PSY 215 Lecture 3 (1/19/2011) (Synapses & Neurotransmitters) Dr. Achtman PSY 215

Transcription

1 Corrections: None needed. PSY 215 Lecture 3 Topic: Synapses & Neurotransmitters Chapters 2 & 3, pages Lecture Notes: SYNAPSES & NEUROTRANSMITTERS, CHAPTER 3 Action Potential (above diagram found on page 41 of textbook) Electrical potential on left compares charge inside cell to charge outside cell Action potential starts at resting point (-70 mv) Resting potential remains stable until neuron is stimulated Page 1 of 12

2 One action potential (AP) takes one millisecond The potential is raised, and raises charge closer to 0 (depolarization) If the neuron hits -50 mv, it is called the threshold of excitation once charge hits -50 mv, it will become excited and fire an AP All-or-none law: it does not matter how much stimulus occurs, so long as it reaches the 50 mv necessary to fire AP o voltage of a certain strength is necessary, but anything past that does not cause AP to become faster or more intense Massive depolarization, potential shoots up far past the strength of the stimulus Rapid depolarization is followed by rehyperpolarization overshoots resting potential and it takes a bit of time for the neuron to come back to normal resting potential Molecular Basis of the Action Potential Sodium ions cause the rapid depolarization they are positive ions, and their entry causes a change in neuron charge Sodium entry is controlled by voltage-gated channels (or voltage-dependent channels) - channels whose permeability is dependent on the voltage difference between inside and outside the membrane Channels are closed at resting potential when voltage hits -50 mv, sodium channels open for 1 msec and shut for 1msec In that 1 msec, sodium ions rush into the neuron to trigger an AP After AP, potassium leaves the cell and causes rehyperpolarization At 0 mv, potassium voltage-gated channels open to let potassium out Page 2 of 12

3 (above diagram found on page 41 of textbook) Red line represents rate of entry of sodium ions into the neuron Blue line represents rate of exit of potassium ions from the neuron Sodium enters during peak of AP, and potassium exits later in opposite direction, which causes the membrane to return to resting potential Summary of Action Potentials Molecular basis sodium ions come in to cause depolarization and potassium leaves to cause rehyperpolarization All-or-none-law once voltage reaches -50 mv, there will be an action potential Refractory periods the time when a neuron cannot fire an AP o Two types of refractory periods: 1. Absolute refractory period membrane cannot produce an action potential, no matter how hard it is stimulated 2. Relative refractory period possible to produce an action potential, but extremely hard and very unlikely Page 3 of 12

4 (above diagram shows voltage levels/time periods at which the AP and RP occur) Please note: RF in diagram should read RP Absolute RP it is impossible for another action potential to be fired during this time happens because sodium voltage-dependent channels are shut and locked Relative RP stronger than usual stimulus is necessary for an AP happens because potassium voltage-dependent channels are still open and need extra stimulation to trigger The Action Potential How does the action potential travel along the axon? Page 4 of 12

5 (above diagram found on page 45 of textbook) Above diagram is of an axon, direction of propagation moving from left to right Rectangles represent myelin (fatty cells that insulate the axon) Node of Ranvier is the space between myelin only location where ions have channels and can pass through Saltatory conduction when action potentials jump from node to node, being carried along through the myelin Why doesn t the action potential travel backwards to the soma? o Absolute refractory period channels are closed and do not allow AP to travel backwards Propagation of an Action Potential Page 5 of 12

6 AP starts in the axon hillock travels along axon via myelin ends in presynaptic terminals triggers release of neurotransmitters AP doesn t bounce back from the presynaptic terminals because the refactory period closes channels and prevents AP from traveling backwards AP can be blocked by: o TTX produced by Puffer fish (sushi made from Puffer fish is called Fugu) - TTX blocks the sodium and potassium channels o Venom of scorpions, bees, and snakes - Deactivates the potassium channels o Venom of tarantulas - Deactivates the voltage-sensitive potassium channels cannot sense voltage cannot open/close o Blocking the action potential can cause death because the action potential is necessary to control processes such as breathing and heart rate Summary of Main Points APs are triggered if the voltage goes above -50 mv APs are caused by the opening of voltage-dependent sodium and potassium channels After an AP, axons go into absolute and relative refractory periods APs can travel along the axon either continuously, or in jumps Myelin Sheath o Jumping of APs from node to node is caused by oligodendrocytes/schwann Cells and is called saltatory conduction Page 6 of 12

