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Physiology 209 > Nerve/Synapse > Flashcards

Nerve/Synapse Flashcards

1
Q

How many neurons comprise the nervous system

A

100 billion

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2
Q

Neuron structure characteristics

A
  • cell body (soma)
  • branching dendrites
  • a single axon (which may extend anywhere from a few milliliters to more than a meter)
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3
Q

Resting Membrane potential of a typical neuron?

A

-60 to -70 mV compared to outside

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4
Q

At rest what is the neuronal membrane highly permeable to?

A

K+

must less permeable to other physiological ions: Na+, Ca++

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5
Q

electrical gradient in cell membrane

A

accumulation of unpaired negative ions inside the cell creates an electrical gradient that tends to pull K+ ions back into the cell.

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6
Q

The Nernst Equation

A

-The membrane potential at equilibrium
-Equation:
Eion = 2.3RT/zF log [ion]out/[ion]in

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7
Q

Leak Potassium channels

A
  • highly selective for K+ over other physiological ions
  • leak channels are open at resting membrane potential
  • causes the resting permeability to K+
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8
Q

What is the membrane potential determines by

A
  • conc. gradients
  • relative permeabilites of membrane to different physiological ions

*The dominant permeability makes greatest contribution to the membrane potential.

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9
Q

Sodium-Potassium Pump

A
  • maintains sodium and potassium gradient
  • uses energy to produce ATP hydrolysis to pump sodium out and potassium in against their concentration gradients
  • Na and K gradients run down faster when the neuron is firing a lot of action potentials
  • the pumps have to keep up with neuronal activity

-2 K+ in and 3 Na+ out

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10
Q

Voltage-gated Sodium Channels

A

The rising (depolarizing) phase of the action potential is caused by sodium ions flowing into the cell through voltage-gated sodium channels. Sodium channels have three critical properties:

  1. They are closed at the resting membrane potential but are open when the membrane depolarizes
  2. They are selective for Na+
  3. The open channel rapidly inactivates, stopping the flow of Na+ ions.
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11
Q

Voltage-gated potassium channels

A
  • secondary factor that contributes to the falling phase of the action potential
  • delayed activation of this channel
  • repolarizes the cell
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12
Q

Absolute refractory period

A

-the membrane is completely unexcitable

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13
Q

Relative refractory period

A

-a brief overshoot in membrane repolarization caused by activation of voltage-gated K channels

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14
Q

Tetrodotoxin

A
  • produced by puffer fish

- an extremely potent inhibitor of sodium channels

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15
Q

Batrachotoxin

A
  • secreted by phyllobates frogs

- a powerful sodium channel activator

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16
Q

Lidocaine, Benzocaine, Tetracaine, and Cocaine are all what?

A

Local Anesthetics

-blocks sodium channels

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17
Q

Phenytoin (Dilantin), Carbamazepine (tegretol), Lamotrigine are all what?

A

Antiepileptics

-blocks sodium channels

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18
Q

Why does size of the axon matter?

A

The thicker the axon the faster is propagates.

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19
Q

Myelin

A
  • acts as an electrical insulator
  • formed by Schwann cells( in the PNS) or oligodendrocytes (in the CNS)
  • interrupted periodically by gaps called Nodes of Ranvier
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20
Q

Nodes of Ranvier

A
  • Gaps along the axon
  • These regions of bare axon contain very high concentrations of voltage-gated sodium channels, enabling the signal to be regenerated at periodic intervals.
21
Q

Multiple Sclerosis

A

-caused by loss of myelin.

22
Q

Three main types of synapses

A
  • Axodendritic
  • axosomatic
  • axoaxonic
23
Q

What triggers neuraltransmitter release

A

-Activation of voltage-gated calcium channels

24
Q

Ligan-gated ion channels in the postsynaptic spine

A

-act as postsynaptic receptors for transmission at brain synapses.

25
Q

Fundamental steps of Chemical Synaptic Transmission

A
  1. the action potential invades the presynaptic terminal. Calcium channels open, resulting in Ca++ influx into the terminal
  2. Synaptic vesicles fuse with the presynaptic membrane, releasing transmitter into the synaptic cleft
  3. Transmitter diffuses across the cleft and activates receptors in the postsynaptic membrane.
26
Q

How vesicles containing neurotransmitters are releases?

A

-Synaptic vesicles and Ca channels are localized to the presynaptic terminal by a complex of proteins that regulates vesicle fusion.

