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53 Cards in this Set
- Front
- Back
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A synapse is a:
Electrical Synapse: |
-point of contact b/t neurons
-Gap junction |
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Electrical Synapse = Gap junction (5)
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-Ion channels
-permits ions/electrical charges to pass b/t coupled neurons -ensure synchronous activity of linked neurons -found in circuits controlling saccades -located in the retina |
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Chemical synapse
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A junction in which a neurotransmitter is released
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The chemical synapse consists of 3 components (5)
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1. A presynaptic membrane or terminal bouton
-vesicles containing neurotransmitter are found in the prsynaptic terminal 2. A synaptic cleft 3. A postsynaptic membrane -postsynaptic membrane has receptors designed to bind secific neurotransmitters |
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Chemical synapse photo
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photo from handout
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Sequence of events leading up to the release of the neurotransmitter (3)
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-Action potential arrives at the presynaptic terminal
-Voltage-gated Ca2+ channels are opened and the Ca2+ diffuses into the presynaptic terminal -Ca2+ ions cause the presynaptic vesicle to fuse with the presynaptic membrane and release the neurotransmitter |
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Photo of sequence of neurotransmitter release
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photo
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Propagation of action potential (3)
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-neurotransmitter diffuses across the synaptic cleft and binds with receptors on the next neuron
-excitatory postsynaptic potential occurs when bound neurotransmitter causes an increased permeability to Na+ ions resulting in a local potential (if strong enough it leads to action potential) -inhibitory postsynaptic potential occurs when the neurotransmitter causes an increased permeability to K+ or Cl- which may lead to hyperpolarizataion |
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Once the neurotransmitter is released from the postsynaptic neuron, the following processes remove it i quickly from the synaptic cleft (3)
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-Catabolism
-Active transport -Diffusion |
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Chemicals used to remove neurotransmitters (5)
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>Acetylcholine ACh
-Acetylcholinesterase (breaks down ACh) -Acetic acid -Choline >Norepinephrine (actively transported back into presynaptic terminal) |
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Neurotransmitters and Neuromodulators
Neurotransmitter is a: |
chemical released by the presynaptic terminal that causes excitation or inhibition of the postsynaptic membrane
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Neuromodulator:
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Influences the likelihood that an action potential will occur in the postsynaptic cell
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Neuromodulator:
-axo-axonic (3) |
-some synapses in the CNS are axo-axonic
-the axo-axonic synapse does not produce an action potential -neuromodulators released at the axo-axonic syapse can influence the amount of neurotransmitter released from the presynaptic terminal |
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Presynaptic inhibitors:
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decrease neurotransmitter release from the presynaptic membrane
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Presynaptic facilitation:
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increase neurotransmitter release from the presynaptic membrane
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Clinical Example:
Endorphins (2) |
-they produce presynaptic inhibition of neurons that transmit pain sensation
-this presynaptic inhibition can reduce or eliminate the postsynaptic action potential that gives the sensation of pain |
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Receptor characteristics of neurotransmitters (2)
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-some can bind to more than one type of receptor
-they can have a different effect depending on which receptor they bind to |
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Receptor characteristics of receptors (2)
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-they are very specific for a neurotransmitter
-they only bind specific neurotransmitters or very closely related substances will bind to the receptor |
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Amino Acid Neurotransmitters/
Neuromodulators: Glutamate (4) |
-Excitatory
-the primary fast excitatory transmitter in the CNS -Elicits neural placticity in learning and development -contributes to cell death after injury in the CNS |
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Clinical Applications: Glutamate (2)
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-Overly active may cause epileptic seizures
-PCP or angle dust blocks glutamate receptors |
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aa.Gamma-aminobutyric acid (GABA) (3)
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-inhibitory
-the major inhibitory neurotransmitter in the CNS -prevents excessive neural activity |
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Clinical application: aa.GABA (4)
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-low levels can lead to seizure
-Benzodiazepines (anti-anxiety and anticonvulasant drugs) activate GABA receptors -Barbituates (tranquilizers activate GABA receptors -Baclfen (muscle relaxant) increases the presynaptic release of GABA reducing excessive muscle activity |
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aa.Glycine (2)
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-inhibitory
-prevents excessive neural activity |
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Clinical application: aa.Glycine (2)
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-low levels can lead to seizures
-strychnine inhibits glycine receptors |
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Cholinergic Neurotransmitter/
Neuromodulator: Acetylcholine (4) |
-found in the neuromuscular junction of skeletal muscle
-it is also involved in autonomic regulation -has a role in the general activity level of the CNS -it can be excitatory or inhibitory |
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cholinergic acetylcholine has two receptors: (2 and what they are)
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-Nicotinic (brief opening)
-muscarinic (slow acting) |
