neuro2 exam learning objectives

Understand how the cells capacitance and resistance determine its response to a current input

• The membrane acts as a parallel resistor-capacitor (RC) circuit.

• Capacitance slows voltage changes: τ=RCτ=RC (time constant).

• The voltage response to a current step is V(t)=IR(1−e−t/τ)V(t)=IR(1−e−t/τ).

Explain why large processes generally have greater lengths constant than small processes

• Length constant λ=rm/riλ=rm​/ri​​.

• Larger diameter → lower internal resistance riri​ → larger λλ, so signals travel farther.

Name the factors that determine how quickly an action potential spreads

• Axon diameter (larger = faster)

• Myelination (increases speed via saltatory conduction)

• Temperature

• Ion channel density

Describe what myelin is and what effect is had on nerve fibers

• Myelin is a lipid-rich sheath from oligodendrocytes (CNS) or Schwann cells (PNS).

• Increases membrane resistance and decreases capacitance → faster AP propagation.

Explain what saltatory conduction is

• AP “jumps” between nodes of Ranvier, where Na⁺ channels are concentrated.

• Much faster than continuous conduction.

Discuss how fiber size affects the electrical properties of nerves

• Larger diameter → lower axial resistance → faster propagation.

Discuss how dendritic action potentials differ from somatic action potentials

Dendritic APs are often smaller, slower, and may not propagate far; they can be graded and modulated by synaptic input.

List five essential functions of glial cells

• Myelination

• Synaptic regulation (uptake of neurotransmitters)

• Metabolic support to neurons

• Homeostasis (K⁺, pH, water)

• Immune surveillance (microglia)

State the key structural feature that distinguishes glial cells from neurons

• Glia are not excitable (do not generate action potentials) and lack axons/dendrites.

list five main types of glial cells and state whether they occur in the CNS or in the PNS

• Astrocytes – CNS

• Oligodendrocytes – CNS

• Schwann cells – PNS

• Microglia – CNS

• Ependymal cells – CNS (line ventricles)

Compare how the physiological properties of the cell membrane in glial cells and neurons

• Glia: resting potential ~ –90 mV, no action potentials, lower resistance, not excitable.

• Neurons: excitable, generate APs, higher membrane resistance.

Explain how electrical coupling between glial cells differs from that between glial cells and neurons

• Glia-glia coupling via gap junctions (connexins) forms a syncytium.

• Glia-neuron electrical coupling is rare or minimal; signaling is mostly chemical.

Explain the concept of spatial buffering

Explain how waves of increased cytoplasmic calcium are evoked in glial cells and what results from such waves

• Triggered by mechanical or chemical stimuli → IP₃ pathway → Ca²⁺ release from ER → Ca²⁺ wave spreads via gap junctions.

• Results in release of gliotransmitters (ATP, glutamate) that modulate neuronal activity.

Describe the structure of electrical synapses and of chemiscal synapses

• Electrical: gap junctions (connexins), direct cytoplasmic connection, bidirectional.

• Chemical: presynaptic bouton with vesicles, synaptic cleft, postsynaptic receptors.

Explain why electrical transmission is faster than chemical transmission

• No delay for neurotransmitter release, diffusion, or receptor binding.

Discuss how electrical transmission and chemical transmission complement one another

• Electrical: fast, synchronous, bidirectional (e.g., escape reflexes).

• Chemical: slower, unidirectional, modifiable (e.g., learning, inhibition)

Distinguish EPSPs and IPSPs

• EPSP: depolarization, reversal potential above threshold (e.g., Na⁺/K⁺ channels).

• IPSP: hyperpolarization or stabilization, reversal potential below threshold (e.g., Cl⁻ or K⁺ channels).

Describe the technique of ionophoresis and how it is applied

• A micropipette ejects charged neurotransmitter via electric current.

• Used to map receptor sensitivity (e.g., ACh receptors at endplate).

Describe two techniques used to assess and the permeability changes produced by acetylcholine

• Voltage clamp – measures synaptic current reversal potential.

• Ion substitution – changes external Na⁺ or K⁺ to see shift in reversal potential.

Explain what the reversal potential is and discuss its significance

• Membrane potential where net synaptic current = 0.

• Indicates which ions carry the current and whether synapse is excitatory or inhibitory.

State two important differences between neuromuscular and CNS synapses

• NMJ: one-to-one, always excitatory, large EPP.

• CNS: many-to-one, excitatory or inhibitory, smaller EPSPs/IPSPs.

