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Conjoint > Neuronal Physiology (Midterm 1) > Flashcards

Neuronal Physiology (Midterm 1) Flashcards

1
Q

Growth Factors necessary for neuron growth? Give two specific examples.

A

Neurotropins. BDNF: brain drive neurotrophic factor and NGF: nerve growth factor.

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2
Q

Tangle of nerves at stump of developing (or cut or damaged) neurons?

A

neuroma

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3
Q

How does the nerve know where to grow?

A

Growth cone on efferent neuron follows cell adhesion molecules.

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4
Q

Cells that surround and support neurons and two examples.

A

neuroglia. 1. astrocytes are most common type and control ISF surrounding neurons and endothelial cells in blood brain barrier. 2. Microglia are counterparts of macrophages.

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5
Q

List the actions in a sensory dendrite of an afferent neuron.

A
  1. deformation of skin causes mechanically gated ion channels to open. 2. net flow of postitive sodium (or calcium) ions into cell causing depolarization of cell. 3. depolarization results in a receptor potential.
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6
Q

Features of receptor potentials.

A
  1. only occur in sensory dendrites of afferent neurons. 2. vary in amplitude. 3. do not travel.
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7
Q

Define Action Potential and list features.

A

Receptor potential is large enough to surpass the threshold leading to depolarization which is the action potential. Travels and is an all-or-nothing. Analagous to a burning fuse.

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8
Q

Describe steps in a postsynaptic potential.

A
  1. action potential triggers release of neurotransmitter at the presynaptic terminal. 2. The neurotransmitter diffuses across the synaptic cleft to the postsynaptic neuron. 3. The neurotransmitter binds to postsynaptic receptors which opens ion channels. 4. depolarization from in-flowing ions leads to a postsynaptic potential.
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9
Q

Describe features of postsynaptic potentials.

A
  1. varies in amplitude. 2. does not travel.
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10
Q

Define summate.

A

When multiple postsynaptic potentials occur in a short period of time, they produce an additive effect to depolarize the membrane above threshold and produce an action potential in the postsynaptic neuron.

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11
Q

What are the equilibrium potentials for K+, Na+, Cl-?

A

K+ -90mV

Na+ +60mV

Cl- -70mV

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12
Q

What is the resting membrane potential? And explain why it is this value.

A

-70mV. It is close to the potassium equilibrium value because the cell has high permeability for potassium. Chloride has the same potential because there is passive diffusion into and out of cell so the equilibrium potential of chloride adjusts to the cells potential.

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13
Q

Name the two factors that influence movement of ions across a membrane.

A
  1. concentration gradient. 2. electrical potential difference. They can act in the same direction or in opposite directions.
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14
Q

Compare what the graph would look like if a voltmeter were placed within the sensory dendrite or in a Node of Ranvier.

A
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15
Q

Define Coding Type.

A

Different neurons code for different types of things. For instance a neuron may code for heat but not touch or vice versa.

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16
Q

Define Coding Intensity

A

The intensity of the receptor potential is measured by the size. It becomes bigger with increasing intensity. Action potentials are measured by frequency. More intense leads to more frequent action potentials.

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17
Q

Define Coding Location.

A

Each neuron goes to a specific spot in the brain. Orderly and organized projections.

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18
Q

Define Coding Change

A

See a high initial response in action potential but the response drops off quickly with a steady stimulus. Tend to react more with novel stimuli.

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19
Q

Define Sensory Adaptation.

A

Receptor potential steadily declines with time, so that you do not have continuing action potential if you are touching something for a very long time (for example).

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20
Q

Desribe the ion channels involved in depolarization and repolarization in action potentials.

A

Voltage gated sodium channel responsible for depolarization. Potassium channels responsible for repolarization.

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21
Q

Describe methods of repolarization in action potentials.

A

depolarization by sodium channels are part of a positive feedback loop.

