Lecture 8:Membrane Mechanisms

Question 1

What factors contribute to the variety of firing patterns observed in neurons,

and how can neurons switch between different firing patterns?

Answer 1

AP Firing Patterns

1. VARIETY OF TEMPORAL FIRING PATTERNS: Many different firing patterns are observed in neurons.
2. PATTERN SWITCHING: Some neurons can SWITCH from one firing pattern to another.

Question 2

Why can’t the variety of firing patterns observed in neurons be explained by a single type of voltage-gated Na⁺ and K⁺ channels? = 3

Answer 2

AP Firing Patterns

1. VARIETY OF TEMPORAL FIRING PATTERNS: Many different firing patterns are observed in neurons.
2. PATTERN SWITCHING: Some neurons can SWITCH from one firing pattern to another.
3. This variety CANNOT BE EXPLAINED by just one type of VOLTAGE-GATED Na⁺ and K⁺ CHANNELS

Question 3

firing patterns on slide 4

Answer 3

Transient:

DELAY
ADAPTING SPIKING
RAPIDLY ADAPTING SPIKING
TRANSIENT STUTTERING
TRANSIENT SLOW WAVE BURSTING
Steady State:

STEADY STATE SILENCE
NON-ADAPTING SPIKING
PERSISTENT STUTTERING
PERSISTENT SLOW WAVE BURSTING
Silence:

DELAY
STEADY STATE SILENCE
Spiking:

ADAPTING SPIKING
NON-ADAPTING SPIKING
Stuttering:

TRANSIENT STUTTERING
PERSISTENT STUTTERING
Bursting:

TRANSIENT SLOW WAVE BURSTING
PERSISTENT SLOW WAVE BURSTING

Question 4

What are some of the membrane
mechanisms involved in modulation of AP
firing patterns? =

Answer 4

1. Voltage-Gated Ion Channels:
   - Na⁺ Channels
   - K⁺ Channels
   - Ca²⁺ Channels
2. Ion Channel Kinetics:
   - Activation Rates
   - Inactivation Rates
3. Ion Channel Distribution:
   - Spatial Localization
4. Synaptic Input:
   - Excitatory Inputs
   - Inhibitory Inputs
5. Modulatory Signals:
   - Neurotransmitters
   - Neuropeptides
   - Hormones
6. Intracellular Signaling:
   - Second Messengers
   - Protein Kinases
7. Membrane Properties:
   - Resting Membrane Potential
   - Capacitance
   - Conductance
8. Channel Interactions:
   - SNARE Proteins

Question 5

Different types of ion channels and receptors: 4

Answer 5

1. ‘Ligand-Gated:’
   — Activated by: Binding of specific molecules (ligands) such as neurotransmitters.
   — Example: NMDA Receptors, AMPA Receptors.
2. ‘Voltage-Gated:’
   — Activated by: Changes in membrane potential.
   — Example: Na⁺ Channels, K⁺ Channels, Ca²⁺ Channels.
3. ‘Mechanically-Gated:’
   — Activated by: Physical deformation of the membrane (e.g., stretching or pressure).
   — Example: Mechanoreceptors in sensory neurons.
4. ‘Always Open:’
   — Activated by: Always open under normal conditions, allowing ions to pass through continuously.
   — Example: Leak Channels (e.g., K⁺ Leak Channels).

Question 6

Basic Chemical Neurotransmission

PRESYNAPTIC: 2

Answer 6

1. RELEASE OF NEUROTRANSMITTER:
   - Via CA²⁺-DEPENDENT EXOCYTOSIS.
2. VOLTAGE-GATED CA²⁺ CHANNELS:
   - Trigger the release of neurotransmitters by allowing Ca²⁺ influx into the presynaptic terminal.

Question 7

Post-Synaptic Receptors - How does receptor variability influence the action of neurotransmitters on target cells? = 5

Answer 7

1. BIND SPECIFIC NEUROTRANSMITTERS
2. HUGE VARIABILITY (subunits/subtypes)
3. RECEPTOR DETERMINES ACTION on target cell
4. ‘IONOTROPIC vs METABOTROPIC ACTION’
5. Example: nicotinic acetylcholine
   receptor (nAChR)

Question 8

What are the differences between homomeric and heteromeric nAChRs in terms of their subunit composition?

