Neuroplasticity Lecture Vocabulary

Definition & Core Idea of Neuroplasticity

• Broadly: the brain’s ability to change its own structure and function.
• Key slogan: “neurons that fire together, wire together.”
  • Repeated/co-ordinated activation → strengthened connections.
• Does NOT require brain injury; happens in everyday learning, therapy, skill practice, etc.
• Plasticity can be beneficial (recovery, mastery) or maladaptive (rumination, PTSD, addiction).

Everyday Examples

• Learning a motor skill (piano, skateboarding, golf).
• Cognitive therapy leading to new thought patterns.
• Adapting to body changes: puberty, weight change, pregnancy, prosthetics (e.g., monkey robotic-arm experiment).
• Remembering where you parked, what you ate for breakfast, the last video you watched—all invoke moment-to-moment synaptic change.

Cellular Anatomy Refresher

• Neuron parts
  • Soma (cell body)
  • Axon: long “wire” transmitting action potentials (APs).
  • Dendrites: branching "input wires"; tens of thousands of synapses per neuron.
  • Terminal buttons: release neurotransmitter into synaptic gap.
• Synapse = space between pre- and post-synaptic neurons where chemical signaling occurs.

Developmental Timeline

• Neurogenesis (birth of new neurons) peaks last trimester before birth.
• Synaptogenesis (new synapses) peaks 0\text{–}2 years; dendritic density highest at ≈2 yrs.

Two Scales of Plasticity

• FORM changes: dendritic growth/retraction, new synapses (synaptogenesis).
• FUNCTION changes: altered sensitivity at existing synapses (receptor-level tweaks).

Synaptic Mechanism: AMPA & NMDA Receptors

AMPA Receptors ("boring but crucial")

• Linear, one-to-one response.
  • Weak neurotransmitter input → weak post-synaptic response.
  • Strong input → strong response.
• Work regardless of firing history; immediate effect.

NMDA (NR) Receptors ("the gatekeepers")

• Largely silent at low neurotransmitter levels.
• Activate only under strong, high-frequency presynaptic firing.
• Once activated, trigger intracellular machinery that creates more AMPA receptors on the post-synaptic membrane.
  • Result: post-synaptic neuron becomes more sensitive to the same future input.

Consequence

• After NMDA-triggered AMPA insertion, the same weak input now produces a stronger output—the physical basis of memory/training.

Long-Term Potentiation (LTP)

• Main form of plasticity in mammals.
• Definition: long-lasting increase in synaptic efficacy following specific patterns of activity.
• Two paths:
  1. Sensitivity Increase – NMDA → more AMPA → amplified chemical response.
  2. Structural Change – repetitive firing patterns → dendritic growth → new synapses (synaptogenesis).
• Time-scale: minutes → days → months → years, depending on reinforcement.

Hebb’s Rule (1949)

• When cell A repeatedly excites cell B, “A’s efficiency at firing B is increased.”
• Anticipated modern receptor-based explanation (NMDA→AMPA).

Specificity Principle

• Only the synapses activated by high-frequency stimulation undergo potentiation; nearby inactive synapses remain unchanged.

Illustration Sequence

1. Before learning: few AMPA receptors, weak input ⇒ weak output.
2. During intense practice: rapid firing floods synapse, activates NMDA.
3. After learning: extra AMPA receptors; even weak input ⇒ strong output (memory trace).

Rate & Pattern vs. "Strength" of APs

• An action potential is all-or-none—no “strong” or “weak” AP.
• Variability arises via:
  • Firing rate (slow vs. rapid bursts).
  • Temporal patterns (distinct sequences encode faces, locations, etc.).

Positive & Negative Plasticity

• Rehearsing trauma or rumination wires negative networks.
• Skill practice or therapeutic reframing wires adaptive networks.

Enhancing or Impairing Plasticity

Natural/Behavioral Enhancers

• Novel learning, enriched environments, physical exercise, attention & motivation.
• Sleep: consolidates LTP-driven changes.

Pharmacological/Technological Enhancers

• Experimental ideas: nicotine micro-dosing, patterned electrical “caps,” trans-cranial stimulation to “tickle” active circuits.
• Potential future use: boost learning, overwrite maladaptive PTSD circuits.

Drugs of Abuse

• Dopaminergic substances (methamphetamine, cocaine, nicotine, opioids) hijack plasticity:
  • Meth floods synapse with ≈1000\times normal dopamine ⇒ massive firing ⇒ homeostatic down-regulation (receptor loss, dendritic pruning).
  • Post-drug: dopamine deficit ⇒ cravings; need larger doses to feel normal.
• Non-dopaminergic hallucinogens (psilocybin, LSD) less physically addictive; studied for therapeutic rewiring when paired with psychotherapy (e.g., MDMA-assisted PTSD treatment).

Types of Plasticity

1. Experience-Dependent (Activity-Dependent / Ecological)

• Unique to individual’s interactions, culture, social milieu.
• Examples: mastering a language, specific memories, trauma associations.

2. Experience-Expectant

• Pre-wired systems awaiting typical environmental input (vision, auditory maps, basic sensory wiring in infants).
• Critical periods: if expected input missing, system reorganizes (e.g., congenital cataract → visual cortex repurposing).

Ethical, Clinical & Real-World Implications

• Therapy leverages plasticity to reshape maladaptive networks.
• Education techniques can target optimal LTP windows.
• Concerns: digital era may re-shape attention networks; reliance on GPS may weaken spatial-navigation circuits.
• Addiction treatment aims to reverse maladaptive dopaminergic rewiring.
• Future neuro-tech (brain caps, targeted stimulation) could accelerate learning—or raise equity/ethics debates.

Numerical / Statistical Nuggets & Key Facts

• Average neuron forms ≈10^{4} ((\approx 12{,}000)) synapses.
• Methamphetamine delivers ≈1000× natural dopamine release.
• Neurogenesis peak: last prenatal trimester.
• Synaptogenesis peak: 0\text{–}2 years, dendritic density max at \approx 2 yrs.
• LTP can last minutes → years depending on reinforcement.

Quick-Recall Bullet List

• AMPA = fast, linear; NMDA = coincidence detector, creates AMPA.
• Action potentials: all-or-none; variation via rate/pattern.
• LTP = cellular basis of memory & skill acquisition.
• "Neurons that fire together wire together"—both blessing (learning) & curse (addiction/PTSD).
• Experience-dependent vs. experience-expectant plasticity: individualized vs. species-typical wiring.
• Dopamine-based drugs exploit plasticity, causing receptor down-regulation, craving cycles.
• Therapies (CBT, exposure, psychedelic-assisted) aim to harness or redirect plasticity.