Introduction to Behavioral Neuroscience

Psych 2701:0AAA - Introduction to Behavioral Neuroscience

Motor System Overview

  • The central nervous system (CNS) governs rhythmic movements, even when not innervated.
  • Muscle types include:
    • Striated muscles: control movement of bones, respiration, speech, and facial expressions.
    • Autonomic nervous system (ANS): controls involuntary activities like peristalsis, blood flow, and blood pressure.

Muscle Anatomy and Contraction

  • Muscles operate through a mechanism of pulling, not pushing.
  • Key muscles involved in arm movements:
    • Triceps brachii
    • Biceps brachii
    • Brachialis
  • Movements:
    • Flexion: Bending action involving muscles like the biceps brachii.
    • Extension: Straightening action involving muscles like the triceps brachii.

Muscle Fiber Structure

  • Muscles consist of fibers, where each fiber equals one cell (e.g., biceps).
  • Axons from the CNS innervate the muscle fibers, facilitating contraction.

Muscle Innervation

  • Muscle innervation is primarily by lower motor neurons:
    • Alpha motor neurons (α-motor neurons): responsible for all muscle contractions. Related to conditions like Amyotrophic Lateral Sclerosis (ALS).
    • Gamma motor neurons (γ-motor neurons): play a role in proprioception, indicating body position and muscle status.

Motor Units and Pools

  • Each muscle fiber is innervated by only one alpha motor neuron; however, one alpha motor neuron can innervate multiple muscle fibers, forming a motor unit.
  • All alpha motor neurons innervating a specific muscle comprise the motor neuron pool.

Control of Muscle Force

  • Temporal summation: influences muscle force based on action potentials (AP).
    • One AP results in one muscle twitch with low-frequency AP leading to a slow and small contraction.
    • High-frequency AP results in fast, large, and smooth contractions.
  • Size principle: Larger motor units are recruited as greater force is needed.

Neuromuscular Junction (NMJ)

  • Muscle fibers have an excitable membrane called the sarcolemma.
  • The primary neurotransmitter at the NMJ is Acetylcholine (Ach), with vesicles containing large quantal content connecting to nicotinic Ach receptors.
  • Upon binding, Na+ and K+ channels open leading to depolarization, known as the end plate potential (EPP).
  • Myasthenia gravis affects this process by blocking Ach receptors.
  • The transmission of signals at NMJ is highly reliable; one AP in an axon results in one AP in the muscle fiber.
  • Termination of transmission occurs via acetylcholinesterase which degrades the neurotransmitter.

EPP to Muscle Contraction

  • EPP leads to the release of Ca²+ from the sarcoplasmic reticulum into myofibrils, resulting in muscle contraction.
  • Contraction process involves:
    • Tropomyosin: blocks actin and myosin interaction.
    • Troponin: senses Ca²+, causing a conformational shift that allows the myosin binding site to be revealed.
    • Myosin head then binds to actin, bends, causing sliding of filaments.
    • The presence of ATP is crucial for myosin head to unbind and prepare for the next contraction cycle.
    • Rigor mortis: occurs due to lack of ATP, keeping myosin bound to actin in the absence of calcium.

Effects of Strength Training

  • Strength training effects include:
    • Increase in muscle cells.
    • Growth of bigger motor units and more myofibrils.
  • Muscle fatigue may result from chronic exposure to leaky calcium channels in the sarcoplasmic reticulum, as proposed by Bellinger et al. (2008).

Neuromuscular Disorders

Amyotrophic Lateral Sclerosis (ALS)
  • Characterized by muscle weakness and atrophy affecting upper and lower motor neurons.
  • Resulting incapacitation leads to loss of voluntary movement within 1-5 years.
  • Other complications include deterioration of speech, swallowing, and respiration, leading to death.
  • Incidence rate: approximately 1 in 20,000.
  • Proposed causes include abnormalities in superoxide dismutase and excitotoxicity, with notable mention of the treatment drug riluzole.
Duchenne Muscular Dystrophy
  • A genetic disorder causing progressive weakening of muscles, affecting approximately 1 in 3500 male adolescents.
  • Linked to a defect in the X chromosome affecting dystrophin, which plays a role in the muscle cytoskeleton but is not essential for muscle contraction.
  • Typically leads to early death from lung disorders, usually by age 25.
Myasthenia Gravis
  • A neuromuscular disorder characterized by fluctuating weakness of voluntary muscles.
  • The condition arises due to an abnormal immune response resulting in antibodies blocking nicotinic receptors at the post-synaptic NMJ.
  • The condition shows improvement with rest and worsens with activity; incidence rate is 1 in 10,000.

Inputs to Alpha Motor Neurons

  • Inputs to alpha motor neurons include:
    • Type 1a axons from muscle spindles.
    • Information from the motor cortex.
    • Inputs from spinal interneurons, both excitatory and inhibitory.

Reflexes

The Myotatic Reflex
  • Utilizes group Ia sensory axons and functions to limit excessive stretching (elongation) of muscles.
  • It helps maintain muscle length and prevents strains and tears.
Reverse Myotatic Reflex
  • Mechanism to prevent injury by limiting excessive muscle tension.
Reciprocal Inhibition
  • Facilitates the coordination of agonist and antagonist muscles during movements.
Flexor Reflex
  • Reflex action that withdraws a limb from noxious stimuli, often associated with protective responses.
Crossed-Extensor Reflex
  • Maintains balance following flexor reflex by triggering contractions in extensor and flexor muscles on opposite sides of the body for stability.