Answer 8

Homomeric nAChRs

HOMOMERIC nAChRs: Composed of identical subunits.
EXAMPLE: NICOTINIC ACETYLCHOLINE RECEPTOR (nAChR)
Heteromeric nAChRs

HETEROMERIC nAChRs: Composed of different subunits.
EXAMPLE: NICOTINIC ACETYLCHOLINE RECEPTOR (nAChR)

Question 9

How do excitatory and inhibitory ‘ionotropic receptors’ differ in their effects on membrane potential? = 4

Answer 9

Ionotropic Receptors

1. LIGAND-GATED ION CHANNELS: Activated by binding of neurotransmitter.
2. FAST ACTION: Rapid response to neurotransmitter binding.

…3. ‘EXCITATORY’: Increase Na⁺ PERMEABILITY.
…4. ‘INHIBITORY’: Increase Cl⁻ OR K⁺ PERMEABILITY.

Question 10

How do NMDA and AMPA receptors differ in their response to glutamate and their roles in neurotransmission? 6

Answer 10

1. ‘Different Ionotropic Receptors for the Same Neurotransmitter.’
   …2. EXAMPLE: GLUTAMATE RECEPTORS
   …3. GLUTAMATE: Most abundant neurotransmitter in CNS of vertebrates.
2. DISTINCTION BETWEEN NMDA AND NON-NMDA (AMPA) RECEPTORS:

…5. NMDA RECEPTORS: Named after NMDA (N-Methyl D-Aspartate), a powerful agonist.

…6. AMPA RECEPTORS: Named after AMPA (α-Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionic Acid), a powerful agonist.

Question 11

How does zinc modulation affect NMDA receptor function and its potential role in preventing glutamate excitotoxicity? = 7

Answer 11

1. Receptor action Can Be Modulated
2. MODULATION OF VOLTAGE-GATED ION CHANNELS: By trace metals.
3. EXAMPLE: NMDA RECEPTOR AND ZINC

…4. PATCH CLAMP IN MOUSE HIPPOCAMPAL NEURONS AND OOCYTES:
— 5. Responses to NMDA strongly antagonized by zinc.

6. FUNCTION OF MODULATION BY ZINC:
   …7. PREVENTING GLUTAMATE EXCITOTOXICITY

Question 12

How do zinc and copper modulate voltage-gated ion channels, and what effects do these trace metals have on neuronal firing? = 6

Answer 12

1. Modulation of Receptors
2. MODULATION OF VOLTAGE-GATED ION CHANNELS BY TRACE METALS: Zinc and copper.
3. INHIBITION OF VOLTAGE-GATED CALCIUM CHANNEL CURRENTS
4. REDUCTION OF NEURONAL FIRING:

…5. Effect on K⁺ CURRENTS.
EXPERIMENTAL MODEL:

…6. Rat olfactory bulb neurons in culture, using VOLTAGE CLAMP and INTRACELLULAR RECORDINGS.

Question 13

How does a rise in calcium contribute to the inactivation of ion channels, and what are the roles of calcium binding and calcineurin activation in this process? = 5

Answer 13

1. Modulation of Ion Channels
2. DIFFERENT MECHANISMS OF INACTIVATION:
3. RISE IN CALCIUM (SELF-LIMITING)

….4….”CALCIUM BINDING” 1A. CALCIUM BINDING DIRECTLY TO ITS OWN CHANNEL: Causes CLOSURE.

….5…..”DEPHOSPHORYLATION” 1B. CALCIUM ACTIVATES CALCINEURIN: This dephosphorylates channels, causing INACTIVATION.

Question 14

How does the refractory period of ion channels contribute to the absolute and relative refractory periods in neurons? = 4

Answer 14

1. DIFFERENT MECHANISMS OF INACTIVATION:
2. SOME CHANNELS HAVE REFRACTORY PERIOD

…3.CHANNELS CLOSED AND NOT AVAILABLE

…4. RESULTS IN ABSOLUTE VS RELATIVE REFRACTORY PERIOD IN A NEURON

Question 15

What are the implications of the refractory period of Na⁺ channels for channel availability and neuronal excitability? = 6

Answer 15

1. implications of the Refractory Period of Na⁺ Channels
2. PROPORTION OF AVAILABLE CHANNELS

…3. % OF Na⁺ CHANNELS AVAILABLE: About 40% of voltage-gated Na⁺ channels are inactivated at normal resting potential.

…4. HYPERPOLARIZATION MAKES MORE VOLTAGE-GATED Na⁺ CHANNELS AVAILABLE: For opening by a subsequent depolarization.

