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Neuro > Lecture 8:Membrane Mechanisms > Flashcards

Lecture 8:Membrane Mechanisms Flashcards

1
Q

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

and how can neurons switch between different firing patterns?

A

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.
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2
Q

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

A

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
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3
Q

firing patterns on slide 4

A

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

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4
Q

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

A
  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
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5
Q

Different types of ion channels and receptors: 4

A
  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).
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6
Q

Basic Chemical Neurotransmission

PRESYNAPTIC: 2

A
  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.
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7
Q

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

A
  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)
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8
Q

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

A

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)

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9
Q

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

A

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.

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10
Q

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

A
  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.

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11
Q

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

A
  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.

  1. FUNCTION OF MODULATION BY ZINC:
    …7. PREVENTING GLUTAMATE EXCITOTOXICITY
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12
Q

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

A
  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.

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13
Q

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

A
  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.

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14
Q

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

A
  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

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15
Q

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

A
  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.

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16
Q

Post-Inhibitory Rebound

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

A
  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.

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17
Q

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

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

…2.SOURCE UNKNOWN.

  1. 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.

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18
Q

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

A
  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.
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19
Q

Which K⁺ channel subtypes exhibit refractory periods and inactivation,

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

A
  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
20
Q

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

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

…2. Will delay depolarization.

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

…4. Become available during afterhyperpolarization.

  1. During Next Depolarization Towards Threshold:

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

…7. Gives Greater Range of AP Firing Rates.

21
Q

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

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

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

  1. 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.

22
Q

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

A
  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.

23
Q

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

A
  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.

  1. IN NEUROPATHIC PAIN ANIMAL MODELS:

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

24
Q

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

Firing Rate Adaptation = 4

A
  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.
25
Q

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

A
  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.

  1. Source Unknown:

…5. EBIO enhances the EFFECTIVENESS of Ca²⁺-ACTIVATED K⁺ CHANNELS, indicating their role in firing rate adaptation.

26
Q

Burst Firing:

HOW DO T-TYPE Ca²⁺ CHANNELS AFFECT BURST FIRING AND EXCITABILITY?

= 5

A
  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.
27
Q

HOW DO H-TYPE CHANNELS CONTRIBUTE TO BURST FIRING AND HYPERPOLARIZATION

Burst Firing: 6

A
  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.

28
Q

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

A

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

29
Q

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

A

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.
30
Q

Metabotropic Receptors: 4

HOW DO METABOTROPIC RECEPTORS DIFFER FROM IONOTROPIC RECEPTORS IN TERMS OF MECHANISM AND EFFECTS?

A
  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.
31
Q

Ligand-Gated Ion Channels: 3

A
  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.
32
Q

G-Protein-Coupled Receptors: 5

A
  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.
33
Q

G-Proteins: 4

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

A
  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.

34
Q

Metabotropic Receptors: 2

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

A
  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.
35
Q

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?

A
  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.
36
Q

Metabotropic Receptors: G-Protein Second Messengers = 3

HOW DO G-PROTEIN SECOND MESSENGERS AFFECT MEMORY FORMATION AND SYNAPTIC PLASTICITY IN NEURONS?

A
  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.
37
Q

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

A

diagram on slide 33

38
Q

Metabotropic Receptors: G-Protein Second Messengers

HOW DO G-PROTEIN SECOND MESSENGERS INFLUENCE GENE EXPRESSION AND TRANSCRIPTIONAL REGULATION IN NEURONS?

2

A
  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.
39
Q

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

Downstream transcription
regulation of genes

A

diagram on slide 34

40
Q

Metabotropic Receptors: Why Have Them? = 3

WHAT ARE THE ADVANTAGES OF HAVING METABOTROPIC RECEPTORS IN TERMS OF SIGNAL AMPLIFICATION AND CELLULAR MODULATION?

A
  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.
41
Q

Why have metabotropic
receptors?

ANSWER:
Signal amplification
mechanism

A

the diagram on slide 35

42
Q

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 =

A
  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.
42
Q

time-Course Differences: Ionotropic vs Metabotropic Receptors

A

diagram on slide 36

43
Q

Other Chemical Messengers = 9

WHAT ROLES DO GROWTH FACTORS LIKE NGF AND BDNF PLAY IN NEURONAL FUNCTION AND DEVELOPMENT?

A
  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.
44
Q

Ion channel diversity
underlies action potential firing pattern

A

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

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