Describe how direct chemical synaptic inhibition differs from direct chemical synapse excitation

• Inhibition: Cl⁻ influx (or K⁺ efflux), reversal potential below threshold.

• Excitation: Na⁺/K⁺ influx, reversal potential above threshold.

explain how direct chemical synaptic inhibition occurs

• Neurotransmitter (e.g., GABA, glycine) opens Cl⁻ channels → Cl⁻ enters (if E_Cl below resting potential) → hyperpolarization or shunting inhibition.

Explain what presynaptic inhibition is and how its function differs from that of postsynaptic inhibition

• Presynaptic inhibition: reduces neurotransmitter release from presynaptic terminal (e.g., via GABAB receptors).

• Postsynaptic inhibition: hyperpolarizes or shunts the postsynaptic cell.

• Function: presynaptic inhibition selectively modulates specific inputs without affecting other inputs to the same neuron.

Explain how indirect synaptic transmission differs from direct synaptic transmission

• Direct: ionotropic receptors, fast (ms), neurotransmitter binds directly to ion channel.

• Indirect: metabotropic receptors (GPCRs), slow (s to min), activate G proteins and second messengers.

Explain how metabotropic receptors differ from ionotropic receptors

• Metabotropic: 7 transmembrane domains, activate G proteins, indirect modulation of channels.

• Ionotropic: subunits forming a pore, direct ion flow, fast response.

Describe the basic structure of G protein-couple receptors (GPCRs)

• Single polypeptide with 7 transmembrane α-helices, extracellular N-terminus, intracellular C-terminus.

Describe the basic structure of G proteins

• Heterotrimeric (α, β, γ subunits). α subunit binds GTP and has GTPase activity.

Explain what happens when a G protein is activated by a transmitter receptor

• GDP exchanged for GTP on α subunit → α and βγ dissociate → both can activate downstream effectors (enzymes, ion channels).

Name the two ways in which G proteins can affect ion channels

• GDP exchanged for GTP on α subunit → α and βγ dissociate → both can activate downstream effectors (enzymes, ion channels).

Discuss how the effects produced by second-messenger systems from those produced by direct interaction of G proteins with ion channels

• Direct: fast, localized, short-lived.

• Second-messenger: slower, amplified, widespread, longer-lasting (e.g., cAMP, IP₃, Ca²⁺).

State what activates the synthesis and release of endocannabinoids

• Postsynaptic depolarization and Ca²⁺ influx.

Explain the concept of retrograde synaptic signaling

• Postsynaptic cell releases messengers (e.g., endocannabinoids) that act on presynaptic receptors to inhibit further transmitter release.

Explain what activates the synthesis and release of nitric oxide

• Ca²⁺/calmodulin activates neuronal NO synthase (nNOS) in response to NMDA receptor activation or increased intracellular Ca²⁺.

Name two roles that nitric oxide plays in human physiology

• Vasodilation (blood vessels).

• Retrograde signaling in synaptic plasticity (e.g., LTP).

List four different mechanisms for regulating cytoplasmic calcium concentration

• Voltage-gated Ca²⁺ channels.

• IP₃ receptors (ER release).

• Ryanodine receptors (ER release).

• Store-operated Ca²⁺ channels (SOC).

• Plasma membrane Ca²⁺ ATPase (PMCA) and Na⁺/Ca²⁺ exchanger (removal).

Discuss two ways in which a rise in intracellular calcium affects neuronal activity and function

• Triggers neurotransmitter release (exocytosis).

• Activates Ca²⁺-dependent K⁺ channels (hyperpolarization).

• Initiates second-messenger cascades (e.g., plasticity, gene expression).

Explain what the relation is between action potential amplitude and transmitter release

Explain what synaptic delay is and what accounts for it

• ~0.5–2 ms delay between presynaptic AP and postsynaptic response.

• Caused by: Ca²⁺ entry, vesicle fusion, transmitter diffusion, receptor activation.

Describe the role of calcium channels in transmitter release

• Voltage-gated Ca²⁺ channels (P/Q-type) open during depolarization → Ca²⁺ influx → triggers vesicle fusion.

Distinguish between calcium nanodomains and microdomains

• Nanodomain: near single open Ca²⁺ channel (~100 nm), fast, high [Ca²⁺].

• Microdomain: near multiple channels or active zone (~1 μm), lower [Ca²⁺].

Explain what the relation is between action potential amplitude and transmitter release

• Release depends on Ca²⁺ influx, which depends on AP amplitude (wider/higher AP → more Ca²⁺ → more release).

Explain what synaptic delay is and what accounts for it

• ~0.5–2 ms delay between presynaptic AP and postsynaptic response.