7 (above diagram is micrograph of myelin) Saltatory conduction increases speed of neural transmission from 10 milliseconds to 120 milliseconds MS (or Multiple Sclerosis) is a disease that affects myelin, causing oligodendrocytes to die o Without myelin, action potentials cannot be carried and messages do not get sent where they need to go o Those affected by MS cannot control muscles Page 7 of 12

8 (above diagram is an illustration of a typical synapse) Axon of presynaptic cell meeting dendrite of postsynaptic cell, but do not touch Space between presynaptic terminal and postsynaptic spine called synaptic cleft (above diagram is a micrograph of a cell) Page 8 of 12

9 Synaptic vesicles (little dots throughout inside of cell) hold neurotransmitters Neurotransmitters are chemical signals that work as a team with the electrical signals of the action potential both are necessary to communicate (above is an illustration of a synapse) Action potential travels along axon Action potential itself does not release neurotransmitter: o Depolarization opens voltage-dependent calcium gates in presynaptic terminal o Within 1 or 2 milliseconds, calcium enters and causes exocytosis o Exocytosis release of neurotransmitter in bursts Neurotransmitter diffuses across synaptic cleft to postsynaptic membrane Neurotransmitter attaches to receptor on postsynaptic spine Page 9 of 12

10 Postsynaptic Effects of Action Potentials Neurotransmitter release can cause graded potentials in postsynaptic neuron Graded potentials membrane potentials that very in magnitude without following the all-or-none law o A local neuron is stimulated produces either a hyperpolarization or depolarization change in membrane potential is conducted to other areas of the cell o Potential decays as it travels Excitatory PostSynaptic Potentials (EPSPs) cause graded depolarizations Inhibitory PostSynaptic Potentials (IPSPs) cause graded hyperpolarizations If the sum of the PostSynaptic Potentials brings the charge of the membrane above its threshold, an AP occurs Temporal and Spatial Summations (above diagram illustrates what types of messages are sent among neurons) Page 10 of 12

11 Interim Summary Temporal summation several impulses from one neuron over time Spatial summation impulses from several neurons at the same time Each neuron is receiving information from numerous sources at one time has to sum up all of the info it s receiving decides what to do based on info Charles Scott Sherrington s contributions: o Presynaptic and postsynaptic terminals are separated by a gap (synaptic cleft) Otto Loewi s contributions o Synaptic transmission involves chemicals known as neurotransmitters and neuromodulators Neurons can integrate Excitatory PostSynaptic Potentials (EPSPs) and Inhibitory PostSynaptic Potentials (IPSPs) over time/space Sequence of Events at a Synapse (above diagram can be found on page 57 of textbook) Page 11 of 12

12 1.) Synthesis of neurotransmitters in cell body 2.) Transport of neurotransmitters to presynaptic terminal 3.) Spike Propagation action potentials travel down the axon 4.) Exocytosis release of neurotransmitters into synaptic cleft 5.) Receptor activation neurotransmitters diffuse across the cleft and bind to receptors 6.) Separation neurotransmitter leaves the receptors 7.) Reuptake neurotransmitter gets taken back up into the presynaptic cell For more information: This YouTube video, called The Schwann Cell and Action Potential further explains and discusses the Schwann cell, myelin, action potentials, and how they travel along the axon, as well as reviewing concepts we covered in the first three lectures. Real-life example: The discussion of Multiple Sclerosis in the lecture touches on one of many diseases of the central nervous system that can have a huge impact on our lives, either as patients or as families and friends of patients. The discussion of what can go wrong with/block the sending and receiving of action potentials is important to understand if you or someone you know is diagnosed with a disease of the nervous system. Page 12 of 12