NEUROSCIENCE 2026 EXAMINERS SET QUESTIONS
AND ANSWERS SURE A+
✔✔Representative Axon Guidance in vitro Experiments - ✔✔if neurons are grown on
collagen media with stripes of laminin, processes tend to grow out along the laminin
stripes
∙experiment highlights importance of ECM molecule laminin in forming a scaffold on
which axons may readily grow and extend
Netrin elicits axon outgrowth
∙floor plate expresses netrin, which attracts processes to the midline
∙placement of a spinal cord explant adjacent to floor plate laeds to growth of axonal
processes towards floor plate
Sema-3A (repelleant molecule which depolymierzes actin) expression results in axonal
growth away from gradient
∙use of blocking antibody against Sema-3A receptor in increasing concentrations results
in gradually decreasing amounts of repulsion as less and less Sema-3A receptors are
active
✔✔Intracellular Axon Guidance Pathways - ✔✔Calcium
∙changes in calcium influence the activity of protein kinases and phosphatases
,∙w/ regards to dendritic spines, rapid and high increases in calcium result in kinase
activation and larger spines
→slow changes stimulate phosphatase activity and spine shrinkage
∙kinase/phosphatase balance is critical to actin effectors (i.e. cofilin) that mediate
polymerization
∙calcium also stimulates focal interlization of adhesions → localized changes in calcium
affect adhesion molecule expression and localization
Cyclic Nucleotides (i.e. cAMP)
∙there exists a complex interplay b/w calcium and cyclic nucleotide-dependent effects on
growth cone guidance
∙distant calcium signaling can be modulated by cAMP, and this can influence an axon's
bidirectional turning response
Rho Signaling
∙Rho GTPase is an establish effector of actin dynamics in axonal and dendritic spine
growth
∙calcium enters the cell to activate changes in Rho to affect actin polymerization
✔✔How are intracellular events initiated? - ✔✔ion channels play an important role in
intracellular calcium concentration
cell adhesion molecules affect kinase/phosphatase activity that regulate actin
polymerization
G protein coupled receptors (GPCR)
∙GPCR function in cell shape and migration as well as axon outgrowth
∙GPCRs are most abundant receptor cell type in brain, are target of many
pharmaceuticals
∙belong to receptor family that contains 7 transmembrane domains
∙activation involves binding of a solbuel agonist to its external domain, leading to
dissociation of the βγ-subunit
→has important effect on overall calcium levels and ultimately actin dynamics
∙GPCRs are also linked intracellularly to an α-subunit
→different GPCRs have different α-subunit functions and effects, but the cell and axon
migration signal is usually transmitted to Rho GTPase through the α-subunit
✔✔Axon Guidance in the Mature CNS - ✔✔same molecules governing axon guidance
are important in regeneration after injury and learning & memory changes
regeneration is inhibited by repulsive adhesion molecules → harder to get regeneration
in mature NS due to much higher expression of repulsive & axon inhibitory molecules
compared to mature PNS
actin polymerization and dendritic protrusions can affect both the number of synapses
and the number of dendritic spines, which are key to learning and memory changes
,✔✔Basic Elements of Neurotransmitter Systems - ✔✔
✔✔Neurotransmitters are involved in synaptic transmission b/w neurons - ✔✔Synaptic
transmission - signal transduction process that begins with an action potential-
dependent release of neurotransmitter from a presynaptic terminal
∙presynaptic neuron gets an electrical stimulus (AP that changes electrical properties)
and converting it into a chemical signal
neurotransmitters then binds and activates postsynaptic receptors that modify the
electrical and biochemical properties of the postsynaptic cell
∙receiving chemical signal, depolarizing/hyperpolarizing cell (based on the signal) and
signal is converted to an electrical signal and propagated to the next neuron in the relay
✔✔Examples of various types of synaptic arrangements in the CNS - ✔✔Axodendritic
∙axon of presynaptic neuron synapsing on dendrite
∙very common in CNS
Axosomatic
∙axon of presynaptic neuron synapsing directly on cell body
Axoaxonic
∙axon of presynaptic synapsing on another axon
✔✔Pre and postsynaptic CNS connections vary in density and size - ✔✔Asymmetrical
synaptic differentiation: Gray's type I synapse, usually excitatory
Symmetrical synaptic differentiation: Gray's type II synapse, usually inhibitory
know that the typical depiction of a presynaptic and postsynaptic neuron is too simple
for the CNS → there are many different ways the synapse can exist (i.e. presynaptic
envelops postsynaptic, presynaptic can bifurcate and synapse many times, etc.)
