Nervous System Notes in Physiology

Nervous System Notes

Membrane Potentials

• Intracellular vs Extracellular
• Higher concentration of Na outside the cell
• Higher concentration of K inside the cell
• Higher concentration of Cl outside the cell
• Higher concentration of Ca outside the cell
• Proteins would want to stay in the cell.

• Na+ equilibrium potential
• If the Na+ protein channel opens, the Na+ ions will rush into the cells until equilibrium, making the cell more positive inside.
• Na+ equilibrium potential= +60 mV

• K+ equilibrium potential
• If the K+ protein channel opens, the K+ ions will rush out of the cell until equilibrium, making the cell more negative inside.
• K+ equilibrium potential= -90 mV

• Resting membrane potential
• Around -70 mV [varies from cell to cell]
• Why is the resting membrane negatively charged?
• Na+/K+ pump /w ATP= move 3 Na+ from the inside of the cell in exchange for 2 K+ from the outside of the cell. Overtime, this will make an overall negative cell.

• Depolarization/Hyperpolarization
• Depolarization is the process of becoming more positive (membrane potential)
• Hyperpolarization is the process of becoming more negative (membrane potential)

In this section, the Central Nervous System and the Autonomic Nervous System are located at the end of the notes.

Factors Affecting Action Potentials

• Hyper/hypokalemia
• Hyperkalemia is the excess of K+ ions in the plasma membrane. The kidneys are not able to excrete the ions and can cause cardiac arrhythmia [neurons regulate the heart rate]and muscle weakness (motor neurons- innervate skeletal muscles)

• Hypokalemia- low K+ in the blood plasma. If a patient is on a diuretic [urination], it is to lower the high blood pressure. Can lose K+ ions to the urination. Can cause heart problems and convulsions.

• Drugs- [-aine]- lidocaine, novacaine, cocaine. Quieting pain neurons. Cause blockage of voltage gated Na+ channels

• Toxins- affect the channels in action potentials
• Puffer fish- blocks sodium channels
• Arrow Dart- keep sodium channels open.

• Heredity- have genetic abnormality in sodium and potassium channels

Synapses

• Types of Synapses

• Synaptic Function in Nervous System
• Voltage-gated calcium channels- After the action potential moves down the axon, it brings a voltage change[synaptic bouton] and opens up the calcium channels [calcium will rush into the cell]
• Calmodulin- calcium ions that are in the cell will bind to calmodulin molecule forming the calcium-calmodulin complex. The complex causes vesicles inside the neuron to fuse with the pre-synaptic membrane. The vesicles contain chemicals [neurotransmitters]
• Exocytosis of neurotransmitter [NT]- NT released into the synaptic cleft. The NT binds to the protein receptor in the post-synaptic membrane (<1 millisecond)
• NT enzyme degradation in cleft, reuptake of NT- if NT stays in cleft too long- extended signal time so do not want NT to stay in the cleft indefinitely.
• Excess NT are either taken back up by the pre-synaptic neurons (endocytosis) or enzymes in synaptic cleft destroys the NT.
• Examples: acetylcholinerterase breaks down ACH into acetate and choline.

• Effect of neurotransmitter of postsynaptic cell- Can either depolarize [make the cell more positive= gets us closer to the threshold=excitory signal] or hyperpolzarize [make the cell more negative by taking it further from the threshold= inhibitory signal]
• Fast EPSP [excitory post synaptic potential]
• NT binds to sodium ion channel [receptor] on the post synaptic membranes and quickly depolarizes the cell
• Slow EPSP
• NT binds to a G-protein [receptor] on the post synaptic membrane and influences another ion channel to open or close an ion channel.
• Example: NT binds to G-protein and then affects potassium channels by closing them so the cell stays more positive
• Fast IPSP [inhibitory post synaptic potential]
• NT binds to Cl- ion channels and chloride ions rush into the cell making the cell more negative
• NT binds to K+ ion channels and potassium ions rushes out the cell making the cell more negative
• Slow IPSP
• NT binds to G-Protein which influences the K+ channels to open as potassium rushes out of the cell

• Graded Potentials- the post synaptic cell takes the summation of IPSP and EPSP from the multiple synapses to achieve an action potential.
• Temporal Summation (time)- achieve action potential by increase frequency of EPSP
• Spatial Summation-more pre-synaptic neurons [releasing more NT] to the post-synaptic
• Synaptic Plasticity- everything depends on the receptor on the post-synaptic cell and are not a fixed number. Can be unregulated or down regulated receptors [learning and memory].
• Exampe: If the pre-synaptic cell is bombarding the post-synaptic cell with NT, the post-synaptic cells will down regulate the receptors so it is not as sensitive to the NT.

• Notes on: Classes of Neurotransmitters




Notes on: Sensory Receptors




• Categories of Receptors
• Tonic- Slow adapting
• As long as the stimulation is there/applied, there will be a sensation and the neuron will continue to produce action potentials. Sensation will continue to be sensed
• Once the stimulus is taken away, the action potential will then stop
• Example: Olfactory sensory neurons- potentially we need to smell bad chemicals so we can get away from bad chemicals
• Example: Nociceptors- if the sensation of pain went away we can badly injure ourselves
• Baroceptor and Osmoreceptor- because we don't want the sensation to go away. However overtime, we can reach a new homeostasis.
• Phasic- fast adapting
• If the stimulus is there, the neuron adapts quickly and slows down/stop the firing of action potentials overtime
• If we take the stimulus away, we get an action potential.
• Example: Thermoreceptors: we do not get the sensation until we take the stimulus away [ to some degree]
• Example: Pressure Receptors
• Receptor Generated Potentials
• If the stimuli is above threshold, the more frequency of action potential
• Threshold can change in sensory neurons

(nervous system)

• Stimulus Localization
• 2 point touch- cutaneous- sensitivity comes down to how close the sensory neurons are together
• Lateral Inhibition- initially we get a wide sensation. But slowly over time, it feels like its narrow. The neurons around the sensation stop firing and sharpens our perception. [cutaneous system and retina]

(nervous system)

• Pain sensation- [nociceptors]- turns on the sympathetic nervous system [flight or fight of the ANS]. Increased: heart rate, blood pressure and breathing rate. Also involves the somatic nervous system [skeletal muscles].
• Types of pain [sensory information]
• Fast- myelinated- sharp and fast pain. Example: needle injection.
• Slow- unmyelinated- "chronic", aching pain. Very poorly localized.
• Unique Example: pain from internal organs poorly localized, we get referred pain.

• Analgesia- the blockage of pain
• Endogenous- come from inside of the body
• CNS inhibits pain by hitting nocicepters with opiod neurotransmitters
• Example: endorphins [chemical] and enkephalins- use very effectively to block pain [sporting events and giving childbirth].
• Exogenous agents- use same molecules as endorphins and enkephalins.
• Stimulation induced analgesia- overriding the pain
• Stimulate other neurons to take away the pain.
• Example: Bengay, capsaicin, TENS- transcutaneous electrical nerve stimulation.

Central Nervous System

Autonomic Nervous System

End of Nervous System Notes

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