Introduction Kandel 2 & Purves 1

• Functions of glial cells
• Parts of neurons and function
• Types of neurons (location in the nervous system)
• Electrical transmission of information (i.e. stretch reflex)

• What are genes?
• Heredity & kinds of mutations
• Per and TIM genes (activity during night and day cycle)
• Genes and relationship to diseases (tables list several)

• How are neurons like epithelial cells? (biologically)
• Cytoskeleton
• Myelin (role of)
• Spines (functional role in signal transduction)

• Translation and transcription (biological steps and organelles involved)
• Protein sorting and packaging
• Protein transport and motors used for transport

• Ion selectivity (ion properties and channel properties)
• Channel kinetics
• Patch clamp technique and application
• Channel gating mechanisms (i.e. ligand, voltage, ect.)

• Ionic gradients influence membrane potential(Vm)
• How is the membrane potential maintained?
• Nernst & Goldman equations(what are they? How are they similar or different?)
• Equivalent circuit and the biological representation with symbols (model)

• Role of input resistance and capacitance in determining Vm properties
• length and time constant ( How does the size of axon effect these?)
• Increase in length constant increases possibility for integration
• Increase in time constant increases probability for summation
• Passive conduction of the action potential (ions and voltage gated channels)
• Flow of current
• Myelin and its effect on properties listed above

• Timing of ionic conductance responsible for the AP (voltage dependence)
• Structure of channels (not too specific)
• Current flow
• Channel kinetics
• Activation and inactivation
• Ball and chain
• Variations on a theme
• Diversity of firing properties
• Delayed firing
• Bursting
• Accommodation
• Mechanisms of voltage gating
• Modulation of firing rate

• Types of synapses- Electrical and Chemical
• Structure of gap junctions
• Structure of Chemical synapse
• Gating mechanisms of transmitter receptors – Direct and indirect (2^nd messenger)
• Metabotropic vs. ionotropic

• End-plate potential- functional properties
• EPP-Na⁺ and K⁺ ions generate the EPP after ACh activation
• EPP synaptic current occurs more rapidly than the EPP - WHY?
• ACh receptor _ Hill of 2 : Five subunits w\ four membrane spanning alpha helixes
• Be prepared for questions that might relate previous to present ie. representative equivalent circuit

• Cause and consequence of inhibitory or excitatory modulation
• Synaptic potentials result in APs if a threshold is reached
• Types of glutamate channels
• NMDA-voltage dependence, multi faceted
• AMPA-Main source of initial membrane depolarization due to glutamate
• Early and late component: application of APV and V dependence
• IPSP\EPSP
• Reversal potential of GABA mediated channels suggest Cl^- or K⁺ current
• Channel structure same for GABA and Glycine(same as ACh)
• Glutamate channels-4 subunits w\ 3 transmembrane domains(M2 domain is a loop)
• Signal integration- spatial and temporal factors
• How do you use the time and length constant to determine temporal summation?
• Synaptic location and properties
• Shunting inhibition

• Know steps of synaptic release
• Amount of transmitter release is dependent on Ca²⁺
• AP-------Ca2+ entry---------EPSP via transmitter release
• Multiple Ca²⁺ channel types
• Quantal release – understand experiments
• Structure of synapse
• Vesicle trafficking, docking, and fusion release mechanisms
• Synapsins(Cytoskeletin)(Substrate of CAMKII)
• Rab3A(trafficking)(GTP dependent)
• VAMPs(synaptobreven), SNAP-25, syntaxin(SNARE protein), neurexin(docking/priming)
• Synaptic vesicle recycling (figure 14-12b)

• Synthesized in neuron, present in presynaptic terminal, can be administered exogenously & mechanisms exist for its removal
• ACh-----Choline acetyltransferase
• Biogenic amines

1. DA--------tyrosine hydroxylase
2. NE-------- tyrosine hydroxylase and dopamine ? hydroxylase
3. Epinephrine------ tyrosine hydroxylase
4. Seretonin------tryptophan hydroxylase
5. Histamine------histadine decarboxylase

• Amino acids

1. GABA-----glutamic acid decarboxylase
2. glycine
3. glutamate

• Neuropeptides (modulated by gene transcription and/or protein production)
• Transmitter removal methods

• Receptor-transducer-primary effector-second messenger- secondary effector
• G_s: GDP+phosphate group = transduction –adenylyl cyclase- cAMP(from ATP)- cAMP binds to regulatory subunit of cAMP dependent protein kinase)
• Most protein kinases have similar interaction w\catalytic and regulatory subunits
• Know differences between PLC and PLA₂ cascade
• 2nd messengers can modulate ionic conductance, other 2nd messengers, gene transcription (Pre and postsynaptically)
• EPSP can be caused by closing K+ channels (table 13-1, Figures 13-11&12)

• Disorder of the neuromuscular junction(synaptic transmission failure)
• reduction of the density of ACh receptors(?-bungerotoxin)
• Auto-immune disease
• antigenic cross-linking of receptors causes an increase in turnover
• Activation of T lymphocytes requires three molecules(immunogenic peptide, MHC and antigenic specific TcR(T-cell receptor)
• Antibodies targeting these molecules may aid in the treatment

• Formation of the nervous system (basic steps)
• Neural tube induction
• Segmentation
• Differentiation of neurons and glia and neuronal diversity
• Fly eye
• Migration
• Neural crest cells

• Axon guidance (factors influencing)
• Molecules involved in growth cone navigation (fig 21-3)
• Distance cues
• Contact cues (know figure P21.7)
• Difference between tropic and trophic factors
• How are topographical maps formed? (i.e. recognition molecules, neurotrophic factors, target interaction)
• methods used to study properties of neural system formation
• Neural cell death
• Figure P21.9
• Neurotrophins
• Regeneration

• What is competition?
• Input or activity specific regulation of topographical maps
• effect of visual deprivation
• Know specific experiments (Figures P22.3-5)
• Critical periods

• Synaptic facilitation, depression, and post-tetanic potentiation and mechanisms
• Long-term potentiation and depression
• Role of NMDA receptor
• Mechanisms of sensitization in Aplysia
• somatosensory map reorganization in the adult cortex (deprivation and heavy use modification)