✔✔Identification Criteria for a Neurotransmitter - ✔✔it is synthesized in the neuron
∙need synthetic enzymes in the neuron to make that neurotransmitter
it is found in the presynaptic terminal in high enough concentrations to exert an effect
it is released in response to presynaptic depolarization and release is Ca++ dependent
specific receptors exist on the post-synaptic cell
when applied exogenously it mimics the action of endogenously released transmitter
specific mechanisms exist which terminate its actions
, ✔✔Life cycle of a neurotransmitter in the regulation of synaptic activity - ✔✔Synthesis
→ storage → release → reception → reuptake/catabolism/diffusion
✔✔Neurotransmitter processing is a target for many CNS drugs and neurotoxins -
✔✔To target synthesis:
∙either decrease precursor or inhibiting specific enzyme activity
∙will decrease concentration of NT in neuron and decrease its activity
To target storage:
∙inhibit vesicular uptake pumps
∙depletes NT in presynaptic neurons
To target release:
∙facilitate release → more NT is released than normal, eventually causing depletion
To inactivate re-uptake or degradation:
∙block reuptake or inhibit enzymatic degradation
∙result in an increased transmitter concentration in the synapse
To target receptor binding:
∙block transmitter binding
∙if you want a specific modulation of NT effect, this is best way to get it
✔✔Characteristics of Specific Neurotransmitters - ✔✔Life Cycle Characteristics:
∙Synthesis and rate-limiting step
∙Metabolism (if there is an enzyme that inactivates it)
∙Termination of action
Central pathways
∙localization and projections
∙physiological/pathological role
✔✔Major Chemical Categories of Neurotransmitters - ✔✔Small Molecule
∙Amino acids (Glutamate, GABA, Glycine)
-->glutamate and GABA predominate by weight (~99%)
∙Biogenic Amines (ACh, serotonin, histamine, catecholamines)
Peptides
∙3-36 amino acids
∙opioid peptide used in this class
another category like gaseous agents, but we won't go there
✔✔Functional divison of neurotransmitters - ✔✔Neural signaling
∙mediate communication b/w neurons
∙Amino acids: Glutamate, GABA and glycine
AND ANSWERS SURE A+
✔✔Representative Axon Guidance in vitro Experiments - ✔✔if neurons are grown on
collagen media with stripes of laminin, processes tend to grow out along the laminin
stripes
∙experiment highlights importance of ECM molecule laminin in forming a scaffold on
which axons may readily grow and extend
Netrin elicits axon outgrowth
∙floor plate expresses netrin, which attracts processes to the midline
∙placement of a spinal cord explant adjacent to floor plate laeds to growth of axonal
processes towards floor plate
Sema-3A (repelleant molecule which depolymierzes actin) expression results in axonal
growth away from gradient
∙use of blocking antibody against Sema-3A receptor in increasing concentrations results
in gradually decreasing amounts of repulsion as less and less Sema-3A receptors are
active
✔✔Intracellular Axon Guidance Pathways - ✔✔Calcium
∙changes in calcium influence the activity of protein kinases and phosphatases
,∙w/ regards to dendritic spines, rapid and high increases in calcium result in kinase
activation and larger spines
→slow changes stimulate phosphatase activity and spine shrinkage
∙kinase/phosphatase balance is critical to actin effectors (i.e. cofilin) that mediate
polymerization
∙calcium also stimulates focal interlization of adhesions → localized changes in calcium
affect adhesion molecule expression and localization
Cyclic Nucleotides (i.e. cAMP)
∙there exists a complex interplay b/w calcium and cyclic nucleotide-dependent effects on
growth cone guidance
∙distant calcium signaling can be modulated by cAMP, and this can influence an axon's
bidirectional turning response
Rho Signaling
∙Rho GTPase is an establish effector of actin dynamics in axonal and dendritic spine
growth
∙calcium enters the cell to activate changes in Rho to affect actin polymerization
✔✔How are intracellular events initiated? - ✔✔ion channels play an important role in
intracellular calcium concentration
cell adhesion molecules affect kinase/phosphatase activity that regulate actin
polymerization
G protein coupled receptors (GPCR)
∙GPCR function in cell shape and migration as well as axon outgrowth
∙GPCRs are most abundant receptor cell type in brain, are target of many
pharmaceuticals
∙belong to receptor family that contains 7 transmembrane domains
∙activation involves binding of a solbuel agonist to its external domain, leading to
