Neuro

Overview of Information Transmission in Nerves

  • Focus on the transmission of information from one nerve to the next.
  • Understanding inputs into the nerve, action potentials, and synaptic transmission.

Neuronal Communication

  • Neurons communicate through the transmission of action potentials.
  • Key components: afferent (incoming signals) and efferent (outgoing signals) pathways.

Pain Pathway Example

  • Utilizes a golden retriever as a model to explore pain pathways.
  • Purpose: Understand how pain travels from the point of injury to the cerebral cortex for conscious awareness.
  • Relevant for subsequent discussions on analgesia in anesthesia.

Pathway of Pain Transmission

  1. Receptors: Sensory information must be gathered via peripheral receptors. Different receptors exist for special senses (e.g., rods and cones).
    • Focus on nociceptors as specific pain pathway receptors.
  2. Threshold and Action Potential:
    • A certain level of stimulation must be reached (threshold) to trigger an action potential.
    • Sodium, potassium, and calcium channels play roles in transmitting the action potential along the axon of afferent neurons.
  3. Spinal Cord Integration:
    • Information enters through the dorsal root into the spinal cord at the dorsal horn.
    • Synapses occur in the spinal cord, transmitting signals via both fast and slow white and gray matter pathways to the brainstem and ultimately to the cerebral cortex.
  4. Thalamus: Acts as a relay center to direct pain signals to the appropriate brain region.

Types of Pain Stimuli

  • Pain can be triggered by various stimuli including:
    • Mechanical Stimuli: E.g., surgery that cuts through tissues.
    • Chemical Signals: E.g., released through the arachidonic acid cascade, such as leukotrienes and bradykinins that stimulate nociceptors.
    • Stretch Receptors: E.g., in the gastrointestinal tract where excessive stretch triggers pain.
    • Temperature Receptors: Hot or cold stimuli exceeding threshold can provoke a pain response.
    • Nociceptors Activation: Chronically stimulated nociceptors become sensitized and may respond to non-painful stimuli, a phenomenon often observed in chronic pain conditions

Properties of Action Potentials

  • Initiating an action potential starts at the axon hillock where threshold influences the opening of sodium channels.
  • An influx of sodium (Na+) causes depolarization, raising the internal charge from about -70 mV to a more positive state.
  • The resulting action potential consists of:
    • Depolarization Phase: Sodium rushes in (opens sodium channels).
    • Repolarization Phase: Potassium channels open, allowing K+ to leave the cell, reverting charge back to resting state.
    • Hyperpolarization: An overshoot can occur leading to even more negative potentials than resting state.
    • Reestablishment of concentrations via sodium-potassium ATPase pump.

Refractory Periods

  • Absolute Refractory Period: After a neuron fires, it cannot be stimulated to fire again until it resets.
  • Relative Refractory Period: A neuron can fire again with a stronger-than-normal stimulus, but this effect is diminished.
  • Importance: Refractory periods ensure action potentials travel in one direction along the neuron.

Conduction Mechanisms

  • Continuous vs Saltatory Conduction:
    • Continuous conduction occurs along unmyelinated fibers where every sodium channel opens in sequence.
    • Saltatory conduction occurs along myelinated axons where action potentials jump between Nodes of Ranvier for faster transmission.
  • Myelination leads to significant advantages in speed and efficiency of signal transmission.
  • Condition Examples: Multiple sclerosis affects the conduction due to damage to oligodendrocytes (myelinating cells in the CNS).

Synaptic Transmission

  1. Chemical Transmission at Synapse:
    • Presynaptic Neuron: Contains neurotransmitter-filled vesicles that release chemicals upon activation.
    • Postsynaptic Neuron: Receives the neurotransmitter through its receptors on dendrites.
  2. Neurotransmitter Effects:
    • Ex excitatory Neurons: Trigger opening of sodium channels leading to depolarization.
    • Inhibitory Neurotransmitters: Trigger potassium channels leading to hyperpolarization, making it harder to reach threshold for firing an action potential.
  3. Common Neurotransmitters:
    • Acetylcholine: Functions in both central and peripheral nervous systems with excitatory and inhibitory effects.
    • Norepinephrine, Epinephrine, Dopamine: Catecholamines that influence sympathetic nervous system function, with various effects based on receptor types.

Central Nervous System and Peripheral Nervous System Interaction

  • Different neurotransmitter effects at different sites related to their receptors.
  • Adrenergic Neurons: Release norepinephrine at target organs, affecting both heart and lungs through alpha and beta receptors. An example would be beta blockers, which can lower heart rate by inhibiting sympathetic stimulation.
  • Cholinergic Neurons: Release acetylcholine affecting glands and smooth muscles in the parasympathetic system.

Enzymatic Breakdown of Neurotransmitters

  • Acetylcholinesterase: Breaks down acetylcholine in the synaptic cleft.
  • Catecholamine Breakdown:
    • Monoamine Oxidase (MAO): Enzyme responsible for breaking down norepinephrine.
    • Catechol-O-Methyltransferase (COMT): Enzyme assisting in repackaging norepinephrine within the presynaptic neuron.
  • Implications of inhibiting these enzymes can lead to prolonged neurotransmitter effects, which has therapeutic and toxicological significance.

Conclusion

  • Summary of the processes involved in neuronal signaling and the importance of neurotransmitter interactions in both normal and pathological conditions.
  • Understanding these concepts is crucial for future lessons on analgesia and patient management in anesthesia contexts.