Neuromuscular junction and dz Flashcards
Anatomy of Neuromuscular junction
- Nerve
- Root (within spinal canal)
- Peripheral nerve - Junction
- presynaptic endplate
- synaptic cleft
- post-synaptic membrane - Muscle
Lower motor neuron reflex arc
- Afferent nerve to
- Synapse in dorsal root ganglion to
- Dorsal horn to
- Synapse in ventral horn to
- Two pathways from there
Resting membrane potential for a large nerve fiber
~-90 millivolts
Depolarization
- inc Na+ permeability, influx of positive
2. Potential may approach zero or….?
Repolarization
- Na+ channels begin to close
- K+ channels open more
- Re-establishment of RMP
Defecit in Ca
Causes Na+ channels to become activated with little increases in membrane potential -> tetany (exciteability)
High extracellular Ca+
Decreases membrane permeability to Na+ and reduces exciteability
Local anesthetics (3)
- Na+ channel blockers
- Act on sodium channel activation gates
- Reduce excitability
When Action Potential strength to excitability threshold is < 1
Nerve impulses are not conducted
Anatomy of the neuron (5)
- Dendrites (receptor endings)
- Perikaryon (cell body)
- Axon
- Collateral branches
- Axon terminals
- Synaptic bulb
Myelin sheath
On CNS nerves I think
-Oligodendroglial cell processes
Schwann cells on
PNS nerves I think
-Rolled up Schwann cell membrane
Things with no myelination (4)
- Initial segment
- Axon hillock
- Nodes of Ranvier
- Axon terminals
Larger nerves have faster
conduction
Saltatory conduction (2)
- Increases velocity
2. Conserves energy with only nodes depolarizing
Presynaptic terminal elements (2)
- Transmitter vesicles
- excitatory or inhibitory - Mitochondria
- Provide ATP for transmitter synthesis
Depolarization of presynaptic membrane (3)
- Depolarized by Action potential
- Opens voltage-gated Ca channels
- Amount of Ca inflow is directly related to transmitter released
Postsynaptic receptor proteins (2)
- Binding component protruding into cleft
2. Ionophore component
Ionophore component (2)
- Ion Channel-rapid
2. Second messenger activator-slow, I think
Ion channel (2)
- Cation channels: allow entrance of Ca ->excitatory
2. Anion channels: allow entrance of Cl- -> inhibitory
‘second messenger’ activator (2)
- For prolonged postsynaptic neuronal changes
2. G-proteins
Neurotransmitters (2)
- Small molecules (rapidly action)
2. Neuropeptides (slowly acting or growth factors)
Small, rapidly acting neurotransmitters (4)
- Class I (ACh)
- Class II: Amines
- norepi, epi, dopamine, serotonin, histamine - Class III: Amino Acids
- GABA, Gly, Glutamate, Aspartate - Class IV (NO)
Neuropeptides, slow neurotransmitters (4)
- Hypothalamic-RH
- TRH, LHRH, Somatostatin - Pituitary peptides
- ACTH, GH, ADH - Peptides GI, Brain
- Enkephalins, gastrin, VIP, insulin, glucagon - Other
- Bradykinin, Angiotensin II
Things affecting synaptic transmission (4)
- Fatigue-dec in d/c of postsynaptic neuron
- pH-alkalosis inc excitability/acidosis depresses excit
- Hypoxia-cessation 3-7 seconds-> unconscious
- Drugs
- Caffeine (reduces threshold)
- Strychnine-inhibits glycine in spinal cord
- Anesthetics-inc threshold for excitation-> decreases transmission
Drugs stimulating muscle fiber by ACh-like action (3)
- Methacholine
- Carbachol
- Nicotine
* These aren’t broken down by cholinesterase (last longer)
Drugs that stim NMJ by inactivating ACh (3)
- Neostigmine
- Physostigmine
- Diisopropyl fluorophosphate
* Results in muscle spasm
Drugs that block transmission at NMJ
Curariform drugs: D-tubocurarine
*Prevents AP