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PHPY 301 > 7. Lectures 15.5, 16, 17 > Flashcards

7. Lectures 15.5, 16, 17 Flashcards

1
Q

What are cys-loop receptors?

A

Characteristic loop formed by a disukfude bond between 2 cysteine residues
13 amino acids apart

4 members of cys-loop family:
Acetylcholine nicotinic (nAChR)- cation selective (Na, K, Ca)
Serotonin (5-HT receptor)- cation selective
Glycine (GlyR)- anion selective (just Cl)
GABA (GABA receptor)- anion selective

Slide 16 lecture 15.5

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2
Q

What is GABA?

A

Main CNS inhibitory neurotransmitter
Mediates large majority of synaptic inhibition in the CNS
GABA and glycine receptors are ionotropic (Cl selective)

Synaptic inhibition is tightly regulated: too much causes loss of consciousness and coma, too little leads to seizure

Slide 17 lecture 15.5

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3
Q

What do benzodiazepines and barbiturates do?

A

Benzodiazepines- increase Cl- conductance
Increase frequency of channel opening

Barbiturates- increase the duration of channel opening

Each binds it’s own specific extracellular site on GABA

Slide 18 lecture 15.5

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4
Q

What is glutamate and it’s 3 ionotropic receptors?

A

Glutamate is the main CNS excitatory neurotransmitter

3 ionotropic glutamate receptors:
AMPA- glutamate site
NMDA- has glutamate and glycine site, blocked by extracellular Mg2+
Kainate- glutamate site

Receptors are tetramers (4 subunits), heteromultimers
Cation non selective

Slide 19-21 lecture 15.5

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5
Q

What are glutamatergic synapses?

A

AMPA and NMDA channels
AMPA- mostly permeable to Na*
NMDA- mostly permeable to Ca (also Na and K)
AMPA and NMDA are never alone they work together

At resting Vm NMDA channels are blocked by Mg, when membrane depolarizes from AMPA, Mg pops out

NMDA are ligand gated and voltage dependant

Slide 23-24 lecture 15.5

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6
Q

What are G protein coupled receptors?

A

Metabotropic receptors
Guanine nucleotide binding proteins
Have ability to bind and hydrolyze guanosine triphosphate (GTP) to GDP

Able to activate or dissociate targets

Slide 4 lecture 16 examples

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7
Q

What is the G protein activation cycle?

A

Cycle on slide 5 lecture 16

GPCR have 7 transmembrane regions, a neurotransmitter binding site (extracellular), and can interact with G proteins (cytoplasmic)
The Gα subunit is a GTPase, bound to GDP at rest, when G protein binds with activated receptor, GDP is exchanged for GTP and G protein splits into Gα and Gβγ

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8
Q

What are the 2 possibilities of the α subunit of GPCR?

A

A receptor coupled to αs (stimulatory) activates adenylate (or adenylyl cyclase)
Receptor coupled to αi (inhibitory) inhibits adenylate
Activated AC converts ATP to cAMP, which then can activate protein kinase A (PKA)

The αt (transducin) activates phosphodiesterase (PDE), which hydrolyzes cGMP closing the cGMP-activated channels

GCPR coupled to αq activates phospholipase C (PLC)

Slides 6-7 lecture 16

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9
Q

Study amplification on slide 8 lecture 16

A

Okay

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10
Q

What are the 4 things all modularity systems in the brain do with diffuse central connections?
(4 of them)

A
  1. A small set of Neurons (several thousand) forms the center of the system
  2. Neurons if they diffuse systems arise from the central core of the brain, most of them from brainstem
  3. Each neuron can influence many others because each one has an axon that may contact more than 100000 postsynaptic neurons spread widely across brain
  4. The synapses made by some of these systems seem designed to release transmitter molecules into the extracellular fluid so they can diffuse to many neurons
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11
Q

What is the locus coeruleus?

How does it’s synaptic modulation work?

A

Involved in regulation of attention, arousal, and sleep-wake cycles, learning and memory, anxiety, pain, brain metabolism

Axons arising from this synapse on pyramidal cells in the cerebral cortex where they release NE
NE acts on β adrenergic receptors in pyrimid cell membrane
A cell exposed to NE reacts more powerfully when it is stimulated by strong excitatory input

NE modulates the cells response to other inputs

Slide 10 lecture 16

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12
Q

What are the 3 sites modulation by second messengers can occur?

A

Presynaptic modulation- phosphorylation can modulate by causing depolarizations (block K channels)
Postsynaptic modulation- modulate synapse by tweaking it tuning receptor responding time neurotransmitter
Modulation in cell body- action potentials changes shape of messages (change or tune signal)

Slide 11 lecture 16

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13
Q

How does muscarinic Rs inhibit M current?

A

Slide 13 lecture 16

M current- typical in autonomic synapses
Muscarinic receptors- fast EPSP (nicotinic) slow depolarization

Depolarization step- Ca, Na blocked, get outward Current due to K

M current is active at rest- current is gone, just a little blip

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14
Q

What are the 4 things phosphorylation affects?

