Physiology 2130 Unit 2: Excitable Cells and Synaptic Transmission

excitable cell

cell use its resting membrane potential (RMP) to generate action poteitnal

action potential = electrochemical impulse

excitable cell VS non-excitable cell

• non-excitable cell = X generate action potentials

• EX → excitable cells = neurons, muscles, some endocrine

• EX → rest of body non excitable

What is an action potential?

• rapid electrical signal generated when an excitable cell depolarizes beyond threshold

• occur when open voltage gated ion channel

• all or nothing response → same magnitude

How do excitable cells communicate through action potentials?

• communicate by generating and propagating action potentials along the neuron

• occur w depolarization events in cell if enough depolarization occurs & excitable cells fire to comm. w adjacent cells

What is depolarization?

• process by which ions move in and out of the cell

• GOAL = inside of the cell INC positive relative to the resting membrane potential

• occur cell constant but only when beyond -55mV, AP trigger

what is ion movement is controlled by?

• controlled by membrane proteins such as channels and pumps on membrane

• chemically/ligand gated & voltage gated channels help movement of ions in & out of cell

What are the 6 main components of an action potential?

1. stimulus & RMP

   • trigger VV depolarization events in excitable cell → inside cell INC +

   • RMP ~ −70 mV

   • K⁺ leak channels leaky & X fully closed at rest

   • voltage gated Na channel & chem gated K channel closed

2. Threshold

   • stimulus reaches approximately −55 mV

   • AP triggered

3. Depolarization

   • Voltage-gated Na⁺ channels open

     • Na⁺ enters cell → inside INC (+) → INC K move out of cell to counteract

     • membrane potential -70mV to -30mV

   • leaky K channel open

   • chem gated K channel closed → need chem bind to open

4. Repolarization

   • Voltage-gated K⁺ channels open

   • K⁺ leaves cell

   • voltage gated Na⁺ channels close

5. Hyperpolarization

   • cell INC (-) than RMP = DEC chance AP occur

   • Relative refractory period occurs → harder to do AP

   • chem gated K+ channel open → INC K+ leave cell

   • voltage gated Na+ channel closed → bc open voltage goated K+ channel

   • all channels move K+ out of cell

6. Return to resting membrane potential & resting state

example of Na+ & K+ channel AP

1. local potential depolarizes trigger zone’s axolemma to threshold of -55mV

2. voltage gated Na+ channel active → Na+ enters, axon section depolarizes

3. Na+ channel inactive & voltage gated K+ channel actives

   1. Na+ X enter

   2. K+ excite axon → repolarize

4. Na+ channel returns resting state, repolarize cont.

5. axolemma can hyperpolarize before K+ channel becomes resting state

   1. then return RMP

During hyperpolarization, channels are more selectively permeable to K than leak channels. True / False

True

What happens to the channels during the resting potential and what are they more permeable to

The leak channels open at rest, 20-25 times more permeable to K+ than to N+

What happens to the channels during the depolarization

The channels are selectively permeable to N+ than to K+

Failed initiations

The depolarization events below threshold

Why are voltage-gated Na+ and K+ channels called "voltage-gated"?

b/c it is a change in voltage that triggers their opening

relative VS absolute refractory period

refractory period = time frame after neuron makes AP & X able to fire

absolute = X stimuli makes AP

relative = another AP possible but need INC strong stimuli

• inside cell = INC (-) & harder to reach threshold

what forms the absolute refractory period of the AP?

• Depolarization and repolarization phases

  • Na channel inactive & X reopen until membrane repolarized enough

• During this time, no AP can be elicited → ensure 1 direction AP travel

An AP can be generated during the relative refractory period T/F?

T, but a larger intensity stimulus would be required to produce an AP because the membrane is hyperpolarized

• refractory period = cell is more negative, reaching approximately -90 mV

• now more difficult to reach the threshold of -55M = INC stimulus needed to reach the threshold bc of how (-) cell is

Because of the absolute refractory period during which time the Na+ voltage-gated channels are closed, two APs cannot be fired one on top of the other. True/ False?

True

how do the channels change during a AP?

• Na+ channels active = INC in membrane potential & start of AP

• K+ channels help membrane repolarize

Why does the closing of the potassium channels cause the inside of the membrane to become more positive?