dissociation of the βγ-subunit
→has important effect on overall calcium levels and ultimately actin dynamics
∙GPCRs are also linked intracellularly to an α-subunit
→different GPCRs have different α-subunit functions and effects, but the cell and axon
migration signal is usually transmitted to Rho GTPase through the α-subunit
✔✔Axon Guidance in the Mature CNS - ✔✔same molecules governing axon guidance
are important in regeneration after injury and learning & memory changes
regeneration is inhibited by repulsive adhesion molecules → harder to get regeneration
in mature NS due to much higher expression of repulsive & axon inhibitory molecules
compared to mature PNS
actin polymerization and dendritic protrusions can affect both the number of synapses
and the number of dendritic spines, which are key to learning and memory changes
,✔✔Basic Elements of Neurotransmitter Systems - ✔✔
✔✔Neurotransmitters are involved in synaptic transmission b/w neurons - ✔✔Synaptic
transmission - signal transduction process that begins with an action potential-
dependent release of neurotransmitter from a presynaptic terminal
∙presynaptic neuron gets an electrical stimulus (AP that changes electrical properties)
and converting it into a chemical signal
neurotransmitters then binds and activates postsynaptic receptors that modify the
electrical and biochemical properties of the postsynaptic cell
∙receiving chemical signal, depolarizing/hyperpolarizing cell (based on the signal) and
signal is converted to an electrical signal and propagated to the next neuron in the relay
✔✔Examples of various types of synaptic arrangements in the CNS - ✔✔Axodendritic
∙axon of presynaptic neuron synapsing on dendrite
∙very common in CNS
Axosomatic
∙axon of presynaptic neuron synapsing directly on cell body
Axoaxonic
∙axon of presynaptic synapsing on another axon
✔✔Pre and postsynaptic CNS connections vary in density and size - ✔✔Asymmetrical
synaptic differentiation: Gray's type I synapse, usually excitatory
Symmetrical synaptic differentiation: Gray's type II synapse, usually inhibitory
know that the typical depiction of a presynaptic and postsynaptic neuron is too simple
for the CNS → there are many different ways the synapse can exist (i.e. presynaptic
envelops postsynaptic, presynaptic can bifurcate and synapse many times, etc.)
✔✔Identification Criteria for a Neurotransmitter - ✔✔it is synthesized in the neuron
∙need synthetic enzymes in the neuron to make that neurotransmitter
it is found in the presynaptic terminal in high enough concentrations to exert an effect
it is released in response to presynaptic depolarization and release is Ca++ dependent
specific receptors exist on the post-synaptic cell
when applied exogenously it mimics the action of endogenously released transmitter
specific mechanisms exist which terminate its actions
, ✔✔Life cycle of a neurotransmitter in the regulation of synaptic activity - ✔✔Synthesis
→ storage → release → reception → reuptake/catabolism/diffusion
✔✔Neurotransmitter processing is a target for many CNS drugs and neurotoxins -
✔✔To target synthesis:
∙either decrease precursor or inhibiting specific enzyme activity
∙will decrease concentration of NT in neuron and decrease its activity
To target storage:
∙inhibit vesicular uptake pumps
∙depletes NT in presynaptic neurons
To target release:
∙facilitate release → more NT is released than normal, eventually causing depletion
To inactivate re-uptake or degradation:
∙block reuptake or inhibit enzymatic degradation
∙result in an increased transmitter concentration in the synapse
To target receptor binding:
∙block transmitter binding
∙if you want a specific modulation of NT effect, this is best way to get it
✔✔Characteristics of Specific Neurotransmitters - ✔✔Life Cycle Characteristics:
∙Synthesis and rate-limiting step
∙Metabolism (if there is an enzyme that inactivates it)
∙Termination of action
Central pathways
∙localization and projections
∙physiological/pathological role
✔✔Major Chemical Categories of Neurotransmitters - ✔✔Small Molecule
∙Amino acids (Glutamate, GABA, Glycine)
-->glutamate and GABA predominate by weight (~99%)
∙Biogenic Amines (ACh, serotonin, histamine, catecholamines)
Peptides
∙3-36 amino acids
∙opioid peptide used in this class
another category like gaseous agents, but we won't go there
✔✔Functional divison of neurotransmitters - ✔✔Neural signaling
∙mediate communication b/w neurons
∙Amino acids: Glutamate, GABA and glycine
