NEUROSCIENCE UPDATED EXAM 2026
COMPREHENSIVE QUESTIONS AND ANSWERS SURE
A+
✔✔Differences b/w Small Molecule NTs and Peptide NTs - ✔✔small molecule NTs are
synthesized in nerve terminal, and packaged into vesicles
∙peptide NTs are formed as pre-propeptides in rough ER (cell body) and activated &
packaged in Golgi (cell body)
∙packaged vesicles then transported to nerve terminal
→at times, peptide NTs are packaged w/ small molecule NTs
small molecule NTs are terminated by re-uptake mechanisms
∙peptide NTs are degraded ocne they are released, not recycled
∙new synthesis and axonal transport must be occurring in order to provide continuous
peptide NT transmission
release of small molecule NTs versus peptide dependent
∙low-frequency stimulation (low frequency APs) lead to localized increase in calcium (at
the terminal) and will stimulate small molecule NT release
∙high-frequency stimulation will lead to diffuse increase in Ca, and thus lead to peptide
NT release
,localization of stimulation refers to projections that are made onto the rest of brain, or
where each specific type of NT will have an effect
∙small molecule NTs are trans-system or multi-system modulators
→project into many areas of brain
∙peptide NTs are within-system modulators
✔✔Neurotransmitter Receptors - ✔✔both pre-synaptic and post-synaptic NT receptors
do exist, but we only discuss post-synaptic NT receptors
2 major types: ionotropic and metabotropic
receptors can act through 2 major mechanisms:
∙direct gating = characteristic of ionotropic receptors
→faster, involves 2 NTs binding directly to an ion channel, channel opening, and then
ion flow
∙indirect gating = characteristic of metabotropic receptors
→slower, NT binds to the receptor which subsequently activates G proteins, which then
act intracellularly to activate nearby ion channel, and then ions can flow
✔✔Principles that apply to all NT receptors - ✔✔Binding is determined by channel
specificity
specificity/selectivity determines whether or not the effects are stimulatory or inhibitory
kinetics of the NT binding to the receptor determines the length of channel opening and
effect
a single NT can activate more than one receptor, and more than one type of receptor
✔✔Ionotropic Receptors - ✔✔post-synpatic NT receptors
have ligand-gated ion channels
made up of 5 transmembrane proteins, which fold in and out of membrane to form ion
channel
major ionotropic receptors can be divided into 2 families based on structural make up:
∙Family #1) nicotinic ACh receptor (nAChR) and GABAA
→5 transmembrane domains w/ 4 membrane-spanning helices, and both N and C
terminus is extracellular
∙Family #2) AMPA, NMDA, Kainate
→5 transmembrane domains w/ 3 membrane-spanning domains and 1 pore loop,
extracellular N terminus, intracellular C terminus
composition of subunits (domains) determines specificity and kinetics of each individual
NT receptors
, ✔✔nAChR - ✔✔made up of 5 transmembrane subunits, each with 4 membrane
spanning helices
∙creates negatively charged ion channel
receptor is only activated when 2 ACh molecules bind, 1 to each alpha subunit of the
receptor
∙when binding of ligands occur, pore opens almost instantaneously
∙highly permeable to Na+, but can also be permeable to Ca++
neuronal AChR desensitizes rapidly (on the order of msec) and is highly influenced by
structural diversity, such that the specific composition of the receptors subunits affects
the rate of desensitization and Ca++ permeability
✔✔GABA Receptors - ✔✔major mediator of inhibitory synaptic transmission in the brain
same overall structure of nAChR, but instead require 2 GABA molecules to be activated
∙when 2 GABAs bind, pore opens and is highly selective for Cl- molecules
∙causes hyperpolarization of membrane
inner core of GABA receptors is positive to attract Cl-
many pharmacological interventions produce allosteric potentiation of GABA receptors
→ CNS depressants
∙i.e. benzodiazepines, barbiturates, steroids)
picrotoxin is a GABA receptor antagonist
∙leads to buildup of glutamate
∙can induce seizures
✔✔Glutamate Receptors - ✔✔major mediator of excitatory synaptic transmission in
brain
have 5 transmembrane domains
∙each domain has 3 membrane-spanning helices and 1 pore loop
∙each domain is composed of 2 repeating subunits → structure differs slight for nAChR
and GABA receptors
3 major glutamate receptors are AMPA, NMDA and Kainate receptors
✔✔AMPA glutamate receptors - ✔✔have fast kinetics
are permeable to Na and K but not Ca