  1. repolarization by potassium channels which open because of depolarization but open slower than the sodium channels.
  2. inactivation of sodium channels within a millisecond of opening.
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22
Q

Describe Features of Potassium Channels

A
  1. open after sodium channels due to depolarization. 2. have no feedback loop, once they open they repolarize the cell causing the channels to close.
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23
Q

Conduction

A

Axons are filled with conducting fluid so that when positive sodium ions enter cell they can flow to the next segment to depolarize and continue the action potential.

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24
Q

Myelinated Axons: Formation and Effect

A

formed from phospholipid bilayer of Schwann cells spriraling around axon. Their effect is insulating which alows ions to flow from node to node to depolarize, in effect speeding conduction.

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25
Q

Sodium Channel Blockers

A

local anesthetics that keep sodium channels in inactive state. These drugs work at low concentrations which reduces negative effects if they get in general circulation. Examples are snakes venom, pufferfish and tetrodotoxin and red tide in mussels. also lidocaine.

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26
Q

Axonal peripheral neuropathy symptoms, features and causes.

A

symptoms: paresthesia (tingling, numbness, burning sensation)
features: affects the longest axons which are the smalles
causes: diabetes mellitus, vitamin B12 deficiency, alcoholism

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27
Q

Guillian Barre

A

demyelinating peripheral neuropathy. results from infection. paralysis is symptom. myelin is being attacked by the immune system.

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28
Q

Charcot-Marie-Tooth

A

genetic demyelinating. characteristic arched foot.

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29
Q

Bell’s Palsy

A

genetic demyelinating. facial nerve. symptom is that only one side of vision when blocked causes paralysis of face.

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30
Q

Carpal Tunnel Syndrome

A

demyelinating. swelling in area. initially is demyelinating but if severe becomes degeneration of axons. symptoms present along medial nerve (middle and index fingers)

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31
Q

Multiple Sclerosis Features and Symptoms

A

Features: axons in CNS, demyelinating, autoimmune, genetic and environmental side (lower levels of Vitamin D), relapsing/remitting cycle. Associated with Epstein-Barr virus

Symptoms: optic neuritis (visual disturbance), paresthesia, ataxia (inability to properly coordinate voluntary movements), muscle weakness.

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32
Q

Why is there a remitting stage in multiple sclerosis?

A

Initially the action potential cannot jump from node to node after demyelination occurs. However, after some time sodium channels become more frequent in the space between nodes which allows for conduction of action potential in the absence of myelin.

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33
Q

DMARD

A

disease modifying anti-rheumatoid drugs. used for treatment of multiple sclerosis.

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34
Q

Treatment options for multiple sclerosis:

A

glucocorticoids for acute relapses. DMARDs for long-term treatment

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35
Q

IFN-beta

A

multiple sclerosis. DMARD. induces anti-viral state

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36
Q

glatiramer

A

multiple sclerosis. DMARD peptide. modify t cell function

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37
Q

natalizumab

A

multiple sclerosis .DMARD. binds to cell adhesion molecules to slow down movement of t cells from the blood into lesions in the blood brain barrier. has serious immunological side effects.

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38
Q

mitroxantrone

A

multiple sclerosis. DMARD. interferes with DNA synthesis.

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39
Q

fingolimod

A

multiple sclerosis. DMARD phospholipid. immunosuppressant. oral. makes it more difficult for lymphocytes to leave lymph nodes.

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40
Q

Name the three origins of vesicles.

A
  1. after exocytosis from the presynaptic neuron the vesicle is recycled through endocytosis back into the neuron.
  2. After exocytosis the vesicle just pops back into the presynaptic neuron
  3. if the neurotransmitter is a peptide, the vesicle is actually formed in the cell body and travels to the presynaptic cleft.
41
Q

Describe the action of botulism toxin

A

Botulism toxin undergoes endocytosis to get into the presynaptic neuron where it diffuses out to the cell and cleaves SNARE proteins preventing the release of Ach. Also injected to reduce unwanted muscle contractions (dystonia)

42
Q

Describe the action of tetanus toxin.