…5. LEADS TO POST-INHIBITORY REBOUND: When hyperpolarization results in increased availability of Na⁺ channels.

…6. AT NORMAL RESTING POTENTIAL: Not all voltage-gated Na⁺ channels are available.

Question 16

Post-Inhibitory Rebound

What causes increased firing in post-inhibitory rebound, and how does this relate to the availability of Na⁺ channels? 3

Answer 16

1. INCREASED FIRING AFTER A PERIOD OF INHIBITION

…2. CAUSED BY INCREASED NUMBER OF AVAILABLE Na⁺ CHANNELS:
– Fewer inactivated channels.

…3. EXAMPLE: RETINAL GANGLION CELLS.

Question 17

No Refractory Period: K⁺ Channels

How does the voltage clamp technique differentiate between Na⁺ and K⁺ currents, and what is unique about the inactivation of K⁺ channels in axons? = 6

Answer 17

1. CLASSICAL VOLTAGE-GATED K⁺ CHANNELS IN AXONS DO NOT INACTIVATE:

…2.SOURCE UNKNOWN.

3. VOLTAGE CLAMP TECHNIQUE:

…4. RECORDS MEMBRANE CURRENTS WHEN Vm IS CONTROLLED.

…5. EARLY INWARD CURRENT: Na⁺ charge movement.

…6. DELAYED OUTWARD CURRENT: K⁺ charge movement.

Question 18

K⁺ Channels

What are the effects of tetrodotoxin (TTX) and tetraethyl ammonium (TEA) on ion channels, and how do selective blockers contribute to the study of K⁺ currents?

= 6

Answer 18

1. SELECTIVE BLOCKERS ALLOW K⁺ CURRENTS TO BE ISOLATED:
   …2. SOURCE UNKNOWN.
2. TETRODOTOXIN (TTX):
   …4. BLOCKS VOLTAGE-GATED Na⁺ CHANNELS.
3. TETRAETHYL AMMONIUM (TEA):
   …6. BLOCKS VOLTAGE-GATED K⁺ CHANNELS.

Question 19

Which K⁺ channel subtypes exhibit refractory periods and inactivation,

and how does the blocking of Na⁺ current with toxins relate to these channels?

Answer 19

1. Some K+ channel subtypes do show refractory
   periods
2. A-TYPE K⁺ CHANNELS (Kv CHANNELS) SHOW INACTIVATION:
   …3. SOURCE UNKNOWN.
3. Na⁺ CURRENT BLOCKED WITH TOXI

Question 20

A-TYPE K⁺ CHANNELS REGULATE INTERSPIKE INTERVAL:

How do A-type K⁺ channels affect the interspike interval and the range of action potential firing rates? = 7

Answer 20

1. A-TYPE K⁺ CHANNELS ONLY AVAILABLE DURING AFTER-POTENTIAL:

…2. Will delay depolarization.

3. Voltage-Gated K⁺ Channels (A-Type) ARE INACTIVATED WHEN Vm < -50 mV:

…4. Become available during afterhyperpolarization.

5. During Next Depolarization Towards Threshold:

…6. Outward current through A-type channels LENGTHENS INTERVALS BETWEEN APs.

…7. Gives Greater Range of AP Firing Rates.

Question 21

A-TYPE K⁺ CHANNELS CAN CAUSE DELAYED FIRING:

How do A-type K⁺ channels affect the timing and initiation of action potentials during different membrane potentials?

= 8

Answer 21

1. A-type K+ channels
2. At NORMAL Vm:

…3. Immediate TRAIN OF ACTION POTENTIALS following depolarization stimulus.

4. At HYPERPOLARIZATION:

..5. FIRST DELAY BEFORE ACTION POTENTIALS:

……6. Caused by A-TYPE K⁺ CHANNELS opening rapidly at depolarization.

……7. Generate SHORT OUTWARD CURRENT, delaying the opening of Na⁺ CHANNELS.

…..8. A-TYPE CHANNELS ARE INACTIVATED AT NORMAL RESTING POTENTIAL.

Question 22

HOW DOES DAMPENED FUNCTION AND EXPRESSION OF Kv CHANNELS IN NEUROPATHIC PAIN AFFECT THE FIRING RATES OF PRIMARY AFFERENT NEURONS AND PAIN PERCEPTION?

A-TYPE K⁺ CHANNELS IN PATHOLOGY:

= 4

Answer 22

1. IN NEUROPATHIC PAIN:
2. Kv CHANNELS SHOW DAMPENED FUNCTION AND EXPRESSION:

…3. May INCREASE FIRING OF PRIMARY AFFERENT NEURONS involved in nociception.

