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Neuroscience > Lecture 4 > Flashcards

Lecture 4 Flashcards

Midterm 2

1
Q

What is the synapse

A
  • the location where neurons and a postsynaptic cell communicate
  • axon terminal from one neuron communicates via neurotransmitter with region of membrane of another neuron, muscle cell or glad to form synapse
  • the primary location of neural communication with another cell
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2
Q

What is the difference between presynaptic and postsynaptic membranes

A
  • presynaptic membranes deliver information in the form of neurotransmitters
  • postsynaptic membranes receive information because they have receptors for neurotransmitters
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3
Q

The process of the synapse

A
  • action potential travels down the axon to the presynaptic terminals which causes the release of chemicals (neurotransmitter) into synaptic cleft
  • Neurotransmitters bind to the postsynaptic cell
  • chemicals released by the presynaptic cell influence a response of the postsynaptic cell (ie a neuron in the brain, spinal cord, etc)
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4
Q

what is a chemical synaptic transmission?

A

release of a chemical at a synapse whereby one cell influences another

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5
Q

7 stages of synaptic communication

A
  1. action potential arrives at the presynaptic terminal
  2. Membrane of the presynaptic terminal depolarizes, opening Ca2+ channels
  3. Influx of CA2+ into the neuron terminal, combined with liberation of Ca2+ from intracellular stores, triggers the movement of synaptic vesicles towards a release site in the membrane
  4. synaptic vesicles fuse with the membrane and release neurotransmitter into the cleft
  5. Neurotransmitter diffuses across the synaptic cleft
  6. neurotransmitter contacts a receptor on the post synaptic membrane and binds to that receptor
  7. Binding causes receptor to change shape
    * SEE DIAGRAM*
    - altered configuration while either open an ion channel associated with the membrane receptor (ligand gated channels) OR activate intracellular messengers associated with the membrane receptor
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6
Q

2 types of synaptic potentials

A
  1. if synapse of neuromuscular, axosomatic or axodendritic: Local potential called postsynaptic potential is generated
  2. If synapse is axoaxonic: Generates local potential called presynaptic inhibition/facilitation
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7
Q

Postsynaptic potentials

A
  • local potential via changes in ion concentration across post synaptic membrane
  • Can cause changes in postsynaptic membrane potential that are either excitatory or inhibitory
  • local depolarization is an excitatory postsynaptic potential
  • local hyper-polarization is an inhibitory postsynaptic potential
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8
Q

excitatory post synaptic potential

A
  • presynaptic neurotransmitters bind to post synaptic cell receptors causing an opening of Na+ or Ca2+ channels
  • causes local depolarization of postsynaptic cell membrane
  • summation of EPSPs lead to generation of action potential
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9
Q

Inhibitory postsynaptic potnetial

A
  • presynaptic neurotransmitters bind to the postsynaptic receptors causing an opening of Cl- (enter cell) or K+ (exit cell) channels
  • causes local hyper-polarization of postsynaptic membrane
  • decreases possibility of action potential
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10
Q

presynaptic facilitation vs presynaptic inhibition

A
  • presynaptic facilitation: occurs when neurotransmitter binding causes local depolarization of the postsynaptic axon terminal resulting in increased release of neurotransmitter
  • presynaptic inhibition: occurs when neurotransmitter binding causes hyper-polarization of the postsynaptic axon terminal resulting in decreased release of neurotransmitter
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11
Q

3 mechanisms for removal of neurotransmitters from the synaptic celft

A
  1. Neurotransmitter transporters: common target for drugs (reuptake inhibitors)
  2. Enzymatic degradation: ie AcH
  3. Uptake by glial cells: Astrocytes
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12
Q

Spatial vs Temporal Summation

A
  • spatial summation: many different synapses must produce EPSPs simultaneously at different locations in the membrane of the postsynaptic cell
  • Temporal Summation: Summation of EPSPs in response to stimuli that occur at the same location in the membrane of the postsynaptic cell but at different times in rapid succession
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13
Q

Integration in postsynaptic cells

A
  • the post synaptic cell has integrated information from many synapses, some of which are EPSPs and some IPSPs
  • integration happens through summation of postsynaptic potentials via synaptic inputs
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14
Q

neurotransmitters and neuromodulators

A
  • both used to convey information among neurons
  • neurotransmitters are released by a presynaptic neuron into the synaptic cleft. They act directly on post synaptic ion channels or indirectly activate proteins inside the post synaptic neuron
  • Neuromodulators are released into extracellular fluid and adjust the activity of many neurons
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15
Q

2 ways that neurotransmitters affect the postsynaptic neuron

A
  1. Directly- By activating ion channels (ionotropic)

2. Indirectly- By activating proteins inside the postsynaptic neuron (metabotropic)

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16
Q

Two types of neurotransmitters

A

Fast Acting: those that act directly (ionotropic). Transmission requires less than 1/1000 of a second. Ie AcH, GABA, glutamate
Slow Acting: Those that act indirectly (metabotrophic). Transmission requires 1/10 of a second to minutes. Ie amines, peptides

17
Q

How do neuromodulators work?