A

Tetanus is a protease that blocks SNARE and acts on inhibitory neurons that are inhibiting the postsynaptic cell. The result is that the postsynaptic cell gets excitable on its own, with no stimulis.

43
Q

Explain what happens in a normal presynaptic neuron to release neurotransmitters from vesicles.

A

The depolarization from the action potential up to the part of the neuron causes voltage-gated calcium channels to open and calcium enters the cell and acts on SNARE to trigger exocytosis.

44
Q

Describe Fast EPSPs

A

They act in milliseconds. The neurotransmitter that was released at the presynaptic neuron binds to a ligand gated ion channel. When the channel opens Na or Ca flow in and cause depolarization. An example is acetylcholine acting on skeletal muscle. Other neurotransmitter can be glutamate.

45
Q

Describe slow EPSPs

A

Take seconds to work and are responsible for emotions, alertness, motivation etc.. Two types are GPCR and NMDA receptors.

46
Q

Describe NMDAs

A

Are slow EPSP receptors that respond to glutamate. Mg cork in channel requires repetitve depolarization to open which comes from adjacent fast EPSPs and repetitve glutamate binding to NMDA. Responsible for chronic pain and memory pathways. Ion that enters through the NMDA is calcium which has long-term effects in the cell.

47
Q

Give an example of a GPCR in slow EPSPs

A

In the heart muscle parasympathetic postganglionic neurons release acetylcholine which binds to a GPCR. The beta and gamma subunits release from the trimeric protein and act on a potassium channel, opening it, and letting potassium in.

48
Q

How are neurotransmitters removed from the synaptic cleft?

A

All neurotransmitters are recycled and transported back into the presynaptic terminal except Acetylcholine. Ach is broken down by acetylcholine esterase in the synaptic cleft. Several drugs target reuptake and prevent it which results in prolonged exposure to the neurotransmitter.

49
Q

Describe IPSPs

A

IPSPs turn off postsynaptic cells. They act in the same manner as EPSPs except the ions that move through the ion channels must inhibit the cell and are therefore K and Cl which both have equilibrium potentials less than the membrane equilibrium.

50
Q

Temporal Summation

A

Summing multiple presynaptic action potentials in a row to reach threshold for a postsynaptic action potential.

51
Q

Spacial Summation

A

Adding up ESPSs from two or more synapses (locations). For example if synapses are occurring near each other they can sum together to form an action potential.

52
Q

Sensors of the Skin - list the types of afferent neurons in the skin.

A
  1. C axons are not myelinated and carry pain, temperature, and crude touch.
  2. A-delta axons are myelinated and carry pain.
  3. A-beta are responsible for fine touch. there are two different kinds. Merkel’s are slow adapting and Meissners and Pasiniens (?) are fast adapting.
53
Q

Afferent neurons in muscles and joints

A

A-alpha. responsible for proprioception which is understanding sense of position.

54
Q

Types of Afferent neurons in visceral receptors.

A

Mainly pain receptors. Stimulants might be decreased blood flow, local conditions in ECF, stretching muscle.

55
Q

Explain the dorsal column tract.

A

From the dorsal horn the neuron synapses to the dorsal column where it travels up to the medulla and synapses. At this point it crosses to the other side of the body and continues to the thalamus then the cerebral cortex. carries fine touch and proprioception.

56
Q

Explain the Anterolateral Tract.

A

Most ancient tract. from the dorsal horn the axon crosses to the opposite side of the body to the anterolateral tract synapses. travels up to the thalamus and synapses. Finally it travels to the cerebral cortex. Carries pain, temperature and crude touch.

57
Q

Describe the organization of the somatosensory cortex.

A

organized in somatotopic. each part of the somatosensory cortex is associated with a location of the body.

58
Q

Name the two pain sensors.

A

A-delta sensors and C-fibers

59
Q

Features of A-delta axons in pain.

A

thinly myelinated. 5-30m/sec. responsible for bright, sharp pain that fades quickly. Nt is glutamate.