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Clinical application of cholinergic acetylcholine (2)
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-botulinum toxin blocks the release of acetylcholine casing paralysis
-Myasthenia Gravis is caused by the destruction of acetylcholine receptors of skeletal muscle membranes |
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Monamine Neurotransmitters/
Neuromodulators: Dopamine (2) |
-has an effect on motor activity, cognition, and motivation
-can be excitatory or inibitory |
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Clinical application of monamine Dopamine: (1)
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-Parkinson's disease results from destruction of dopamine-secreting neurons
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Monamine Neurotransmitters/
Neuromodualtors: Norepinephrine (4) |
-Role in increasing attention to sensory information
-transmitter in the synaptic system -Alpha1, alpha2, beta1, and beta2 receptors -can be excitatory or inhibitory |
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Clinical application of Norepinephrine: (4)
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-panic disorder and post-traumatic stress disorder involve excessive levels of norepinephrine
-MAO inhibitors increase the affect of norepinephrine by decreasing the activity of monamine oxidase -Cocain blocks the reuptake of norepinephrine -Amphetamines increase the release and block the reuptake of norepinephrine |
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Monoamine Neurotransmitters/
Neuromodulators: Serotonin (2) |
-role in general arousal level, mood, and suppressing sensory information
-generally inhibitory |
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Clinical applications: Monoamine serotonin (3)
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-low levels of serotonin are associated with depression and suicide
-prozac, zoloft, and paxil block serotonin reuptake -serotonin levels are increased with schizophrenia |
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Peptides Neurotransmitters/
Neuromodulators: Endorphins (2) |
-associated with pain perception
-generally inhibitory |
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Clinical application: peptide Endorphine (1)
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-morphine and heroin reduce pain by inhibiting neurons involved in pain perception
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Myasthenia Gravis: Cause (2)
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-the body produces antibodies to the nicotinic receptors on the skeletal muscle cells
-normal amounts of acetylcholine are released into the synaptic cleft, but the receptors are insufficient to cause an action potential in the postsynaptic cell |
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Myasthenia Gravisa: Onset (2)
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-Age 20-30 years in women
-Age 60-70 years in men |
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Myasthenia Gravis: Prevalence: (1)
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- 14 per 100,000
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Myasthenia Gravis: Symptoms (7)
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-muscle weakness with repetitive movement
-muscle movement commonly affected -eye movement and eyelids are often affected first -facial expression -swallowing, chewing, talking -proximal limb movement -respiration |
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Myasthenia Gravis: Ocular symptoms of Lid drop (4)
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-found in almost all MG patients
-this is the presenting symptom in 50% of patients -diminished or absent on wakening and progresses through the day -may involve on or both lid asymmetrically |
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Myasthenia Gravis: ocular symptoms of double vision (1)
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-worsens as the day progresses
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Myasthenia Gravis: Ocular Signs #1 (with 3 explinations)
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Ptosis
-accentuated when the patient maintains upgaze for 2 minutes -physical elevation of the more ptotic lid will cause the other eyelid to droop more -Cogan's sign: when the patient looks in downgaze and then to primary position the eyes overshoot and then come back to normal position |
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Myasthenia Gravis: sign #2
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ocular motility disorder and misalignment
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Myasthenia Gravis: sign #3
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Saccades slow with fatigue
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Myasthenia Gravis: sign #4
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Eyelids open easily when the patient is trying to force lid closure indicating orbicularis weakness
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Myasthenia Gravis: In-office testing (Ice-test) (3)
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-Ice is placed over the ptotic lid for 2 minutes
-ptosis will be greatly improved in MG patients -ocular motility disorder will improve if ice is left over the eye for 5 minutes |
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Myasthenia Gravis: In-office testing (rest test) (1)
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ptosis improves in MG patients after 20 minutes of keeping their eyes closed
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Myasthenia Gravis: lab testing (IV test = Tensilon test) (1 whats the name and what does it do?)
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-IV injection of edrophonium chloride causes an improvement in the ptosis and muscle disorders for approximately 2 minutes
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Myasthenia Gravis: Electromyography (1)
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-a decreased response of muscle fibers after repeated stimulus indicates MG
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Myasthenia Gravis: Imaging (1)
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-chest imaging to determine thymus dysfunction should be performed in MG patients
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Myasthenia Gravis: what organ function test should be performed
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thymus function should be tested in MG patients
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Myasthenia Gravis: Treatment (4)
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-Anticholinesterase medications: drugs that allow acetylcholine to stay in the synaptic cleft longer (inhibit breakdown)
-removal of the thymus gland -immunosuppressive drugs -plasmapheresis (filter the blood) |
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Myasthenia Gravis: Prognosis (1)
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-greater than 90% survival rate
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