I.

Levels of Organization & Classification

Behavior and Cognition: interactions between the brain, body,
and external world
CNS: gross anatomy; the organization of the neural pathways,
comparative neuroscience, coordination of activity across entire
CNS
Systems: multiple connected regions work together to support a
single common function
Maps: individual brain regions with consistent responses to Intracellular transport: along microtubule
stimuli in the external environment; specific types of information • Retrograde: towards soma; dynein & dynactin
processing • Anterograde: towards axon; kinesin
Circuits/Networks: coordination of activity in small groups of
connected neurons; demonstrates intricate connectivity within
brain
Neurons: morphology of single neuron affects how it processes
electrochemical signals
Synapses: site of electrochemical interactions between neurons
Molecules: mediate neuronal changes and development and
signal transmission

Connectivity: brain region

• Principal/projection neuron: axons extend to one or more
distant brain regions
• Interneuron: axons and dendrites remain in single local brain
region
Structure: unipolar, bipolar, multipolar
Physiological responses: frequency & threshold of firing
Genetic & Neurotransmitter: ion channels, receptors, etc.

II. Soma III. Glia

Nissl stain: rough endoplasmic reticulum Gap junctions: direct connection of cytosol between two cells via
Golgi stain: entire neuron ion channels
Microtubule Associated Protein (MAP) tau: stains soma,
dendrites, and axon red; MAP2 stains soma and dendrites 1. Ependymal cells: produces cerebral-spinal fluid (CSF)
only green • Choroid plexus: lining made of ependymal cells found in
ventricles and canal of spinal cord
Reticular theory: nervous system is continuous • Tight junctions form blood-CSF barrier
Neuron doctrine: neurites end freely in nervous system; • CSF cushions skull & circulates nutrients & waste
communication through contact (contiguous) exchanged with cells and blood
Law of dynamic polarization: propagation of nerve impulses is 2. Microglia: processes extend from soma; secretes immune
unidirectional, towards dendrites and soma and away from axon response molecules and engulf damaged tissues in response to
injury (ATP-sufficient); removal of neurites (pruning for
Protein synthesis: 2º alpha helix & beta sheet, 3º polypeptide adaptation to changing environment) or entire neurons
subunit folds due to residue group interactions; exon, intron, 3. Myelin sheath: spiral wrapping that insulates axon
promoter: DNA à mRNA • Oligodendrocytes: can wrap axons from multiple neurons in
Ribosomes: proteins synthesized by free ribosomes remain in CNS
cells; for insertion in cell membrane or out of cell if synthesized • Schwann cells: wrap only one axon in PNS
by ribosomes on rough ER 4. Astrocytes: communicate via gap junctions
Smooth endoplasmic reticulum: protein folding, regulation of • Blood-brain barrier: formed by endothelial cells of
Ca2+ capillaries, pericytes, and astrocytes that limits permeability
Golgi apparatus: modifies post-translational proteins to of substances from bloodstream to brain
determine their final destinations o Astrocytes’ end-feet wrap around capillaries
Cytoskeleton: microtubule (tubulin), neurofilament, • Tripartite synapse: astrocytes surround pre-/postsynaptic
microfilament (actin) neuron
o Segregate neighboring neuron spatially via isolation of
chemical release
Axon collaterals: branches along axon o Increase in Ca2+ in microdomains (which can eventually
Axon terminal: abundance of ATP, no microtubules spread further) in response to NT release due to NT
Dendritic spines: highly specialized protrusions influence receptors
dendritic strength o Neurotransmitter reuptake & gliotransmitter release that
affects transmission
 o Release factors that can influence the development (e.g. • Ligand-gated/ionotropic receptor: neurotransmitter binding
silent synapses) or modification of synapses (including to protein
removal by microglia, increasing NT receptors); can • Voltage-gated: membrane potential threshold; may require
influence transmission without initiating structural NT
changes (e.g. higher NT release)
• Phagocytosis: direct (silent synapses) and indirect (signals Investigating selective permeability:
microglia) • Chemical: toxins selectively block specific ion channels
• Genetic: mutations affect protein structure
• Electrophysiological: changes in voltage across cell
membrane
• X-ray crystallography: maps out amino acids necessary

Na+/K+ pump: uses ATP to create concentration gradient; 3 Na+

out and 2 K+ in
Ca2+ pump: Ca2+ binds to Plasma Membrane Ca2+ ATP-ase,
which uses ATP to throw Ca2+ out of cell
Na+/Ca2+ exchanger: uses energy produced by 3 Na+ flowing
down [Na+] gradient into cell to pump 1 Ca2+ out of cell

IV. Membrane Potential

Ohm’s Law: I = gV = V/R
Capacitor: stores electrical energy
• Membrane acts like a capacitor: intracellular cations are
attracted to extracellular anions due to potential difference,
but there is no open channel (net difference occur at
surfaces)
Depolarization: decrease in potential difference across
membrane; Vm becomes less negative
Hyperkalemia: too high [K+]o which cause muscle weakness and
irregular heartbeat; high [K+]o leads to depolarization, lowering
ion driving force of Na+
K+ spatial buffering: high [K+]o flows through K+ channels on
astrocytes, which release to other microdomains with less [K+]o
• Blood-brain barrier limits [K+] flow into serum

Equilibrium potential: electric potential difference that exactly

counterbalances ion concentration gradient when membrane is
permeable to only one single ion
Ion driving force: difference between actual membrane potential
and Eion drives Vm towards Eion once the membrane is
permeable to the ion; magnitude of force proportional to
magnitude of the difference
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Nernst Equation: 𝐸!"# = ln  ( )
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Goldman-Hodgkin-Katz: 𝑉!  !"#$ = ln  ( )
! !!"! !"! ! !!!! ! ! !
• PK = 40PNa at resting potential

Transmembrane ion channel: different properties of R-groups

and size of pore formed by polypeptide subunits determine ion
channels’ permeability to selective ions; hydrophobic parts keep
channel suspended in membrane; 4-6 subunits
• If mutation happens: R-groups affect 3º structure due to
hydrophobic/hydrophilic interactions with other amino acids
on the same polypeptide chain à structure of polypeptide
subunits is changed à shape of pore no longer fits ion à
channel is no longer permeable to that ion
Ion channel gating: selective opening and closing