60
Q

Describe the C-fibers in pain.

A

not myelinated. 0.1-1m/sec. responsible for burning, persistent pain. important for chronic pain. Nt is glutamate and Substance P (peptide involved with inflammation).

61
Q

Describe Gate-Control Hypothesis in reduced pain sensation

A

A-beta axon inhibits C afferent neurons from taking its message to the brain. A-beta axons are more myelinated and faster and thus have more “priority”

62
Q

Opiates and opioid receptors.

A

morphine is the active ingredient. naloxone is a competitive inhibitor of morphine. opioid receptors are GPCR and found in three areas of CNS: periaguaductal gray (brain), medulla and dorsal horns.

63
Q

What are opioid peptides?

A

enkephalins, dimorphins, beta-endorphins. come from periaguaductive to medulla to interneuron which releases peptides onto the synapse in the dorsal horn.

64
Q

symptoms of neuropathic pain

A

allodynia (pain to stimulus that isn’t normally a stimulus), hyperalgeria (something you think would be a small thing is overwhelming and more cutting than burning), abnormal parasthesia.

65
Q

Describe the “wind-up” phenomenon in neuropathic pain.

A

As a person is exposed to strong pain, the tendency is for the perception of pain to get bigger and bigger. Substance P and glutamate are responsible.

66
Q

Explain the role of substance P in the wind-up phenomenon.

A

Substance P is released and are broken down more slowly and act longer than axons. They can also diffuse out of the synaptic cleft to other surrounding neurons and act there. They promote the growth of neighboring neurons.

67
Q

Explain the role of glutamate in the “wind-up” phenomenon.

A

Glutamate produces fast EPSPs. With prolonged depolarization glutamate starts opening NMDA channels which results in Calcium flowing into the cell. Neuron remodeling occurs due to calcium’s actions in the cell.

68
Q

Define phantom limb pain.

A

occurs in amputees. still feel pain in limb through afferent neurons that used to innervate it. deafferentation pain is the general pain due to the loss of afferent neurons going to the CNS.

69
Q

Describe sympathetic maintained pain

A

Give a drug that blocks sympathetic nervous system sometimes helps with pain and nobody knows why. only with certain pain syndromes.

70
Q

Visceral Pain sensation

A

also referred pain. No somatotopic organization like in somatic pain. instead visceral pain converges on somatic pain so that the pain felt is somatic in the same region.

71
Q

drugs to treat pain (non-neuropathic)

A

NSAIDS (central and peripheral action), APAP (central), opiates (central)

72
Q

neuropathic treatments

A

TCA’s block re-uptake in presynaptic terminals giving Nt more effect. anticonvulsents like gabapentin. NMDA antagonist is memantine.

73
Q

Cerebrovascular events

A
  • most common cause of damage to localized region of brain
  • two kinds: Transient Ischemic Attack (TIA) is breif and reversible
  • stroke results in permanent damage.
74
Q

Causes of Strokes

A
  1. blood vessel is clogged by a clot due to damage to vessel wall by atherosclerosis.
  2. sometimes due to hemorrhage (bleeding) usually in elderly with long-standing high blood pressure.
75
Q

Symptoms of Stroke

A

symptom: aphasia is difficulty with language if stroke happens on left side.

76
Q

Results of Stroke

A

necrosis of cells. apoptosis of neurons. outward diffusion of glutamate increases intracellular calcium levels which causes activation of caspases (results in apoptosis)

77
Q

Epilepsy definition and results

A

characterized by recurrent disorderly discharge of nervous tissue. results are altered consciousness, improper motor activity, distorted sensory perceptions, inappropriate behavior.

78
Q

Partial Seizures

A

begin at specific region of brain called focus. usually happens in hippocampus and other parts of limbic system.

79
Q

Generalized seizures in epilepsy

A

synchronous discharges in both cerebral hemispheres.

80
Q

absence seizures in epilepsy

A

generalized seizure. loss of consciousness and fluttering eyelids. usually a child.