27
Q

Postsynaptic response to

A

two options

  1. An excitatory postsynaptic potential (EPSP) which depolarizes the postsynaptic membrane
  2. Inhibitory postsynaptic potential (IPSP), which hyperpolarizes the postsynaptic membrane.
28
Q

Glutamate

A

-the main excitatory neurotransmitter in the brain

29
Q

Two types of ionotropic glutamate receptors

A
  • ion channels that open in response to binding of small molecuels (eg. neurotransmitter) to receptor sites on their external surfaces.
  • the rapid excitatory transmission at synapses is primarily due to the actions of glutamate on these receptors
  1. AMPA receptors
  2. NMDA receptors
30
Q

AMPA receptors

A
  • ionotropic glutamate receptor

- responsible for the “fast” EPSP at excitatory synapses

31
Q

Excitatory Postsynaptic potential (EPSP)

A
  • small, transient depolarization of the postsynaptic spine
  • in typical brain synapses, the depolarization caused by a single EPSP is (>/=) a few millivolts and last around 20 msec
  • depolarization cause by a single EPSP is too small to depolarize the axon initial segment to threshold.
  • from 50 to 100 EPSPs must sum at the initial segment to initiate an action potential
  • These near-simultaneous EPSPs can come from multiple synapses acting in synchrony and/or from individual synapses, activated at high frequencies.
32
Q

NMDA receptors

A

Key Properties

  • At resting membrane potentials, the pore is blocked by Mg++; depolarization expels, Mg++, enabling the pore to conduct.
  • The open pore is highly permeable to Ca++ as well as monovalent cations.
33
Q

Synaptic Plasticity

A
  • when highly active excitatory synapses become stronger (i.e. the EPSPs become larger)
  • involves NMDA receptors
34
Q

Long-term potentiation (LTP)

A
  • model of synaptic plasticity
  • high frequency activity depolarizes the postsynaptic spine, removing Mg++ block of NMDA receptors and enabling them to conduct Ca++.
  • EPSPs are larger, hours after inductions of LTP

-Control –> induction –> LTP

Shows that highly active synapses will get stronger

35
Q

Long-term (LTD)

A

-a complementary synaptic phenomenon, suggests that active strengthening and weakening of brain synapses, sculpts out networks of neuron connectivity.

36
Q

Exitotoxicity

A
  • high concentrations of glutamate are toxic to neurons
  • thought to involve Ca influx through NMDA receptors
  • likely to contribute to neuronal degeneration after stroke and in some neurodegenerative diseases.
37
Q

Y-aminobutyric acid (GABA)

A
  • main inhibitory neurotransmitter

- postsynaptic receptor responsible for the IPSP is called the GABA receptor

38
Q

GABAa Receptor

A
  • ionotropic receptor
  • activation causes influx of Cl- which hyperpolarizes the postsynaptic membrane.
  • potentiated by a variety of drugs including benzodiazepines (Xanax), barbiturates, and ethanol
39
Q

Site of excitatory inputs

A

on the dendritic spines

40
Q

Site of inhibitory inputs

A

often clustered on or near the cell soma. Where the effect is maximal

41
Q

Glutamate synapses have both:

A
  1. ionotropic receptors (AMPA and NMDA receptors)

2. Metabotropic glutamate receptors (mGLuR’s)

42
Q

Whtat does activation of mGluR’s by glutamate do

A

it relays a chemical signal to the inside of the postsynaptic neuron.

43
Q

What does activation of mGluR’s do?

A

-activation of mGluR’s by glutamate generates a chemical signal, called a second messenger, inside the postsynaptic spine.

44
Q

Second Messengers

A
  • activate a range of cellular proteins, including
  • ion channels
  • protein kinases (affects the neurotransmitter receptors and enzymes)
  • transcription factors(activates transcription factors –> nucleus)
45
Q

Neuromodulators

A

Many types of neurotransmitters interact mainly or entirely with metabotropic receptors.

  • Dopamine
  • Serotonin
  • norepinephrine
  • neuropeptides like Substance Y
  • endorphins

Not directly involved in the fast flow of neural information but modulate global neural states, influencing alertness, attention and mood.

46
Q

Neurons that release neuromodulators originate in?

A
  • the small brain stem or midbrain nuclei
  • their axons project diffusely throughout the brain

SA- Substantia Nigra
VTA - Ventral Tegmental Area

47
Q

Neuromodulator systems

A
  • important targets for wide range drugs
  • e.g. antidepressants, such as Prozac affect serotonergic transmission whereas amphetamines, cocaine and other stimulants typically affect dopamine and norepinephrine transmission
48
Q

Axoaxonic Synapses

A

-modulate neurotransmitter release from the presynaptic terminal

  • unmodulated transmission (synapse directly to neural cell)
  • Presynaptic inhibition (synapse at synapse to decrease release)
  • Presynaptic facilitation (synapse at synapse to increase release).

Physiology 209 (9 decks)

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