Mar 26
Overview of Synaptic Changes
Facilitation and Depression
The figure presents three sections demonstrating different calcium conditions affecting excitatory postsynaptic potentials (EPSPs).
Sections of the Figure:
Low Calcium Solution (Section A)
Initial EPSP is noted.
Subsequent EPSPs show greater amplitude.
A test pulse is higher than the initial EPSP, indicating facilitation.
High Calcium Solution (Section B)
Initial EPSPs have high amplitudes.
Subsequent EPSPs demonstrate depression (smaller amplitudes).
No test pulse is present because vesicles are depleted.
Normal Physiological Calcium (Section C)
Initial EPSP is recorded followed by subsequent EPSPs which also show increased amplitudes, but taper off.
Test pulse is lower than the initial EPSP, indicating depression.
Key Insights:
Facilitation occurs in low calcium conditions, while depression is more pronounced in high calcium conditions. Normal conditions exhibit both effects.
Facilitation
Definition:
A short-term increase in synaptic strength during repeated stimulation.
Mechanism:
Residual calcium accumulates in the presynaptic terminal, boosting the release probability of neurotransmitters during subsequent EPSPs as calcium levels rise but fade back to baseline over time.
Supporting Evidence:
Calcium chelators reduce facilitation.
Calcium currents increase during stimulus trains.
Depression
Definition:
A temporary decrease in synaptic strength that occurs with continued stimulation.
Causes:
Large initial neurotransmitter release that depletes vesicles in presynaptic cells.
Reduced presynaptic calcium current contributing to lower release probability.
Recovery Mechanism:
Vesicles are replenished alongside calcium returning to baseline levels.
Augmentation
Definition:
An intermediate increase in synaptic strength over seconds, distinct from facilitation.
Mechanism:
Result of increased release probability due to additional presynaptic action potentials.
Key Difference from Facilitation:
Unlike facilitation, there's no change in the total number of available vesicles.
Post-tetanic Potentiation (PTP)
Definition:
Long-lasting increase in neurotransmitter release after high-frequency tetanic stimulation.
Mechanism:
Resulting from increased presynaptic calcium levels and enhanced vesicle release probability.
Total number of release-ready vesicles increases as well.
Magnitude Factors:
Relies on stimulation frequency and train duration.
Decay Phases:
Fast Phase: Release probability returns to baseline quickly, similar to augmentation.
Slow Phase: Vesicle pool numbers recover more gradually.
Long-Term Plasticity
Definition:
Persistent synaptic changes resulting from repeated synaptic activity; affects synaptic strength for hours to days.
Importance:
Key for memory and learning processes.
Long-Term Potentiation (LTP)
Definition:
An increase in synaptic strength caused by a large influx of postsynaptic calcium.
Consequences:
Activation of AMPA receptors at postsynaptic sites increases sensitivity.
Long-Term Depression (LTD)
Definition:
A decrease in synaptic strength due to smaller postsynaptic calcium signals.
Characterization:
Involves removal of AMPA receptors from postsynaptic sites.
Temporal Differences in Forms of Plasticity
Visualize Plasticity Over Time:
Facilitation occurs within milliseconds.
Augmentation and depression occur over seconds.
PTP persists for minutes.
LTP extends for hours to days.
Memory Formation and Synaptic Plasticity
Importance of Hippocampus:
Essential in memory and learning, linked to findings from Brenda Milner's work on patient H.M.
Concept of "cells that fire together wire together" emphasized as significant in memory studies.
Brenda Milner’s Contributions
Noteworthy Case Study:
Patient H.M. had significant memory loss following a surgical procedure.
Memory studies revealed distinctions between short-term and long-term memory.
Discoveries:
H.M. could retain immediate information through repetition but couldn't create new long-term memories.
Distinction between declarative memory (facts and information) and procedural memory (skills) emerged through her studies, showcasing different brain mechanisms involved.
Trisynaptic Loop in Hippocampus
Key Components:
The pathway involves entorhinal cortex, dentate gyrus, CA3 pyramidal cells, and CA1 pyramidal cells.
Importance for memory consolidation emphasized.
Mechanisms of LTP and LTD
LTP Mechanisms:
Calcium influx activates signaling cascades leading to AMPA receptor insertion.
Associative LTP:
Coincidence of signals from two inputs necessary for LTP, underpinning associative learning principles.
LTD Mechanisms:
Various pathways including NMDA dependent, metabotropic glutamate receptor dependent, and endocannabinoid signaling.
Maladaptive Plasticity Examples
Addiction:
Linked with increased synaptic strength through LTP mechanisms.
Phantom Limb Pain:
Occurs due to mismatched sensory inputs and neural rewiring following limb loss.
Epilepsy:
Characterized by hypersensitivity in neuronal circuits, most commonly treated with cortical surgery.
Tinnitus:
Results from compensatory reorganization in the auditory cortex after hearing loss.
Dystonia:
Overlapping motor maps leading to motor control issues due to repeated muscle use.
Conclusion
Importance of Understanding Maladaptive Plasticity:
Recognition of how synaptic changes contribute to various neurological disorders.
Engaging in volunteer opportunities and community involvement recommended for student development.
Quiz Preparation:
Key terms and concepts reviewed, such as activation of signaling pathways and receptor types.
Miscellaneous Notes
The visual representations of EPSC (excitatory postsynaptic currents) and their correlations with synaptic changes are used to further emphasize the mechanisms discussed.
Additional context provided includes volunteer opportunities emphasizing community engagement and benefits for future academic and career pathways.