81
Q

Tonic-Clonic seizures in epilepsy

A

generalized seizure. most common. loss consciousness, convulsive jerking, confusion afterward

82
Q

Axonal Transport of Viruses disorders

A

herpes zoster: virus usually resides in cell bodies of sensory neurons at the spinal level. After it moves out along the afferent axons it causes shingles.
rabies virus: moves toward the CNS, causing neuronal damage once it reaches spinal cord and brain.

83
Q

Two neuromuscular blocking agents

A

succinylcholine: depolarizing neuromuscular blocking agent used to relax skeletal muscles during surgeries. channels move to a closed formation.
curare: nondepolarizing. prevents contraction of skeletal muscle. used as poison on arrow darts.

84
Q

Prolonged Transmitter Action - 2 examples.

A 
cholinesterase inhibitors (anticholinesterases) block acetylcholinesterase in the synaptic cleft inhibiting removal of neurotransmitter. Used to treat myasthenia gravis and Alzheimer's. 
blocking reuptake: examples are cocaine with norepinephrine. and various antidepressant drugs like fluoxetine block reuptake of serotonin.
85
Q

Enhanced Transmitter Action

A

diazepam, barbituates bind to separate sites on GABA receptor increasing the effectiveness of GABA

86
Q

Blocking Inhibition

A

strychnine binds to and blocks the postsynaptic receptor for glycine (major inhibitory transmitter in the spinal cord and brain). results in increasing excitation of CNS.

87
Q

Duchenne Muscular Dystophy

A

genetic, males, degeneration of skeletal muscle fibers. death from respiratory failure in 20’s. defect in gene for dystrophin, an intracellular structural protein

88
Q

Myasthenia Gravis

A

reduced number of Ach receptors on skeletal muscle. muscles around eyes are most commonly affected. antibody attacks receptors.

89
Q

Training

A

during weight lifting (training for strength) more myofibrils are added in fast muscle fibers. during endurance training there is little effect on growth of myofibrils and ATP-generating machinery increases in slow muscle fibers.

90
Q

Denervation

A

myofibrils then muscle fibers will start to degenerate over a period of months. Shows the integrity of a muscle fiber relies on trophic factors released by a functioning efferent neuron.

91
Q

Jacksonian March

A

type of partial seizure. seizure begins furthest distal spot and moves proximal toward trunk. results from abnormal discharge moving sequentially through the primary motor cortex.

92
Q

Babinski Sign

A

damage to the corticospinal tract causes the appearance of the Babinski Sign on the foot.

93
Q

Parkinson’s Disease

A

symptom is bradykinesia (difficulty in initiating new movements), resting tremor, hypertonia.

there is decreased levels of dopamine in the brain due to degeneration of neurons in substantia nigra that project to the basal ganglia. dopamine does not cross the blood-brain barrier and does not work as a drug. Treatment options are L-dopa and dopamine agonists and deep brain stimulation.

idiopathic. protein aggregations in the brain of alpha-synuclein called Lewy bodies.

94
Q

Chorea

A

excessive, uncontrollable movements. In Huntington’s chorea, neurons with the nt GABA degenerate in the basal ganglia. In Huntington’s disease have a defective gene (huntigtin) with CAG repeats. begins with fidgeting, clumsiness.

95
Q

Athetosis.

A

involuntary movements that are slow. degeneration of basal ganglia usually the result of cerebral palsy (variety of motor abnormalities around the time of birth). common symptom is spasticity.

96
Q

Encephalitis Lethargica

A

result of severe flu outbreak in 1916. caused lethargy and somnolence. damage to the substantia nigra so several people had symptoms similar to Parkinsons. symptom was extreme lack of movement.

97
Q

define nystagmus.

A

symptom of multiple sclerosis. The eyeball is jerky.

98
Q

Axon Reflux

A

With C fibers certain branches of the afferent neuron move peripherally. Functions so that certain painful stimuli lead to the release of Substance P locally which causes inflammation due to histamine release and dilation of blood vessels.

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