• closing of potassium channels slows the outward flow of K⁺

• cause the inside of the membrane to become less negative (or slightly more positive) before it fully returns to the resting potential

neurons

• excitable cells

• comm. w AP

structure

1. Soma (cell body)

2. Dendrites

3. Axon

4. Axon terminals

5. Myelin sheath

6. Schwann cells

7. Nodes of Ranvier

Soma

(cell body)

has nucleus & most organelles

Dendrites

• branch-like projections from soma

• get signals & info from other neurons → soma

• direct AP → soma

Axon

projections of cell body

AP AWAY from soma

Axon terminals

ends of axon

Release neurotransmitters to communicate with next cell

Myelin sheath

Fatty acid & protein insulating layer surrounding the axon

speeds signal transmission

myelin

• rapid move of APs thru saltatory conduction thru axon

• prevent decay of AP when travel along axon

Schwann cells

Produce myelin and support neuron survival in the PNS

cell surround axon

Nodes of Ranvier

-Gaps in the myelin sheath rich in ion channels that aid rapid AP propagation

-Unmyelinated axon membrane

What is the direction in which an action potential propagates?

Dendrites → Soma → Axon → Axon terminals

DSAAT

saltatory conduction

• occurs in myelinated neurons

• AP jumps from one Node of Ranvier to the next instead of traveling continuously along every section of membrane

Advantages of saltatory conduction

• INC transmission speed by 10-15 times compared with unmyelinated neurons

• INC efficiency

• rapid communication over long distances

• conserve E because fewer ions cross the membrane

What is the all-or-nothing principle of an action potential?

• if membrane depolarization reaches threshold (~−55 mV) → an action potential occurs

• if threshold is not reached → no action potential occurs

• action potentials always same amplitude

What determines the direction of the propagation of an action potential?

The direction is determined by the refractory periods, especially the absolute refractory period.

What happens during the absolute refractory period?

• Voltage-gated Na⁺ channels become inactive

• Another action potential cannot immediately occur in the area that just fired

• Because the membrane behind the AP cannot fire again immediately, the signal moves forward only, preventing backward propagation.

Another AP cannot be elicited while the previous one is in the absolute refractory period. Why?

Because the ion channels are inactive during this time.

The relative refractory period (or hyperpolarization phase) makes the membrane more negative relative to the resting potential. T/F?

T, As a consequence, it is harder to reach threshold. The depolarization of the membrane will ONLY move in one direction

The AP only travels in one direction due to the absolute refractory period in only myelinated neurons. T/F?

False, both myelinated and unmyelinated neurons.

propagation of AP

• propagate 1 direction in neuron

  • dendrite → soma → axon → axon terminals

1. neurotransmitter released from presynaptic neuron

2. bine to ion channel in postsynaptic cell & depolarize

   1. depolarize = inside INC + than RMP & INC chance AP occur bc + inside closer to -55mV

3. signal propagates to soma

   1. speed vary if axon myelinated or unmyelinated

how is AP propagation unidirectional?

• bc refractory period & another AP X happen when previous one in absolute refractory period

• ion channels inactive

• only move in 1 direction towards axon terminals from soma

BUT during relative refractory period/hyperpolarization, membrane INC (-) can possible but INC force needed bc harder to reach threshold

what cells are in the brain?

• neurons → info transmit & process for body

• gilal cells → make enviro for neuron f(x)

What are glial cells?

• neuroglia

• support cells of the nervous system

• provide the environment necessary for neurons to function properly

• ~ 90% of the brain

Unlike neurons, gilal cells do not primarily transmit electrical signals. T/F?

T

Glial roles include:

Support

Protection

Nutrient delivery

Insulation (myelin production)

Maintenance of neuronal environment

What are different types of neurons present in the brain?

for mammals

• Bipolar neurons

• Unipolar neurons

• Multipolar neurons

Bipolar neurons

• 1 axon + 1 dendrite w branches (2 processes extend from cell body)

• mainly in specialized sensory structures such as the retina

Unipolar neurons

• 1 process extending from the cell body

• straight connect axon & dendrite → soma separate on side

• mainly sensory neurons in the PNS → send sinals to & from spinal cord

Multipolar neurons

• 1 axon with many dendrites

• most common neuron type in the CNS & connect CNS w effector organs

What are 6 examples of glial cells?

