Neurophysiology Notes

Neurophysiology

  • Study of electrical and chemical processes in neurons.

Information Flow

  • Within a Neuron: Electrical signals.
  • Between Neurons: Chemical signals.

Neuronal Function

  • Electrical and chemical signaling enables physical actions and cognitive processing.
  • Neurons use electrical signals to communicate.
  • All living cells are more negative inside than outside.
  • Neurons adapted electrical properties for information processing.

Resting Membrane Potential

  • Neuron at Rest: Charge of about -50 to -80 mV (typically −65-65 mV).
  • Ions: Electrically charged molecules (anions and cations).
  • Intracellular and extracellular fluid separated by lipid bilayer.
  • Selective Permeability: Membrane is selectively permeable to K⁺.
  • Diffusion: K⁺ moves out of the cell.
  • Electrostatic Pressure: Negative charge pulls K⁺ back in.
  • Sodium-Potassium Pump:
    • Removes 3 Na⁺ from the cell.
    • Brings in 2 K⁺ into the cell.
    • Consumes energy.
  • Nernst Equation: Predicts equilibrium potential for an ion.
  • Goldman Equation: Predicts overall membrane potential.

Action Potential

  • Brief, large change in neuron’s electrical charge.
  • Originates in axon’s initial segment.
  • Encoded through patterns of action potentials.
  • Hyperpolarization: Membrane becomes more negative.
  • Depolarization: Membrane becomes less negative.
  • Threshold: Depolarization reaches about -40 mV.
  • All-or-None Principle: Fires at full strength or not at all.
  • Afterpotentials: Electrical oscillations as neuron returns to rest.

Ionic Mechanisms of Action Potential

  • Hodgkin & Huxley: Studied giant axon of the squid.
  • Na⁺ Ions: Enter neuron through voltage-gated Na⁺ channels.
  • At peak, action potential reaches +40 mV.
  • Voltage-Gated Na⁺ Channels: Open when depolarization reaches threshold.
  • Refractory Periods:
    • Absolute: No stimulus can trigger another action potential.
    • Relative: Stronger stimulus needed.
  • Role of Axon: Action potentials generated in axons.

Action Potential Propagation

  • Series of regenerated electrical spikes.
  • +40 mV depolarization triggers depolarization in next segment.
  • One-Way Direction: Axon hillock to axon terminals.
  • Axon Diameter: Larger axons = faster conduction.
  • Myelin: Increases speed (saltatory conduction).
  • Nodes of Ranvier: Gaps in myelin.
  • Blocking Action Potentials: Drugs/toxins block Na⁺ channels.

Ion Channels and Selectivity

  • Selective ion channels allow only certain ions to pass.
  • Channelopathies: Diseases caused by ion channel malfunctions.
  • Toxins: Tetrodotoxin (TTX), Saxitoxin (STX), Batrachotoxin, Scorpion toxins, Spider venom.
  • Medical Applications: Anesthetics block Na⁺ channels.

Synapses and Postsynaptic Potentials

  • Action potential travels down axon to terminal.
  • Electrical signal converts to chemical signal (neurotransmitter release).
  • Neurotransmitters modify postsynaptic membrane potential.
  • Excitatory Postsynaptic Potentials (EPSPs): Depolarize neuron.
  • Inhibitory Postsynaptic Potentials (IPSPs): Hyperpolarize neuron.
  • Integration: EPSPs and IPSPs combine to determine if neuron fires.

Spatial and Temporal Summation

  • Neural Integration: Neurons combine synaptic inputs.
  • Spatial Summation: Inputs from different synapses combine.
  • Temporal Summation: Multiple EPSPs from same synapse in rapid succession.
  • Threshold: Neuron fires if combined inputs reach threshold at axon hillock.

Synaptic Transmission Sequence

  • Action Potential Arrival: At axon terminal.
  • Calcium Channel Activation: Ca²⁺ enters terminal.
  • Neurotransmitter Release: Vesicles fuse, releasing neurotransmitter.
  • Receptor Binding: Neurotransmitters bind to postsynaptic receptors.
  • Generation of EPSP/IPSP: Ion flow alters membrane potential.
  • Neurotransmitter Clearance: Degradation or reuptake.
  • Autoregulation: Autoreceptors regulate neurotransmitter release.

Neurotransmitter Release Mechanism

  • Calcium Influx: Opens voltage-gated Ca²⁺ channels.
  • Vesicle Fusion: Neurotransmitters released via exocytosis.
  • SNARE Proteins: Mediate exocytosis.
  • Synaptotagmin: Ca²⁺ sensor.
  • Toxins: Botulinum and tetanus toxins block neurotransmitter release.

Receptor Molecules

  • Neurotransmitters like keys fitting into receptor locks.
  • Ligand: Any molecule that binds to a receptor.
  • Receptor Type: Determines if ACh is excitatory or inhibitory.
  • Endogenous vs. Exogenous Ligands: Internal vs. external.
  • Neurotoxins: Curare and bungarotoxin block ACh receptors.
  • Agonists: Mimic neurotransmitters (muscarine, nicotine).
  • Antagonists: Block neurotransmitters (curare, bungarotoxin).
  • ACh Receptors: Nicotinic and muscarinic.
  • Loewi’s Experiment: Discovery of chemical transmission.

Ion Channels Controlled by Receptors

  • Ionotropic Receptors: Directly open ion channels.
  • Metabotropic Receptors: Activate G proteins, leading to indirect effects.
  • G Proteins: Activate ion channels or second messengers.
  • Second Messengers: Amplify neurotransmitter effects (cAMP).
  • GPCRs: 80% of neurotransmitters use G protein-coupled receptors.

Termination of Synaptic Transmission

  • Brief Action: Neurotransmitter effects must be short-lived.
  • Degradation: Enzymes break down neurotransmitters (acetylcholinesterase).
  • Reuptake: Transporter proteins reabsorb neurotransmitters.
  • Autoreceptors: Regulate neurotransmitter levels.

Nonclassic Synapses

  • Axo-axonic: Control neurotransmitter release from another axon.
  • Retrograde: Postsynaptic cell signals presynaptic neuron.
  • Dendro-dendritic: Direct communication between dendrites.
  • Ectopic Transmission: Neurotransmitter release outside synapses.
  • Varicosities: Release neurotransmitters broadly.

Neural Circuits

  • Analogous to electrical circuits.
  • Neural Chains: Simple connections of neurons.
  • Stretch Reflex: Sensory to motor neuron via synapse.

Brain Activity Detection

  • Electrical Potentials: Detectable outside the skull.
  • Spontaneous Potentials: Appear without stimulation.
  • Evoked Potentials: Triggered by stimuli.
  • EEG: Records spontaneous brain potentials (brain waves).

Seizure Disorders

  • Epilepsy: Synchronized brain activity.
  • EEG Patterns: Abnormal "spike-and-wave".
  • Generalized Seizures: Affect entire brain.
    • Tonic-clonic (grand mal): Tonic and clonic phases.
    • Simple Partial (Absence): Brief loss of awareness.
  • Complex Partial Seizures: Affect part of the brain.
  • Treatments: Antiepileptic drugs, surgery.