….4. Potentially leads to HYPERSENSITIVITY.

Question 23

HOW DOES THE FUNCTION AND EXPRESSION OF Kv1.2 AND Kv1.4 CHANNELS IN NEUROPATHIC PAIN MODELS AFFECT ACTION POTENTIAL FIRING AND INTERSPIKE INTERVAL?

Kv CHANNELS AND THEIR FUNCTION: 7

Answer 23

1. αNTID is responsible for FAST N-TYPE INACTIVATION in Kv1.4 channels.
2. βNTID of the accessory Kvβ1 SUBUNIT confers N-type inactivation to Kv1.1 and Kv1.2 channels.
3. Kv1.4 CHANNELS:

…4. Found in SOMA and AXONS, including the JUXTA PARANODAL REGION of the NODES OF RANVIER.

…5. LOW VOLTAGE-ACTIVATING, potentially regulating AP FIRING and INTERSPIKE INTERVAL.

6. IN NEUROPATHIC PAIN ANIMAL MODELS:

…7. Kv1.2 and Kv1.4 channels exhibit DAMPENED FUNCTION and EXPRESSION.

Question 24

HOW DOES THE ACTIVATION OF Ca²⁺-ACTIVATED K⁺ CHANNELS CONTRIBUTE TO FIRING RATE ADAPTATION IN NEURONS?

Firing Rate Adaptation = 4

Answer 24

1. Depolarizing Stimulus causes Ca²⁺ INFLOW via VOLTAGE-GATED Ca²⁺ CHANNELS.
2. This ACTIVATES Ca²⁺-ACTIVATED K⁺ CHANNELS, leading to LATE HYPERPOLARIZATION.
3. Ca²⁺-ACTIVATED K⁺ CHANNELS:
4. Involved in ADAPTING FIRING RATES by contributing to the LATE HYPERPOLARIZATION.

Question 25

WHAT EVIDENCE SUPPORTS THE ROLE OF Ca²⁺-ACTIVATED K⁺ CHANNELS IN FIRING RATE ADAPTATION? Evidence of Involvement of Ca²⁺-Activated K⁺ Channels in Firing Rate Adaptation = 5

Answer 25

1. Provides EVIDENCE for the involvement of Ca²⁺-ACTIVATED K⁺ CHANNELS in firing rate adaptation. 2. Normal Firing Rate Adaptation: ...3. Ca²⁺ ENTRY BLOCKED: Shows that the adaptation process relies on Ca²⁺-ACTIVATED K⁺ CHANNELS. 4. Source Unknown: ...5. EBIO enhances the EFFECTIVENESS of Ca²⁺-ACTIVATED K⁺ CHANNELS, indicating their role in firing rate adaptation.

Question 26

Burst Firing: HOW DO T-TYPE Ca²⁺ CHANNELS AFFECT BURST FIRING AND EXCITABILITY? = 5

Answer 26

1. Example 1: Low Threshold Ca²⁺ Channels (T-type) 2. INACTIVATED (NOT AVAILABLE) at NORMAL MEMBRANE POTENTIAL. 3. AVAILABLE at HYPERPOLARIZED MEMBRANE POTENTIAL (e.g., -75 mV). 4. DIFFERENT RESPONSE to the same DEPOLARIZING STIMULUS due to channel availability. 5. FIRING PROPERTIES and EXCITABILITY change when DIFFERENT CHANNELS are made available or unavailable.

Question 27

HOW DO H-TYPE CHANNELS CONTRIBUTE TO BURST FIRING AND HYPERPOLARIZATION Burst Firing: 6

Answer 27

1. Small Depolarization opens Ca²⁺ Voltage-Gated Channels and subsequently the “USUAL” Na⁺ Voltage-Gated Channels. 2. Example 2: H-Type Channels ...3. OPEN in response to HYPERPOLARIZATION, causing SMALL DEPOLARIZATION. ...4. OPEN to both Na⁺ and K⁺. ...5. STRONG DEPOLARIZATION from action potentials CLOSES H-Type Channels and Ca²⁺ Voltage-Gated Channels. ...6 Allows HYPERPOLARIZATION to develop, leading to another BURST.

Question 28

So ionotropic receptors and ion channels show large variety and their action can be modulated in several ways

Answer 28

So ionotropic receptors and ion channels show large variety and their action can be modulated in several ways

Question 29

WHAT ARE THE MAIN MECHANISMS OF MODULATION FOR IONOTROPIC RECEPTORS AND ION CHANNELS?