CNS →

• Astrocytes

• Oligodendrocytes

• Ependymal cells

• Microglia

PNS →

• Schwann cells

• Satellite cells

Astrocytes (Astrocytes are the most abundant cells in the brain.)

• #1 in brain

• star shape

• Physical and nutritional support

• Transport nutrient to neurons

• Hold neurons in place

• Remove debris

• Digest dead neurons

• Regulate extracellular environment

• Promote synaptic connections

• Participate in injury response

Schwann cells

• gilal cells of PNS

• surrond neruons & keep alive by cover w mylein

• work for dvlp, maintain, f(x) & regen peripheral nerves

Oligodendrocytes

Produce myelin in CNS → layered phospholipid membrane support & insulate axon

1 cell can myelinate several axons

Ependymal cells

• line ventricles of brain & spinal cord

• Regulate ion and glucose movement

• Help distribute hormones and signal molecules associated with the CNS

• shape of cuboidal w cillia & microvilli used to circulate & make cerebrospinal fluid (CSF)

Microglia

• immune defense cells → dynamic move to look invaders

• emove damaged tissue and pathogens → engulf

• small cells sparsely located

• remove previously formed synapses X needed

Satellite cells

• Support neurons in the PNS

• Provide nutrients and structural support → bundle axons together & stop from touching

• like astrocytes of CNS

Multiple Sclerosis (MS)

• autoimmune disease → 2X W get

• can stop natural flow AP & X transmission occur

• progressive disease of CNS → X cure

• chronic inflame response for myelin sheath & immune system attack them around axons

EFFECTS

• myelin damage slows or blocks action potential transmission

• Communication between neurons becomes impaired

• Muscles may fail to receive signals

• lead to weakness or paralysis → if nerve damaged connected to muscle & X contract

nervous system formation

1. central nervous system (CNS)

   • brain

   • spinal cord

2. peripheral nervous system (PHS)

   • somatomotor → voluntary w skeletal

   • autonomic → automatic w organs & control brain

   • nerves go from CNS to muscles & organs

central nervous system (CNS)

• Brain + Spinal cord

Main function:

• integrates and processes information

• Coordinates responses and body functions

Peripheral Nervous System (PNS)

• nerves connecting the CNS to the rest of the body

• carry signals between organs and the CNS

(1) Somatomotor system

• voluntary w skeletal

(2) Autonomic nervous system

• automatic involuntary w organs & control brain

Compare the central and peripheral nervous system

Comparison: Both systems communicate through neurons and action potentials, but the CNS mainly processes information while the PNS transmits it.

what are the anatomical and functional structures of the brain?

• 2 cerebral hemispheres → L & R

  • contralateral control → L control R, R control L

    • control muscles, sensory info

• gyri = bumps on brain

• sulci = dips/valley

• 4 lobes

  • frontal

  • temporal

  • parietal

  • occipital

what is the use of gyri and sulci?

• INC SA of brain

• landmarks divide cerebral hemispheres into lobes (4)

Frontal lobe

• planning & perception of stimuli

• (1) Primary motor cortex → process input from skeletal muscles

• (2) Premotor cortex → motor association area

  • work w/ prefrontal cortex → integrates info abt movement w other sensory input to make perception of stimuli

• (3) Prefrontal cortex

Temporal lobe

• olfaction

• short term memory → mediate storage & recall

• sound

• get & process signals from auditory nerve & integrate w other sensory input

  • (1) primary auditory cortex

  • (2) auditory association area

Parietal lobe

• touch and sensory integration

• (1) primary somatosensory cortex → get input from major senses

  • EX →

• (2) somatosensory association areas → intergrate sensory info w other association areas

Occipital lobe

• vision & visual processing

• (1) primary visual cortex → input from optic nerve

• (2) visual association area → process visual info & integrate w other sensory information

Cerebellum

• posterior → under occipital lobe & above brain stem

• ROLES →

  • process sensory info to

  • coordinate moves

• #1 # of neurons in the brain → get input for many things

  • somatic receptors

  • receptors for equilibrium

  • balance and motor neurons from higher centers of the brain

Brain stem

• controls some basic functions of body → heart rate & respiration

• includes 9 cranial nerves

• formation → midbrain, pons, medulla oblongata

  • medulla is continuous to the spinal cord

Corpus callosum

• dense bundle nerve fibers

• path & connect 2 cerebral hemispheres → help integrate sensory & motor info both sides & coordinate whole body movement & f(x)

diencephalon

• (1) thalamus → get sensory input from spinal cord & integrates before send to cortex