A
  • Alter neural function by acting at a distance away from the synaptic cleft
  • Effects manifest more slowly and usually last longer than those of neurotransmitters which happen in seconds
  • Effects last from minutes to days
18
Q

What is substance P?

A
  • One of the most common neuropeptides
  • stimulates nerve endings at the site of injury and then in the CNS
  • Acts as a neurotransmitters carrying information from the spinal cord to the brain
  • response to pain
19
Q

How are synaptic receptors named and how do they produce actions?

A
  • typically named for neurotransmitter or neuromodulator to which they bind
  • several types of receptors can bind to same neurotransmitter
  • Effect is due to type of receptor
  • product direct or indirect action
  • direct: when the receptor and ion channel make up single functional unit
  • Indirect: Using a cascade of intracellular molecules to activate ion channels or cause other changes within the postsynaptic neurons
20
Q

Three mechanisms that postsynaptic receptors use to transduce signals

A
  1. Directly open ion channels-fast synaptic transmission
  2. Indirectly open ion channels: Slow synaptic transmission
  3. Indirectly activate a cascade of intracellular events-including activating genes and regulating cell processes. Slow synaptic transmission.
21
Q

direct activation of ion channels (ligand gated ion channels)

A
  • ligand gated ion channels consist of proteins that function as both receptors for the neurotransmitter and as ion channels
  • channels open in response to specific chemical ligand binding to the receptor surface
  • gates are closed in resting state
  • fast acting transmission (rapid and brief opening of membrane channels with neurotransmitter binding)
  • ion channel receptors act like a lock and key
22
Q

Indirect activation of ion channels (G-proteins)

A
  • ion channels open indirectly using metabotropic receptors
  • receptor stimulation results in release of G-protein which binds to specific ion channels resulting in their opening
  • G protein can affect more than one channel
  • G protein subunit attached to receptor can be activated and deactivated
  • G protein bound to receptor when inactive
23
Q

G protein second messenger system

A
  • responsible for most profound and long lasting changes in the nervous system
  • ability to effect multiple effector sites and dramatically amplify signal
24
Q

Via second messenger systems the activation of the receptors will…

A
  • activate genes, resulting in changes in quantities of neurotransmitters and receptors
  • open ion channels
  • Regulate intracellular Ca2+ concentrations (cell metabolism)
25
Q

AcH (neurotransmitter and receptor)

A
  • major neurotransmitter of PNS
  • utilized at neuromuscular junction
  • AcH receptors fall into 2 categories:
    1. Nicotinic: ionotropic excitatory at NMJ, autonomic ganglia and some areas of CNS
    2. Muscarinic: G protein receptors. Excitatory or inhibitory acting regulating cardiac muscle, smooth muscle and glands
  • involved in myasthesia gravis and alzeimer’s disease
26
Q

Glutamate

A
  • Main excitatory neurotransmitter of CNS
  • ionotropic or metabotropic
  • involved in long term potentiation (important to learning and development)
  • decreased levels associated with depression
  • increased levels associated with epileptic procedures
27
Q

GABA

A
  • most common fast acting inhibitory neurotransmitter
  • binds to 2 different receptors
    1. Gaba a- ionotropic (Cl- channels producing hyperpolarization, drugs inhibit neural excitation, benzodiazepines (antianxiety), barbiturates (sedation)
    2. GABA b- slow acting receptors linked to ion channels via second messenger. Baclogen (muscle relaxant used in treating muscle contracture in spinal cord injury)
28
Q

Opiods

A
  • inhibit neurons in CNS involved in perception of pain

- ie opium, oxycodon, morphine

29
Q

dopamine

A
  • slow acting inhibitory neurotransmitter which suppresses Ca2+ channels
  • drugs acting on dopamine receptors alter movement, motivation and thinking
  • low levels associated with parkinson’s disease
  • high levels associated with schizophrenia
  • involved with reward mechanisms of the brain
30
Q

Norepinephrine

A
  • flight or fight response
  • excessive levels in panic disorders
  • G protein mediated inhibitory and excitatory
  • two major subtypes:
    1. A Receptors (inhibitory)-relaxation of smooth muscle
    2. B Receptors (excitatory)-contraction of cardiac muscle
31
Q

Serotonin

A
  • responsible for general arousal level
  • affects mood, perception of pain, arousal levels
  • high levels=alertness
  • low levels= REM sleep, depression, suicide
  • Prozac and MDMA: antidepressents which are seratonin reuptake inhibitors
32
Q

Neurotransmitter agonists and antagonists

A

agonists: are drugs that bind to a receptor and mimic the effect of naturally occuring neurotransmitters
Antagonists: are drugs that prevent the release of neurotransmitters or bind to the receptor and impede or block the naturally occuring transmitters

33
Q

pathologies affecting receptors and channels: myasthenia gravis

A
  • disease in which antibodies attack and destroy nicotinic receptors on muscle cells
  • adequate AcH is released into the synaptic cleft but few receptors are available to bind
  • repetitive use of muscles lead to increased weakness
  • symptoms: drooping eyelids, distorted facial expression, problems breathing and swallowing
  • proximal limb weakness causes difficulty climbing stairs, reaching overhead and rising from a chair
  • treatment includes plasmapheresis, immunosuppression and thymectomy

Neuroscience (2 decks)

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