Answer 29

ionotropic Receptors and Ion Channels: - LARGE VARIETY in types and functions. - MODULATION of their action can occur through several mechanisms. Key Points: - IONOTROPIC RECEPTORS: Ligand-gated ion channels activated by neurotransmitters. They can be EXCITATORY (increase Na⁺ permeability) or INHIBITORY (increase Cl⁻ or K⁺ permeability). - ION CHANNELS: - VOLATAGE-GATED: Activated by changes in membrane potential. - LIGAND-GATED: Activated by neurotransmitter binding. - MECHANICALLY-GATED: Activated by mechanical forces. - ALWAYS OPEN: Continually allow ions to pass through.

Question 30

Metabotropic Receptors: 4 HOW DO METABOTROPIC RECEPTORS DIFFER FROM IONOTROPIC RECEPTORS IN TERMS OF MECHANISM AND EFFECTS?

Answer 30

1. INDIRECT PATHWAY: Do not directly open ion channels. 2. OFTEN INVOLVES G-PROTEIN PATHWAY: Activate G-proteins that initiate intracellular signaling. 3. ENZYME CASCADE: Leads to a chain reaction of events within the cell. 4. SLOW ACTION, COMPLEX EFFECTS: Effects are longer-lasting and more complex compared to ionotropic receptors.

Question 31

Ligand-Gated Ion Channels: 3

Answer 31

1. NEUROTRANSMITTER BINDS: - The Neurotransmitter binds to the receptor. 2. CHANNEL OPENS: - The channel undergoes a conformational change and opens. 3. IONS FLOW ACROSS THE MEMBRANE: - Ions move through the channel and across the membrane.

Question 32

G-Protein-Coupled Receptors: 5

Answer 32

1. NEUROTRANSMITTER BINDS: Neurotransmitter binds to the receptor. 2. G-PROTEIN IS ACTIVATED: The binding activates the G-protein. 3. G-PROTEIN SUBUNITS OR INTRACELLULAR MESSENGERS MODULATE ION CHANNELS: The activated G-protein subunits or messengers influence ion channels. 4. ION CHANNELS OPEN: The ion channels open as a result of modulation. 5. IONS FLOW ACROSS THE MEMBRANE: Ions move through the open channels and across the membrane.

Question 33

G-Proteins: 4 WHAT IS THE FUNCTION OF G-PROTEINS IN THE ACTIVATED AND INACTIVATED STATES, AND HOW DOES THIS AFFECT CELLULAR SIGNALING?

Answer 33

1. SPECIALIZED PROTEINS: G-proteins are specialized proteins involved in cell signaling. 2. BIND NUCLEOTIDES: They can bind guanosine triphosphate (GTP) and guanosine diphosphate (GDP). ...3. GTP ACTIVATED STATE: When bound to GTP, the G-protein is in its activated state. ...4. GDP INACTIVATED STATE: When bound to GDP, the G-protein is in its inactivated state.

Question 34

Metabotropic Receptors: 2 HOW DO G-PROTEINS MODULATE ION CHANNELS DIRECTLY IN THE SHORT-CUT PATHWAY OF METABOTROPIC RECEPTORS?

Answer 34

1. SHORT-CUT PATHWAY: -- Metabotropic receptors can use a short-cut pathway. 2. G-PROTEINS MODULATE ION CHANNELS DIRECTLY: -- G-proteins can modulate ion channels directly without requiring intermediate steps.

Question 35

Metabotropic Receptors: Modulation of Excitability ...5 HOW DOES THE ACTIVATION OF β-ADRENERGIC RECEPTORS LEAD TO CHANGES IN POTASSIUM CHANNEL FUNCTION THROUGH THE G-PROTEIN PATHWAY?

Answer 35

1. B RECEPTOR BINDING TO NE: Noradrenaline (NE) binds to β-adrenergic receptors. 2. G-PROTEIN ACTIVATION: This activates the G-protein. 3. ATP TO cAMP: ATP is converted to cyclic AMP (cAMP) by adenyl cyclase. 4. cAMP ACTIVATES PROTEIN KINASE: cAMP activates protein kinase. 5. PROTEIN KINASE MODULATES POTASSIUM CHANNEL: Protein kinase modulates potassium channels, affecting their function and thereby modulating neuronal excitability.