• (2) hypothalamus → regulates endocrine function w hormone release

Thalamus

• get sensory input, process & integrate sensory info BEFORE send to cortex

• get info as it travels from the spinal cord

Hypothalamus

USES →

• regulates endocrine functions w hormone release

• regulate homeostasis systems

  • temp

  • body water

  • hunger/ food intake

  • cardiovascular

  • circadian clock

  • emotions

  • thirst

ANATOMY →

• base of brain, anterior brain stem, under thalamus

• use negative feedback system

  • stimuli trigger homeostasis change

  • sensor see info

  • control center sends info →

    • effector

    • mechanism (effector also uses this to send info back to stimuli integration center to regulate signaling)

Midbrain

• mesencephalon

• bridge lower brainstem & upper diencephalon

• f(x)

  • eye movement

  • visual and auditory reflexes

Pons

• USE → relay station w cerebellum & cerebral cortex

• regulate breathing w medulla

Medulla

• main control 4 involuntary f(x)

  • breathing

  • blood pressure

  • swallowing

  • hear rate

• corticospinal track fibers from motor cortex cross to opp sides of spinal cord →innervate muscles on opp sides

pituitary gland/hypophyse

• controlled by hypothalamus

• diff parts secrete diff hormones & diff anatomy

• USE →

  • regulates endocrine organs

  • hormones secret differ based on each section

    • EX → stress, lactation, growth, dvpmt, rpxdtn

• anterior pituitary → from epithelial tissue of pharynx

• posterior pituitary → from neural tissue of hypothalamus

Hormones

• chemicals cells use to comm over "long-distance" w blood stream

• info → growth, stress, development, homeostasis regulation from higher integration centers to effector organs

  • EX→ skin, muscles and other tissues

Because myelin is required for fast saltatory conduction, damage significantly impairs communication throughout the nervous system. T/F?

T

The premotor cortex (motor association area) works with the prefrontal cortex to integrate movement information with other sensory inputs to generate perception (or interpretation) of stimuli. T/F?

T

synapse

• where impulses passed by neurons to comm. w cells

• (1) electrical

• (2) chemical → presynaptic, synaptic clef, post synaptic neruon

electrical synapse

• site of cell to cell comm

• neurons directly exchange ions w channels → create AP in next cell

• channels = 2 communicating cell long

chemical synapse

• site cell to cell comm. w excitable cell release neurotransmitter to comm.

• 2 neurons X have channel → separated by synaptic cleft

• components

  • presynaptic neuron

  • synaptic clef

  • post synaptic neuron

neurotransmitter

• chem. released by neuron @ axon terminals

  • GOAL = comm. w other neurons

PROCESS

1. synthesized & stored w synaptic vesicles

2. when released w/ AP, diffuse synaptic cleft

3. bind to receptor/ ion channels on post synaptic cleft → ion influx in the cell

   • binding neurotransmitter to channel = electrical impulses that are EPSP, or IPSP

presynaptic neuron

• transmit info → synaptic cleft (w axon & axon terminals) → dendrites next neuron

synaptic cleft

small space btwn axon terminals of 1 neuron & dendrites another

area where neurotransmitters released

post synaptic neuron

transmit info ← synaptic cleft from dendrites & toward soma

what is the exact process of synaptic transmission?

1. AP @ axon terminal → depolarizes pre-synaptic membrane

2. Voltage-gated Ca²⁺ channels open

   • voltage change by AP = channel open & Ca2+ enter

   • on synapse, membrane axon terminal

3. Ca²⁺ enters cell

   • trigger biochemical rxn w release neurotransmitter

   • synaptic vesicles fuse w pre-synaptic membrane w exocytosis

4. neurotransmitters released from synaptic vesicle → synaptic cleft

   1. bind to receptors on the post-synaptic membrane → diffuse out of synapse down [gradients]

   2. break down by enzymes on synaptic cleft→ re-uptake into pre-synaptic cell to be recycled

5. neurotransmitters bind = open ligand-gated receptors on post-synaptic membrane

