Ch 4: Neural Conduction & Synaptic Transmission This chapter is about introducing the function of neurons How they conduct & transmit electrochemical signals through the nervous system Resting Membrane Potential Function of neurons centers around the
membrane potential The difference in electrical charge between the inside & outside of the cell Can measure membrane potential using a microelectrode Measure the charge inside the cell & the charge outside. Resting Potential A neurons resting potential is -70mV
Meaning, the charge inside the cell is 70mV less than the charge outside Inside < Outside Because this value is beyond 0, it is said to be polarized So at rest, neurons are polarized. Ionic Basis It is polarized due to the arrangement of ions The salts in neural tissues separate into + and
charged particles called ions 4 main ions are responsible: 1. K+ (potassium) 2. Na+ (sodium) 3. Cl-(chloride) 4. - charged proteins Ionic Basis The ratio of to + ions is greater inside a neuron than out, so you have a more charge inside
Again, why the neurons resting potential is polarized 2 things cause this imbalance & 2 things try to equalize (homogenize) Contributing Factors to Resting Potential Equalizers (homogenizers) 1. Random motion 2. Electrostatic pressure Cause imbalance 1. Passive flow
2. Active transport Equalizers Random Motion Ions are in constant random motion Tend to be evenly distributed because they move down their concentration gradient 1.
2. Move from areas of higher concentration to lower concentration Electrostatic Pressure Ions with the same charge will repel each other Opposite charges attract Contributing Factors to Resting Potential
Concentrations of Na+ and Cl- are greater outside the neuron (extracellularly) K+ concentration is greater inside the cell (intracellularly) Negatively charged proteins generally stay inside the neuron Imbalancers Passive Flow
1. Does not require energy The membrane is selectively permeable to the different ions K+ and Cl- ions easily pass through the membrane
Na+ ions have difficulty passing through Ions passively flow across the membrane via ion channels Special pores in the membrane Active transport 2. Needs energy to power the pumps
Imbalancers Active transport 2. Requires energy to power the pumps that transport the ions Discovered by Hodgkin & Huxley
Nobel prize winning research Why is there high Na+ and Cl- outside and high K+ inside? Why are they not passively flowing down their concentration gradients & reaching equilibrium? Calculated the electrostatic pressure (mV) that would be necessary to counteract the passive flow down the concentration gradient (aka keep the concentrations uneven across the membrane) & how this differed from the actual resting potential Active pumps cont. Discovered that there are active pumps that
counteract the passive flow of ions in & out of the cell (specifically for Na+ and K+) Sodium-potassium pumps Actively (using energy) pumps Na+ out & K+ in 3 Na+ ions out for every 2 K+ ions pumped in Other types of active transporters also exist *Summary Table 4.1 (pg. 79)* Postsynaptic Potentials Remember: At a synapse, the presynaptic neuron
releases NT that bind with receptors on the postsynaptic neuron, to transmit the signal from one neuron to the next When the NT bind with the postsynaptic neuron, they have either of 2 effects 1. Depolarize the membrane Decrease the resting potential **this means become less negative, aka approach zero** Hyperpolarize the membrane
2. Increase the resting potential ** make it more negative; further from zero** hyperpolarize hyperpolarize MV -70
depolarize depolarize 0 MV Postsynaptic Potentials Postsynaptic depolarizations: Excitatory postsynaptic potentials EPSPs Increase the likelihood that the neuron will fire
Postsynaptic hyperpolarizations: Inhibitory postsynaptic potentials IPSPs Decrease the likelihood that the neuron will fire Graded responses Weak signals cause small PSPs; strong signals cause large PSPs PSPs Travel passively
Very rapid (practically instantaneous) Like a cable Deteriorate over distance Lose amplitude as they go along Fade out Like sound Integration of PSPs Individual PSPs have almost no effect on getting a neuron to fire However, neurons can have thousands of synapses on them & combining the PSPs from all of those can initiate firing
Called integration Add all the EPSPs + IPSPs Remember: PSPs are graded & have different strengths ExcitatoryPSPs increase the likelihood of firing & InhibitoryPSPs decrease the likelihood Integration of PSPs Neurons integrates PSPs in 2 ways 1. Over space: spatial summation
EPSP + EPSP = big EPSP EPSP + IPSP = 0 (cancel each other out; assuming of equal strength) IPSP + IPSP = big IPSP Over time: temporal summation 2.