Question 36

Metabotropic Receptors: G-Protein Second Messengers = 3 HOW DO G-PROTEIN SECOND MESSENGERS AFFECT MEMORY FORMATION AND SYNAPTIC PLASTICITY IN NEURONS?

Answer 36

1. G-PROTEIN SECOND MESSENGERS: Involved in signaling pathways inside the neuron. 2. EFFECTS INSIDE THE NEURON: Influence various cellular processes such as enzyme activation, changes in ion channel activity, and alterations in gene expression. 3. ROLE IN MEMORY: Critical for processes like synaptic plasticity and memory formation, impacting long-term potentiation (LTP) and other memory-related functions.

Question 37

Metabotropic receptors G-protein second messengers: effects inside the neuron

Answer 37

diagram on slide 33

Question 38

Metabotropic Receptors: G-Protein Second Messengers HOW DO G-PROTEIN SECOND MESSENGERS INFLUENCE GENE EXPRESSION AND TRANSCRIPTIONAL REGULATION IN NEURONS? 2

Answer 38

1. G-PROTEIN SECOND MESSENGERS: Affect various intracellular processes in neurons. 2. DOWNSTREAM TRANSCRIPTION REGULATION: G-protein signaling can influence gene expression by regulating transcription factors and other molecular pathways.

Question 39

Metabotropic receptors G-protein second messengers: effects inside the neuron Downstream transcription regulation of genes

Answer 39

diagram on slide 34

Question 40

Metabotropic Receptors: Why Have Them? = 3 WHAT ARE THE ADVANTAGES OF HAVING METABOTROPIC RECEPTORS IN TERMS OF SIGNAL AMPLIFICATION AND CELLULAR MODULATION?

Answer 40

1. SIGNAL AMPLIFICATION MECHANISM: Metabotropic receptors can amplify signals through second messenger systems, leading to significant and prolonged changes within the cell. 2. MODULATION: They allow for modulation of neuron excitability and synaptic strength over a longer time frame compared to ionotropic receptors. 3. VARIETY OF EFFECTS: Through diverse signaling pathways, metabotropic receptors can influence various cellular processes, including gene expression, protein synthesis, and long-term changes in synaptic plasticity.

Question 41

Why have metabotropic receptors? ANSWER: Signal amplification mechanism

Answer 41

the diagram on slide 35

Question 42

HOW DO THE TIME-COURSE AND MECHANISMS OF IONOTROPIC AND METABOTROPIC RECEPTORS DIFFER IN TERMS OF THEIR IMPACT ON EPSPs AND EXCITABILITY? Time-Course Differences: Ionotropic vs Metabotropic Receptors =

Answer 42

1. iONOTROPIC RECEPTORS: 2. FAST EPSPs: Cause rapid excitatory postsynaptic potentials. 3. SHORT-TERM EFFECTS: Act quickly, leading to immediate changes in membrane potential. 4. DIRECT ACTION: Directly open ion channels upon neurotransmitter binding, allowing ions to flow across the membrane. 5. METABOTROPIC RECEPTORS: 6. SLOW EPSPs: Cause slower excitatory postsynaptic potentials. 7. LONG-TERM EFFECTS: Have longer-lasting effects, influencing cellular processes and synaptic plasticity over time. 8. INDIRECT ACTION: Utilize G-protein-coupled pathways and second messengers to modulate ion channels and other intracellular targets, resulting in a more gradual and sustained response.

Question 42

time-Course Differences: Ionotropic vs Metabotropic Receptors

Answer 42

diagram on slide 36

Question 43

Other Chemical Messengers = 9 WHAT ROLES DO GROWTH FACTORS LIKE NGF AND BDNF PLAY IN NEURONAL FUNCTION AND DEVELOPMENT?

Answer 43

1. NEURONS AND GLIA: 2. Have receptors for signals beyond neurotransmitters. 3. CHEMICAL SIGNALS: 4. NERVE GROWTH FACTOR (NGF): Involved in neuron survival and differentiation. 5. BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF): Plays a role in synaptic plasticity and neurogenesis. 6. OTHERS: NT-3, CNTF, EGF, FGF, etc. 7. RECEPTORS: 8. TYROSINE KINASE (trk) PROTEIN FAMILY: Many growth factor receptors are part of this family. 9. ROLES: Critical for neuron growth, development, and survival.

Question 44

Ion channel diversity underlies action potential firing pattern

Answer 44

Ion channel diversity is key to the variety of action potential firing patterns.