Synaptic Plasticity I
Synaptic facilitation occurs because of this at the synaptic cleft
Prolonged calcium elevation
This postulate states that correlated activity between two neurons will potentiate their connection
Hebb's Rule: "Cells that fire together, wire together."
This serves as self regulation and prevents over-excitation of neurons
Feedback inhibition
These two proteins (one forms plaques and the other forms tangles) are the classic hallmarks of Alzheimer’s disease
Amyloid-B plaques and tau tangles
I speak without a mouth and hear without ears. I have no body, but I come alive with sound. What am I?
An echo
Augmentation and Post-Tetanic Potentiation improve calcium’s ability to do this
Trigger fusion of synaptic vesicles
Late phase LTP is induced by changes in these 2 things
Gene expression and protein synthesis
Activation of phosphatases by small, slow Ca2+ influx causes this
Long term depression (LTD)
This allele of the APOE gene is the strongest known genetic risk factor for late-onset Alzheimer’s disease
What is APOE-e4
The more of me there is, the less you see. I’m not fog, I’m not sleep. What am I?
Darkness
Lowering calcium levels slows the rate of PPD by reducing this
Probability of release
Blocking NMDA receptors blocks LTP, but not this
Low frequency stimulations
This mechanism regulates between strengthening synapses or weakening them based on order of firing
Spike Timing Dependent Plasticity (STDP)
This Alzheimer’s medication works by binding inside NMDA receptor channels to limit Ca2+ influx and reduce excitotoxicity
What is memantine (namenda)
I can fly, but I have no wings. I can cry, but I have no eyes. Wherever I go, darkness flies. What am I?
A cloud
This is decreased in short term habituation to decrease glutamate release
Number of voltage gated calcium channels responding to AP
These synapses show NMDA currents only at depolarized potentials and produce no AMPA-mediated response at resting membrane potential until LTP inserts new AMPA receptors and ‘awakens’ them
Silent synapses
The hypothesis supported by severed axons unable to maintain LTP into the late phase
Synaptic tagging hypothesis
One major argument against the amyloid hypothesis is that this protein’s deposition does not reliably correlate with cognitive decline, even though tau pathology does.
Amyloid-B
I’m taken from a mine, locked in a wooden case, never released, yet almost everyone uses my work. What am I?
Pencil lead
Activation of this heterosynaptic neuron increased the motor EPSP in sensitization
Serotonergic modulatory interneuron
These 2 enzymes are activated by Ca2+ in early LTP
Protein kinase C and Calmodulin Kinase 2
A persistently active PKC isoform maintaining LTP
PKMζ (zeta)
According to the tau prion hypothesis, tau pathology spreads because tau monomers adopt these distinct, self-propagating conformations that drive different tauopathies
Tau shapes
I’m always running but never walk, often murmuring but never talk. I have a bed but never sleep. What am I?
A river