2 PSPs in rapid succession coming Action Potentials If the sum of the PSPs reaching the axon hillock area at any one time is enough to reach the threshold of excitation, an action potential is generated The threshold is -65mV So the resting membrane potential must be depolarized 5mV for the neuron to fire
Action potential Massive, 1ms reversal of the membrane potential -70 to +50mV Not graded; they are all-or-nothing responses Either fire at full force or dont fire at all Conduction of APs APs are generated & conducted via voltage-activated ion channels When the threshold of excitation is hit, the voltage-activated Na+ channels open &
Na+ rushes in The Na+ influx causes the membrane potential to spike to +50mV This triggers the voltage-gated K+ channels to open & K+ flows out After 1ms, Na+ channels close End of rising phase Conduction of APs cont. Beginning of repolarizing phase K+ continues to flow out until the cell has been repolarized; then the K+ channels close
Cell returns to baseline resting membrane potential Refractory Periods For about 1-2ms after the AP, it is impossible to fire another one Absolute refractory period
Followed by a period during which another AP can be fired, but it requires higher than normal levels of stimulation Relative refractory period Afterwards, the neuron returns to baseline & another AP can be fired as usual Conduction in Myelinated Axons Ions can pass through the membrane at the nodes of Ranvier between myelin segments
APs move instantly through myelinated segments to the next node, where concentrated Na+ channels allow the signal to be recharged and sent to the next Saltatory Conduction Overall, this allows APs to be conducted much faster than in unmyelinated axons, because the AP jumps from node to node and effectively skips the lengths covered in myelin (saltatory
conduction) Velocity of Axonal Conduction Speed of conduction is faster with myelin Faster in thicker axons Ex: mammalian motor neurons are thick & myelinated & can conduct signals at around 224 mph!! Structure of Synapses Different types of synapses based on the
location of the connection on each neuron Axodendritic Normal synapses Terminal button of axon on Neuron1 dendritic spine of Neuron2 Axosomatic Axon of N1 to soma of N2 Dendrodendritic Axoaxonic to Neurotransmitters
2 categories of NTs Large: Neuropeptides Small: Made in terminal buttons & stored in vesicles Release of NTs NTs are released via exocytosis At rest, NTs are in vesicles near membrane of presynaptic neurons When an AP reaches the terminal button, voltage-activated Ca2+ channels open &
Ca2+ rushes in Ca2+ causes the vesicles to fuse with the membrane & release contents into the synaptic cleft Activation of Receptors by NTs NTs released from the presynaptic neuron cross the cleft & bind to receptors on the postsynaptic neuron Receptors contain binding sites for only certain NTs Any molecule that binds is a ligand
There are often multiple receptors that allow one kind of NT to bind: receptor subtypes Different subtypes can cause different reactions Receptors There are 2 general types of receptors 1. Ionotropic
NT binds & ion channel opens & ions flow through Immediate reaction Metabotropic 2. NT binds & initiates a G-protein to trigger a second messenger, which moves within the
cell to create a reaction Slow, longer lasting effects More abundant Autoreceptor A special type of metabotropic receptor Located on the presynaptic neuron & bind with NTs from its own neuron Function to monitor the # of NTs in the synapse If too few, signal to release more Too many, signal to slow/stop
release Reuptake, Degradation & Recycling In order to allow the synapses to be available to signal again, the extra NT in the synaptic cleft need to be cleaned up by: Reuptake Most of the extra NT are quickly taken back into the presynaptic neuron by transporters to be repackaged in vesicles for future release
Enzymatic degradation NTs in the cleft are broken down by enzymes Ex: acetylcholine broken down by acetylcholinesterase Even these pieces are taken back into the neuron & recycled Gap Junctions
Unique signal transmission alternative to traditional synapses Called electrical synapses Narrow gaps between neurons connected by fine tubes called connexins that let electrical signals pass Very fast & allow communication in both directions Not yet fully understood in mammalian systems
Neurotransmitters Amino Acid NTs Monoamine NTs Acetylecholine Unconventional/Misc. NTs Neuropeptides Amino Acid NTs AAs are the building blocks of proteins Glutamate Most common excitatory NT in the CNS
Aspartate Glycine GABA Most common inhibitory NT Monoamines 2 groups with a total of 4 NTs in this class Catecholamines: 1. Dopamine (DA)
Made from tyrosine/L-Dopa Norepinephrine (NE) 2. Made from dopamine Epinephrine 3.
Made from NE Indolamines: Serotonin (5-HT) 4. Made from tryptophan Acetylcholine (Ach) Functions at neuromuscular junctions, in
ANS & CNS Extra is mostly broken down in the synapse; by acetylcholinesterase Receptors for Ach are said to be cholinergic Unconventional/Misc. NTs Act differently than traditional NTs Nitric oxide & carbon monoxide Gases that diffuse across the membrane, across the extracellular fluid & across the membrane of the next neuron
Endocannabinoids Essentially, the brains natural version of THC (main active chemical in marijuana) Ex: annandimide Neuropeptides Dont worry about the specific types Just know that they are another type of NT Generally large NTs Drugs & Synaptic Transmission
Pharmaceutical drugs generally affect synaptic in 2 ways Agonists facilitate the effects of a NT Can bind to a receptor & activate it like the NT would Antagonists inhibit Can bind to a receptor & block it so NTs cannot bind Example Acetylcholine has 2 types of receptors 1. Nicotinic
Many in the PNS between motor neurons & muscle fibers Ionotropic Nicotine: agonist Curare: antagonist (causes paralysis) Botox: antagonist Muscarinic
2. Many located in the ANS Metabotropic Atropine: antagonist, receptor blocker Misc. Endogenous Compounds naturally made within the body
Ex: enkephalins & endorphins The bodys endogenous opioids An exogenous opioid is morphine Opioids are analgesics (pain relievers)
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