dendrodendritic synapses: dendrite – dendrite (can go both ways, often electrical as opposed to chemical) o Axoaxonal synapses: axon-axon (presynaptic modification of a signal) o Chemical Synapses: 5 msec (inhibitory or excitatory and different types of neurotransmitters)  Coexistence: one neuron can release more than one neurotransmitter  Many neurons synthesize and release only ONE neurotransmitter o Electrical Synapses: faster (limited, only excitatory, only one type of signal good for synchronizing cells, synchronizing beating of the heart, SANODE)  Membrane coupling through Gap Junctions which allows the free transit of small molecules and ions (ie. Sodium), passive spread of depolarization. 6 connexins 1 connexon, 2 connexon  1 gap junction  Bidirectional  Direct transmission  More common in invertebrates 4.6 Neurotransmitters  Neurotransmitters: o Synthesis: in the cell body then o Bigger peptides/proteins: somal vesicle packaging in Golgi. Then active (use E) axoplasmatic transport (~40cm/day) using the microtubules and stuff o Small molecules: axonal travel – usually passive (concentration gradient) button vesicle packaging o Types of Release:  Direct synapse release: into synaptic cleft to post-synaptic neuron membrane  Non-direct synapse release: release into extracellular fluid  Release of Neurotransmitters: 1. the action potential reaches the synaptic terminal 2+ 2. Activates voltage-activated calcium (Ca ) channels open 3. Ca ions influx, activate SNARE proteins on the vesicles and on presynaptic membrane, they match/bind 4. Presynaptic vesicles fuse (dock) with the cell membrane 5. Release of neurotransmitter in the synaptic cleft 6. Exocytosis PSYC 2410 – Chapter 4  Receptor Activation o Receptor: a protein that contains the binding site for a specific neurotransmitter (ligand). Receptor can have many different binding sites. o Receptor Subtypes: eg. Dopamine has 5 receptors subtypes: D1, D2, … 5 .  Differential brain distribution  different functions o Ionotropic Receptor: ligand-activated ion channel. Neurotransmitter binds and opens channel, allowing ions to move across the membrane along the concentration/electrostatic gradient.  Fast effect  Open – Close  Examples:  Excitatory postsynaptic potentials, EPSP (depolarization): often Na channels open, Na rushes in + -  Inhibitory postsynaptic potentials, IPSP (hyperpolarization) often K or Cl channels open, they flow out. Gets even more negative. o Metabotropic Receptor: associated with signal proteins and G proteins (guanosine-triphosphate (GTP) – sensitive)  Slower effect. Longer lasting.  Varied responses.  Neurotransmitter binds to receptor on post-synaptic membrane, activates G protein on the intracellular membrane of the cell. G protein can detached and bind to another protein, such as a channel, to open it and let ions flow.  G protein can also be a second messenger causing a cascade leading to differences in DNA transcription. o Autoreceptor: metabotropic receptors on the PRE-synaptic neuron terminal region, soma, or dendrites. Binds to own neurotransmitter. Often affect intracellular processes (eg. Neurotrans release)  Self-regulation through inhibitory feedback o Heteroreceptors: pre-synaptic inhibition. Slightly depolarizes other cell, so signal at the button is weaker. Inhibiting primary presynaptic cell using excitation itself. Calcium channels respond to difference in change in potential. Less calcium influx, less synaptic release. Butif u stimulate the cell from scratch, you have a bigger change in membrane potential, causing a larger influx of calcium into the button and a larger release of neurotrans. Only inhibition. o Post-synaptic Inhibition + Facilit
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