Study Notes on Synaptic Plasticity, Neurogenesis, and Extra Credit Opportunities

  • 10 extra credit points available on the final exam.
      - Relevant to Chapters 2 and 3, which cover foundational concepts such as action potentials and cell types.
      - Recommends students review these chapters thoroughly.

Synaptic Plasticity

  • Synaptic plasticity refers to the ability of synaptic connections to change in strength.
      - This modification can occur in various forms, including:
        - Increasing neurotransmitter release.
        - Adjusting the number of receptors.
        - Altering the size of pre- and postsynaptic elements.

Hebbian Theory

  • Introduced by Donald Hebb (1940s-1950s) who proposed the mechanism of learning through synaptic strengthening:
      - Active synapses strengthen connections.
      - Inactive synapses weaken or may disappear.
      - Stated as "cells that fire together, wire together."

  • Explanation of strong vs weak synapses is based on their ability to regulate the activity of postsynaptic neurons.

  • Neurons that frequently communicate strengthen their connections, while infrequently communicating neurons may atrophy.

Experimental Evidence of Synaptic Plasticity

Long-Term Potentiation (LTP)

  • Discovered in the 1970s by observing changes in synaptic strength after high-frequency stimulation.

  • The typical experiment involves:
      - Two neurons: one presynaptic and one postsynaptic.
      - Use of electrodes to stimulate the presynaptic neuron and measure the excitatory postsynaptic potential (EPSP) in the postsynaptic neuron.

  • Procedure:
      1. Low-frequency stimulation leads to a slight depolarization of the postsynaptic neuron, often insufficient to trigger an action potential.
      2. A high-frequency stimulation (tetanus) induces a significant increase in the release of neurotransmitters and resultant EPSP.

  • After tetanus, applying low-frequency stimulation results in a potentiated response, indicating increased synaptic strength due to LTP.

Mechanisms of LTP Induction

  • Key Components:
      - AMPA Receptors: Primary mediators of excitatory neurotransmission.
      - NMDA Receptors: Require both ligand binding (glutamate) and depolarization (removes magnesium block) to activate.

  • Calcium Influx: Essential for activating intracellular signaling pathways (e.g., CAMKII) which lead to synaptic changes.
      - CAMKII is responsible for inserting more AMPA receptors into the membrane, enhancing synaptic response.

  • Efficiency of Learning: Strengthens synapses that are repeatedly activated.

Neuroplasticity Beyond LTP

Cortical Reorganization

  • Occurs after brain damage (e.g., stroke) and may involve reallocation of functions to healthy brain regions.

  • Example: Stroke affecting left brain leads to reduced control of the right hand. Recovery can result in neuroplastic changes allowing partial regain of function.

  • Active therapy and engagement are crucial for stimulating cortical remapping.

Neurogenesis

  • Refers to the creation of new neurons, which occurs mainly in the hippocampus and olfactory bulb; essential for learning and memory.

  • Adult neural stem cells are limited to producing:
      - Neurons
      - Oligodendrocytes
      - Astrocytes

  • Process includes:
      - Asymmetrical division of stem cells to produce progenitor cells.
      - Progenitor cells differentiate into specialized cells based on environmental signals.
      - Brain incorporates new cells into existing circuits, emphasizing the integration process.

  • Engagement in learning and physical activities can enhance neurogenesis.