Old Stuff

Front 1

How a neuron maintains resting potential

Back 1

•Action of theNa+-K+ pump (3 Na+ out, 2 K+ in) •Movement of K+across the membrane (via non-voltage gated channels)

Front 2

The steps of how an action potential is fired

Back 2

• From a neuron atresting potential (approx. –70 mV), postsynaptic potentials depolarize theneuron’s membrane voltage to threshold (near –55 mV). At threshold,voltage-gated sodium channels open and sodium enters neuron.

• As sodium rushesin, neuron rapidly depolarizes and membrane potential actually become positive(up to approx. +40 mV); as neuron depolarizes, voltage-gated K+ channels beginto open and K+ begins to leave the cell

• Near +40 mV,voltage-gated Na+ channels close and become refractory (absolute refractoryperiod begins)

• K+ continues toleave the neuron and neuron membrane becomes more negative (repolarizes),slight undershoot or hyperpolarization of resting potential

• Voltage-gated K+channels close, flow of K+ out of neuron decreases

• Voltage-gatedNa+ channels reset (neuron becomes relatively refractory); extracellular K+diffuses away from cell; neuron returns to resting potential (approx. –70 mV)

Front 3

The steps of how a chemical synapse works

Back 3

• Action potentialpropagates to the end of the axon, and depolarizes the terminal region

• Depolarizationopens voltage-gated Ca2+ channels; Ca2+ flows into the terminal

• Ca2+ activatesenzymes in the terminal that cause synaptic vesicles to dock at release zoneand fuse with membrane; NTs released into cleft
• NTs diffuseacross cleft, and bind with postsynaptic receptors at the active zone; Bindingof NTs to receptors causes local, graded changes in the voltage of thepostsynaptic cell (‘postsynaptic potentials’, or PSPs)

• NT signal isended via enzymatic degradation and reuptake by transporters

• NTs activateautoreceptors on the presynaptic terminal; autoreceptors inhibit the activityof terminal region
  

Front 4

Distinguishing ionotropic receptors andmetabotropic receptors

Back 4

• Ionotropic:fast-acting, and fast inactivating; activation opens an ion channel to cause arapid inhibition or excitation of neuron

• Metabotropic:slower-acting and slow inactivating; activation leads to stimulation of aG-protein, which activates a ‘second messenger’ inside the cell; causing either ion channels to open and/or other changes insidethe cell, including gene transcription.

Front 5

Proper experimental controls in neuroscienceresearch

Back 5

• Importance of experimental controls
• For surgery: ‘sham’ surgery
• For drug injections: vehicleinjections (e.g., saline)
• For other manipulations: makesure your subjects experience all of the steps of treatment except for the step that you think will cause an effect
• This isn’t as easy as itsounds…
• Without proper controls, youcannot conclude anything definitively from your experiment