   • ion channels OR trigger events that open ion channels

   • RESULT → graded potentials

6. neurotransmitter bind = receptors de/hyper polarization post-synaptic cell (based on which channel opens)

graded potential

small localized subthreshold depolarizations of membrane

• diff size occur & amts stack up → based on stimuli magnitude

• made by opening ligand gated ion channels

• decay when farther from stimulation site

• X make AP

• (1) EPSP (depolarizing potentials)

• (2) IPSP (hyperpolarizing potentials)

excitatory post synaptic potential (EPSPs)

• X make AP

• localized → depolarization 1 area on membrane

• summed → stack to make INC depolarization & INC # bring closer to AP

• graded → INC stimuli = INC depolarization

• decay → when propagate across membrane (INC far depolarization from stimuli = smaller)

occur when neurotransmitter:

(1) open K+ channel → move out cell = inside INC (-) & depolarization occur

• mainly Na move in & little K move out, both needed bc EPSP use non selective cation channel

(2) open Na+ channel → move in cell = inside INC (+) & depolarization occur

inhibitory post synaptic potential (IPSPs)

• localized → hyperpolarized on 1 area membrane

• graded → INC stimuli = INC hyperpolarization

• summed → stack to make INC hyperpolarization & INC # farther from AP

• decay → when propagate across membrane (INC far depolarization from stimuli = smaller)

• decay → when propagate across membrane (INC far depolarization from stimuli = smaller)

occur when neurotransmitter:

(1) open K+ channel → move out cell = inside INC (-) & hyperpolarization occur

(2) open Cl- channel → move in cell = inside INC (-) & hyperpolarization occur

EPSP vs IPSP

EPSP → depolarize below threshold & INC inside (+)

• turn on neuron

IPSP → hyperpolarize below RMP & INC inside (-) than RMP

• shut off neuron

size of stimuli = INC change membrane potential

both graded potential b/c size based on stimuli

how do EPSP & IPSP affect AP production?

• @ 1 time → 1 post synaptic cell get many inputs (EPSP or IPSP) from many presynaptic cells

  • vary based on →

    • (1) type of presynaptic neuron synapsed onto post synaptic neuron

    • (2) type of neurotransmitter released

• AP formed based on sum of IPSP & EPSP when get to axon hillock

  • AP = all or nothing so need to reach threshold to occur

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IMAGE

• (1) IPSP & EPSP decay as get to axon hillock

• (2) IPSP & EPSP summed there

• (3) BUT threshold X met here so X AP made

axon hillock

trigger zone that determines if AP will occur

• AP generated based on sum IPSP & EPSP @ this location

why does depolarization have to occur at axon hillock?

• dendrites & soma & have voltage gated channels → need for AP formation

• voltage gated channels occur INC [ ] @ axon hillock & axon membrane

how does decay affect graded potentials ?

• farther from site of stimuli = DEC intensity

• for enough depolarization need strong & large enough current of EPSP to spread from synpase on axon hillock

  • use temporal & spatial summation

how do graded potentials activate APs?

• use summation to ensure depolarization large & strong enough reach threshold

• effect of EPSP & IPSP sun at axon hillock & if above threshold, AP fire

spatial summation

• ADD effect

• many EPSP made at diff synapses on SAME POSTsynaptic neuron at SAME time

• many neurons fire same time

same for IPSP but opp effect → INC hyperpolarization

temporal summation

• ADD effect

• many EPSP made at SAME synapse by many high frequency APs on PREsynaptic neuron

• 1 neuron fire many times

same for IPSP but opp effect → INC hyperpolarization

what are the types of neurotramitters?

1. acetylcholine

   • acetyl choline

2. biogenic amines

   • catecholamine → epinephrine, norepinephrine

   • catecholamine → dopamine

   • serotonin

3. amino acids

   • glutamate & aspartate

   • GABA & glycine

4. neuropeptides

   • endogenous opioids → endorphins

   • vasoactive intestinal peptides

acetylcholine (ACh)

• excitatory

• CNS & PNS

• muscles control & memory → w release @ NMJ

USES →

• neurotransmitter @ NMJ

• bind to nicotinic receptors in NMJ + autonomic ganglion

• bind to muscarinic receptors @ target organ of PSYN

• neurotransmitter of autonomic ganglion

epinephrine & norepinephrine

• excitatory

• biogenic amines → catecholamine

• PNS → adrenal gland in medulla

• fight/flight response