Overview of the Neurons, Neuronal Signaling, and Neural Networks (Part I)

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Charcot-Marie-Tooth disease (MOA and S/Sx)

- AKA CMT -Loss of PNS axons leading to peripheral neuropathy -Signs & Symptoms •Motor dysfunction, sensory loss, muscle atrophy •Podiatry: Foot drop, high-stepped gait, hammertoe

Guillain-Barré (MOA and S/Sx)

-1-2 weeks following a viral infection -***Selectively attacks and damages PNS myelin (e.g. motor nerves)*** -Weakness is progressive and may require ventilatory assistance -Most get better over time but often with residual complications

Myasthenia Gravis (MOA)

-Autoimmune destruction of postjunctional nicotinic receptors -Decreases the availability of acetylcholine receptor sites

Lambert-Eaton Myasthenic Syndrome

-Ca2+ is blocked from entering presynaptic motor nerve terminals -Inhibits the release of acetylcholine

Tetrodotoxin (source and MOA)

-From Pufferfish -Concentrated in liver and ovaries of pufferfish -Prevents depolarization by preventing Na+ from entering

Anesthesia Considerations in MS

-Increase in body temperature can cause exacerbation -Increased seizure risk in these patients -Peripheral blocks, epidural, or spinal anesthesia? A) Epidural > Spinal, epidural is safer -Peripheral blockade has not been shown to exacerbate -Possible sensitivity with non-depolarizers A) Avoid succinylcholine (only depolarizing agent) -Consider steroid supplementation perioperatively

Multiple Sclerosis (MOA)

-Neuroinflammatory disease that impacts myelin -***Plaques occur due to an autoimmune attack of CNS myelin***

Tx for Multiple Sclerosis

-No cure, only symptom control/slowing progression -Corticosteroids -Interferon-B (beta) therapy -Immunosuppressants: e.g. Mitoxantrone (cardio toxic), Methotrexate

S/Sx of Multiple Sclerosis

-Optic nerve: visual disturbances -Cerebellum: gait disturbances -Spinal cord: Limb paresthesias, Limb weakness, Urinary incontinence, and Impotence

Curare

-Plant extract -Causes paralysis by binding to nicotinic receptors at NMJ -used with induction and surgery eventually

Botulism (MOA)

-Prevents presynaptic attachment and fusion of vesicles -Inhibits the release of acetylcholine

Multiple Sclerosis (Forms)

-Relapse-remitting: Exacerbations and remissions -Primary progressive: Slow continuous debilitation

Role of membrane proteins

-Serve as anchor points for cytoskeletal elements -Surface recognition molecules -Assist in movement of lipid insoluble nutrients (glucose) -Regulate the passage of ions into or out of the cell

What do Corticosteroids do in MS?

-Shortens duration of relapse -Accelerates recovery

Steps of Chemical Synaptic Transmission 5 steps

1) Synthesis of the neurotransmitter 2) Presynaptic concentration & packaging (e.g. vesicles) 3) Release into the synaptic cleft 4) Binding to receptors on postsynaptic membrane 5) Termination of neurotransmitter action

What is special about nodes of ranvier?

Contain high concentration of Na channels

Name two demyelinating diseases

Guillain-Barré Syndrome and Multiple Sclerosis

Treatment of choice for relapse-remitting MS?

Interferon-B (beta)

Fast synaptic receptors

Ionotropic receptors (ligan gated)

What three diseases interfere with neuromuscular transmission

Lambert-Eaton Myasthenic Syndrome Botulism Myasthenia Gravis

Slow synaptic receptors

Metabotropic receptors (g-protein)

Type of conduction from node to node along myelinated axons

Saltatory conduction

Relative Refactory Period (RRP)

This represents a time when a greater-than-normal stimulus may initiate an impulse.

Equilibrium potential of K+

Wants ot move out of cell (-94 mV)

Equilibrium potential of Na

Wants to more into cell (+60 mV)

Equilibrium potential of Ca2+

Wants to move into cell (+136 mV)

Equilibrium potential of Cl-

Wants to move into cell (-86mV)

What do we know about unmyelinated axons?

propagation is slow & continuous

Absolute Refractory Period

time during which another action potential is impossible; limits maximal firing rate


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