9/17/09 8:08 PM Figure 6.19 Right after Step 6- After hyperpolarization Open sodium channels, close sodium channels repolarization (Step 6) Action potential Nodes in between myelin Saltatory conduction- jumping of depolarization from node to node Myelination makes speed of conduction much faster Size of nerve fiber influences speed greatly Bigger in diameter nerve fiber is, the faster it will go Lack of myelin can cause serious diseases Figure 6.27- Neurotransmitter storage and release Synaptic bulb- swelling at the end of an axon terminal At end of dendrite, open Na channels with stimulus -70 mv Depolarization If threshold reached (-55mv) Open voltage gated Na channels Action potential- remains the same across neuron due to all or none and non-decrimental Down at end of axon Calcium goes in because more calcium outside Calcium binds to proteins and causes release of neurotransmitter Released into space between synaptic bulbs called synaptic cleft Fates of neurotransmitter: 1. Diffuse away from neurons and not do anything 2. Bind to receptor on post-synaptic membrane Could change membrane permeability Produce membrane potential Could activate enzymes Could bind to receptor that opens sodium channels Depolarizes- Excitatory post synaptic potential Could bind to receptor that activates chlorine channel Inhibitory post synaptic potential Can?t be excitatory and inhibitory on same cell 3. Bind to receptor on presynaptic membrane- negative feedback (neuromodulators) Regulate release of neurotransmitter 4. Bind to enzyme that breaks it down Need to get rid of neurotransmitter so that another message may be sent out Reuptake transporter protein- on presynaptic membrane Release neurotransmitter and pull it back in to the cell Has chance to bind so the receptors become free If it does not reach the threshold, nothing happens Repolarizes and goes away If before it polarizes you send another weak signal Temporal summation General Classes of Neurotransmitters 1. Acetylcholine (ACh) Synthesized from coenzyme A and choline within the neurons Broken down by acetylcholinesterase- very important enzyme present in synaptic cleft Can also bind to cholinergic receptors Two main classes of cholinergic receptors Nicotinic- ligand gated ion channel that is permeable to both Na and K Muscarinic- couples to other membrane proteins via G proteins Can be excitatory or inhibitory depending on signal transduction pathway and location of acetylcholine and what receptor is there Drug interactions and things that can interfere with this Agonist- binds to receptor and does same thing as the neurotransmitter Antagonist- binds to receptor but does not initiate signal transduction Blocks the signal because it binds on the site you need to get message to Atropine- antagonist that will bind to receptor even though there is too much acetylcholine, not as much will bind 2. Biogenic amines Catecholamines- major subclass Dopamine (DA) Norepinephrine (NE) Adrenergic- things that are going to bind or secrete epinephrine 2 min classes Alpha adrenergic Uses various second messengers depending on which type Beta adrenergic Both use G proteins and second messengers Beta uses cAMP pathway Epinephrine (Epi) Adrenergic Monoamine oxidase breaks down epinephrine, norepinephrine, and dopamine Serotonin (5-hydroxytryptamine, 5-HT) Use different amino acids as bases and then modify them Levels are not controlled by enzymes, but by reuptake transporters (serotonin reuptake transporter) MAOI prescribed to knock out monoamine oxidase to increase epinephrine level- serotonin levels increase SSRI prescribed to interfere with protein that pulls serotonin back into cell- serotonin levels increase Histamine 3. Amino acids Excitatory amino acids such as glutamate Inhibitory amino acids such as gamma-aminobutyric acid (GABA) and glycine GABA not involved in protein synthesis but will activate chlorine channels and cause a hyperpolarization 4. Neuropeptides For example, endogenous opioids, oxytocin, tachykinins Oxytocin comes from neuron within pituitary gland Endogenous (within the system) opioids (opium) comes from plant ovary Derivatives of plants are agonists Very important in pain pathways Afferent neuron Neurotransmitter released is neuropeptide called substance P that sends message Need pain to tell us we are doing damage to ourselves Neurons on synaptic bulb can inhibit release of substance P which causes no pain 5. Miscellaneous Gases such as nitric oxide Purines such as adenosine and ATP Chemical messengers could be hormones Release from glands and binds to receptor Paracrine agents- things released by a cell and have actions on nearby cells Neurotransmitters are paracrine agents but we call them neurotransmitters Reflexes- protective responses Knee-jerk reflex keeps you from falling down Tells you that nerve pathway to spinal cord is intact and working No reflex = nerve damage, muscle damage, spinal cord damage, etc. Petellar tendon- sends information from stretch receptors up into spinal cord and stimulates action potential in afferent pathway Synapse directly on motor fiber that goes into muscles Hits inhibitory neuron- releases inhibitory neurotransmitter and inhibits muscles, leads to contraction of muscles (spinal reflex, brain not needed at all) Monosynaptic response- just spinal reflex More synapses- slower response Figure 10.19 Activates movement on both sides of body Signal from brain overrides reflex Sympathetic Nervous System?TEST QUESTION?EVERYTHING BELOW THIS Somatic Goes to skeletal muscle Conscious control 1-fiber pathway (1 neuron from CNS to muscle) Single neuron comes from spinal cord or brain, goes all the way out to the muscle ACh released Receptor is nicotinic receptor, response always excitatory (to contract) All or none response, excitatory Autonomic Graded response Excitatory or inhibitory Goes to smooth muscle, cardiac muscle, glands Unconscious control 2-fiber pathway (2 neurons from CNS to muscle) Sympathetic- fight or flight Comes from thoracic/lumbar regions Comes from middle Ganglia are close to CNS Preganglionic fibers release ACh Postganglionic fibers have nicotinic receptors on dendrites Postganglionic fibers release norepinephrine Effectors have either alpha or beta receptors Viscera, face, skin, and blood vessels Parasympathetic- rest digest Comes from cranial/sacral regions Comes from top and bottom Ganglia are close to effector (muscle) Preganglionic fibers release ACh Postganglionic fibers have nicotinic receptors on dendrites Postganglionic fibers release ACh Effectors have muscarinic receptors Mostly viscera and face IN SUMMARY ALL somatic motor fibers release acetylcholine Skeletal muscle has nicotinic receptors ALL autonomic preganglionic fibers release acetylcholine ALL autonomic postganglionic dendrites have nicotinic receptors Parasympathetic postganglionic fibers release acetylcholine Parasympathetic effectors have muscarinic receptors Sympathetic postganglionic fibers release norepinephrine Sympathetic effectors have alpha or beta receptors Autonomic nervous system Cranial nerve 10- Vagus nerve Goes to intestines, heart, lungs, stomach Provides most of parasympathetic input Sympathetic Pathway outside spinal cord = sympathetic trunk Phrenic nerve- goes to diaphragm Comes out from neck and goes outside the spinal cord Cord damage can occur but can still breathe on your own Table 6-11 Neurotransmitters 9/17/09 8:08 PM 9/17/09 8:08 PM
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