• Caused by: Ca²⁺ entry, vesicle fusion, transmitter diffusion, receptor activation.

Explain what the active zone of a nerve terminal is and what role it plays in transmitter release

• Specialized presynaptic membrane region with docked vesicles and Ca²⁺ channels.

• Site of vesicle fusion and transmitter release.

Describe how synaptic vesicles release their contents by exocytosis

• Vesicle fuses with presynaptic membrane via SNARE proteins → fusion pore opens → transmitter released into cleft.

Describe the kiss and run mode of exocytosis

• Fusion pore opens briefly, releases some transmitter, then closes; vesicle detaches and is reused without full collapse.

Explain what ribbon synapses are and name two types of cells in which they occur

• Synapses with a dense ribbon tethering many vesicles for continuous release.

• Occur in: photoreceptors, auditory hair cells.

Describe what happens to vesicles after they release their contents

• Membrane retrieved via endocytosis (clathrin-mediated or kiss-and-run), vesicle recycled and refilled.

Describe the two basic pathways by which depleted vesicles are retrieved and recycled

• Kiss-and-run: direct reuse.

• Clathrin-mediated endocytosis: vesicle collapses, membrane internalized via clathrin, then recycled.

Describe the roles played by glutamate, GABA, and glycine, in the vertebrate CNS

• Glutamate: main excitatory NT (AMPA, NMDA, kainate receptors).

• GABA: main inhibitory NT in forebrain (GABAᴀ Cl⁻ channel).

• Glycine: main inhibitory NT in brainstem/spinal cord (Cl⁻ channel).

Name five indirect transmitters that enhance or reduce transmission through synaptic pathways in the CNS

• Endocannabinoids, nitric oxide, ATP (via P2Y), adenosine, neuropeptides (e.g., orexin).

Describe the roles played by glutamate, GABA, and glycine, in the vertebrate CNS

• Immunohistochemistry (antibodies against NT or synthesizing enzyme).

• Pharmacology (agonists/antagonists to mimic or block action).

describe two different methods used to identify neurotransmitters and their receptors

• Immunohistochemistry (antibodies against NT or synthesizing enzyme).

• Pharmacology (agonists/antagonists to mimic or block action).

List three ways in which peptides differ from small molecule transmitters such as amino acids and monoamines

Synthesized as larger precursors, stored in dense-core vesicles, act via GPCRs (slower, prolonged effects).

Describe the functions of orexins

• Hypothalamic peptides regulating feeding, arousal, and sleep–wake stability.

• Orexin KO causes narcolepsy.

Explain how low molecular weight transmitters and neuropeptides differ in their synthesis, storage, and release

• Small-molecule: synthesized locally in terminal, stored in small clear vesicles, rapid release.

• Neuropeptides: synthesized in soma (precursor), stored in dense-core vesicles, released with high-frequency stimulation.

Explain how the synthesis of ach and other low molecular weight transmitters is controlled to meet the demands of release

• Rate-limiting enzymes (e.g., ChAT, GAD) and precursor availability (choline, glutamine) regulated by demand.

Explain why only a few molecules of a peptide are needed to influence a target cell

• Peptides act via GPCRs → signal amplification via second messengers.

Describe the difference between vesicles that store low mol weight transmitters and those that store neuropeptides

• Small clear vesicles: store ACh, glutamate, GABA.

• Large dense-core vesicles: store neuropeptides.

Explain how the accumulation of transmitter in vesicles is mediated

• Vesicular transporters (SLC family) use H⁺ gradient (V-ATPase) to drive uptake.

Explain the concept of co-storage and co-release

• Same neuron stores and releases two or more transmitters (e.g., ATP + norepinephrine).

Distinguish between axoplasmic flow and axonal transport

• Axoplasmic flow: slow movement of cytoplasm (0.1–1 mm/day).

• Axonal transport: fast (up to 400 mm/day), uses motor proteins.

Distinguish between anterograde transport and retrograde transport

• Anterograde: soma → terminal (kinesin).

• Retrograde: terminal → soma (dynein).

Describe the role of microtubules in axonal transport

• Tracks for motor proteins (kinesin, dynein) to move cargo.

Describe three mechanisms that remove transmitter from the synaptic cleft

• Enzymatic degradation (e.g., AChE).

• Reuptake via plasma membrane transporters (e.g., EAAT, GAT).

• Diffusion away from cleft.

Discuss why the prompt removal of transmitter is important for normal synaptic function

Preives receptor overstimulation, excitotoxicity, and loss of temporal precision.