A

Ion selectivity
Gating
Po
Traffic and insertion to the membrane

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15
Q

What is synaptic strength?

A

The mean amplitude if the postsynaptic response

Many synapses synaptic strength depends on their previous activity

The sensitivity of a synapse to its past activity can lead to a long term change in it future effectiveness, which is all we need to build memory into a neural circuit

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16
Q

What is low frequency stimulation of presynaptic terminal?

Why is high frequency stimulation of presynaptic terminal?

A

Low frequency stimulation of presynaptic terminal triggers the release of only the small transmitter

Bursts of high frequency stimulation of presynaptic terminal is required for the release of both types of vesicles (small and large)

Slides 4-5 lecture 17

17
Q

What is working memory?

What is long term memory?

A

Working memory- lasts seconds, continual series of fleeting memories that we use during the course of the day to remember facts and events, why was just spoken to us, where we put the phone down, etc
Thought to depend on persistent neural firing

Long term memory may last for hours to decades and strongly resist disruption and replacement, allows accumulation of knowledge over lifetime
Thought to involve long lasting changes in the strength of synaptic connections

18
Q

What is the breakdown of high frequency stimulation?

A

Facilitation- lasts 10-100s of msec
Augmentation- lasting several sec
Potentiation- lasting sec to several min and outlasting the period of high frequency stimulation
Depression (short term decreases)- can occur during high frequency stimulation

Slide 7 lecture 16

19
Q

What is the breakdown of low frequency stimulation?

A

Habituation- a slowly progressing decrease

Slide 7 lecture 16

20
Q

What are the 2 explanations for short term increases in synaptic strength?

A
  1. The presynaptic terminal may release more transmitter for each action potential
  2. The post synaptic receptors may be more responsive to transmitter because of a change in their number or sensitivity

Both of these explanations can occur simultaneously

21
Q

What is the explanation for short term decrease in synaptic strength (habituation)?

A

Aplysia: withdraws it’s gill in response to a stimulus to its skin, that withdrawal becomes less vigorous when the stimulus is presented repeatedly (the animal habituates)
Synaptic habituation is due to fewer transmitter quanta release per AP

22
Q

What is the hippocampus synaptic circuit?

A

Hippocampus neurons can undergo a long term increase in synaptic efficacy called long term potentiation (LTP)

Because the hippocampus is important for learning and memory, LTP is considered one of the possible mechanisms underlying these tasks

LTP requires activation of the presynaptic terminals and depolarization of the post synaptic terminals

Slide 9-11 lecture 16

23
Q

What is LTP induction and expression?

A

Slide 13 lecture 16

Early LTP- lasting 1-3 hours
Does not require new protein synthesis, cAMP, or PKA activation

24
Q

What is the sequence of events during normal low frequency synaptic transmission?

A

Glutamate released acts in both NMDA and AMPA receptors in post synaptic membrane of dendritic spines
Sodium and K flow through the AMPA receptors but not through the NMDA receptors because their pore is blocked by Mg at negative membrane potentials

25
Q

What are the early and late phases of LTP?

A

Early- one train of APs produces a phase of LTP lasting 1-3 hours
It does not require new protein synthesis, cAMP, or PKA activation

Late- 4 or more trains of synaptic stimulation induce a late LTP lasting up to 24 hours
It does require cAMP and PKA, as well as changes in gene transcription and the synthesis of new proteins

Synapse “AMPAfication” occurs in both early and late and keeps synapse going

Slide 15 lecture 16

26
Q

How is early LTP induced?

A

A single tetanus induced early LTP by activating NMDA receptors, which triggers Ca influx into postsynaptic cell and activation of a set of second messengers
With relegated tetanus the Ca influx also recruits an adenylyl cyclase which generates cAMP then activates PKA which activates MAP kinase which translocates ti the nucleus where is phosphorylated CREB-1…. etc etc

27
Q

What would happen if synaptic connections could be enhanced and never attenuated?

A

Synaptic transmission might rapidly saturate

The strength of the synaptic connections might reach a point beyond which further enhancement is not possible

28
Q

What’s the similarities of LTP and LTD (long term depression)?

A

LTD requires activation of the same receptors involved in LTP

Like LTP, LTD is thought ti require Ca influx though the NMDA receptors into the postsynaptic neuron

Slide 20 lecture 17

29
Q

How can activation of a single type of receptor leading to elevated levels of a single second messenger, Ca2+, produce both potentiation and depression?

A

Different induction

30
Q

What is long term depression (LTD)?

A

The low frequency tetanus produces a modest EPSP and thus is much less effective at relieving the Mg block if the NMDA receptors

The increase in postsynaptic Ca2+ concentration is much smaller than observed during induction of LTP

the low conc of Ca is thought time be insufficient to activate LTP

LTD is thought to result from the activation of that calcium dependant phosphatase

Slide 18 lecture 17

31
Q

What’s the difference between early LTP and late LTP in terms of how they go away?

A

Early LTP goes away with phosphatases

Late LTP doesn’t go away with phosphatases
Need to remove synapse

PHPY 301 (13 decks)

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