desensitize rapidly
COMPREHENSIVE QUESTIONS AND ANSWERS SURE
A+
✔✔Differences b/w Small Molecule NTs and Peptide NTs - ✔✔small molecule NTs are
synthesized in nerve terminal, and packaged into vesicles
∙peptide NTs are formed as pre-propeptides in rough ER (cell body) and activated &
packaged in Golgi (cell body)
∙packaged vesicles then transported to nerve terminal
→at times, peptide NTs are packaged w/ small molecule NTs
small molecule NTs are terminated by re-uptake mechanisms
∙peptide NTs are degraded ocne they are released, not recycled
∙new synthesis and axonal transport must be occurring in order to provide continuous
peptide NT transmission
release of small molecule NTs versus peptide dependent
∙low-frequency stimulation (low frequency APs) lead to localized increase in calcium (at
the terminal) and will stimulate small molecule NT release
∙high-frequency stimulation will lead to diffuse increase in Ca, and thus lead to peptide
NT release
,localization of stimulation refers to projections that are made onto the rest of brain, or
where each specific type of NT will have an effect
∙small molecule NTs are trans-system or multi-system modulators
→project into many areas of brain
∙peptide NTs are within-system modulators
✔✔Neurotransmitter Receptors - ✔✔both pre-synaptic and post-synaptic NT receptors
do exist, but we only discuss post-synaptic NT receptors
2 major types: ionotropic and metabotropic
receptors can act through 2 major mechanisms:
∙direct gating = characteristic of ionotropic receptors
→faster, involves 2 NTs binding directly to an ion channel, channel opening, and then
ion flow
∙indirect gating = characteristic of metabotropic receptors
→slower, NT binds to the receptor which subsequently activates G proteins, which then
act intracellularly to activate nearby ion channel, and then ions can flow
✔✔Principles that apply to all NT receptors - ✔✔Binding is determined by channel
specificity
specificity/selectivity determines whether or not the effects are stimulatory or inhibitory
kinetics of the NT binding to the receptor determines the length of channel opening and
effect
a single NT can activate more than one receptor, and more than one type of receptor
✔✔Ionotropic Receptors - ✔✔post-synpatic NT receptors
have ligand-gated ion channels
made up of 5 transmembrane proteins, which fold in and out of membrane to form ion
channel
major ionotropic receptors can be divided into 2 families based on structural make up:
∙Family #1) nicotinic ACh receptor (nAChR) and GABAA
→5 transmembrane domains w/ 4 membrane-spanning helices, and both N and C
terminus is extracellular
∙Family #2) AMPA, NMDA, Kainate
→5 transmembrane domains w/ 3 membrane-spanning domains and 1 pore loop,
extracellular N terminus, intracellular C terminus
composition of subunits (domains) determines specificity and kinetics of each individual
NT receptors
, ✔✔nAChR - ✔✔made up of 5 transmembrane subunits, each with 4 membrane
spanning helices
∙creates negatively charged ion channel
receptor is only activated when 2 ACh molecules bind, 1 to each alpha subunit of the
receptor
∙when binding of ligands occur, pore opens almost instantaneously
∙highly permeable to Na+, but can also be permeable to Ca++
neuronal AChR desensitizes rapidly (on the order of msec) and is highly influenced by
structural diversity, such that the specific composition of the receptors subunits affects
the rate of desensitization and Ca++ permeability
✔✔GABA Receptors - ✔✔major mediator of inhibitory synaptic transmission in the brain
same overall structure of nAChR, but instead require 2 GABA molecules to be activated
∙when 2 GABAs bind, pore opens and is highly selective for Cl- molecules
∙causes hyperpolarization of membrane
inner core of GABA receptors is positive to attract Cl-
many pharmacological interventions produce allosteric potentiation of GABA receptors
→ CNS depressants
∙i.e. benzodiazepines, barbiturates, steroids)
picrotoxin is a GABA receptor antagonist
∙leads to buildup of glutamate
∙can induce seizures
✔✔Glutamate Receptors - ✔✔major mediator of excitatory synaptic transmission in
brain
have 5 transmembrane domains
∙each domain has 3 membrane-spanning helices and 1 pore loop
∙each domain is composed of 2 repeating subunits → structure differs slight for nAChR
and GABA receptors
3 major glutamate receptors are AMPA, NMDA and Kainate receptors
✔✔AMPA glutamate receptors - ✔✔have fast kinetics
are permeable to Na and K but not Ca
desensitize rapidly
