Synaptic Plasticity

Question 1

Synaptic Plasticity is

Answer 1

the ability to reorganise by creating new neural pathways to adapt

Question 2

Mechanisms of synaptic plasticity could include:

Answer 2

• altering the amount of
  neurotransmitter released
• changing the no. receptors post-
  synaptically
• changing signaling molecules inside
  neuron
• changing gene transcription

Question 3

Synaptic efficacy/strength changes with —–, many of these changes are ——- dependent

Answer 3

• time
• activity

Question 4

Learning:

Answer 4

involves adaptive changes in synaptic connectivity which will in turn alter behaviour

Question 5

Hebb’s Rule:

Answer 5

synapses can change conformation depending on how active or inactive it is

Question 6

Hebb’s Cell Assembly:

Answer 6

internal representation of an object consists of the cortical cells that are activated by it - cell assembly - cells were reciprocally interconnected

Question 7

Hebb’s cell assembly hypothesis:

Answer 7

• activation of the cell assembly
  persisted long enough leading to
  consolidation/growth process
• reciprocal connection would be more
  effective; fire together and wire
  together
• subsequently, if only a fraction of
  assembly cells were activated by a
  later stimulus, the strengthened
  connections could cause the whole
  assembly to activate

Question 8

Rules of Synaptic Modification:

Answer 8

• fire together wire together
• fire out of sync lose their link
• individual stimulation may be
  insufficient to fire an action potential
• summation of two signals is
  acceptable

Question 9

Connectome:

Answer 9

• system of neural pathways in a brain
  or nervous system considered
  collectively

Question 10

Long-Term Potentiation:

Answer 10

• mechanism underlying synaptic
  strengthening
• describes a phenomenon whereby
  high frequency stimulation of a
  neurone leads to increased EPSP to a
  subsequent single stimulus pulse
• long-term changes in expression of
  genes and turnover of peptides
  undelry this phenomenon = a form
  of plasticity

Question 11

An example of long term potentiation is

Answer 11

high frequency electrical stimulation of the perforant pathway

Excitatory postsynaptic potential can last hours

Question 12

Cellular Physiology of LTP:

Answer 12

• Glutamate release onto membrane
  at resting potential
• AMPA receptor activated to create
  EPSP
• NMDA receptor blocked by Mg2+
• depolarisation from AMPA activation
  not sufficient to expel Mg2+
• Glutamate release continued onto
  active (depolarised) cell
• AMPA receptor activated
• Mg2+ block on NMDA removed
• Na+ enters through AMPA and
  NMDA channels
• Ca2+ through NMDA receptors
• leads to the activation of protein
  kinase C, CaMKII (Calcium
  calmodulin-dependent protein
  kinase II)

1)phosphorylates existing AMP
receptors increasing their
effectiveness
2) stimulates the insertion of new
AMPA receptors into the membrane

Question 13

CaMKII Molecular Switch:

Answer 13

• has autocatalytic activity so becomes
  phosphorylated
• constitutively active; no longer
  requires Ca2+
• maintains phosphorylation, insertion
  of AMPA after depolarising stimulus
  has receded
• molecular switch which maintains
  increased excitability of neuron for
  minutes to hours

Question 14

Early Phase Long-term potentiation:

Answer 14

• a minute to an hour
• explained by the actions of Ca2+ and
  the subsequent enhancement of
  AMPA receptors, presynaptic events
  etc

Question 15

Late Phase Long-Term Potentiation:

Answer 15

• hours, days, months
• requires new protein synthesis
• can involve morphological changes
  and new synapses
• Ca2+ activated signal transduction

Question 16

Before and after of what?

Answer 16

Question 17

Long-term potentiation and Pre-synaptic Events:

Answer 17

• post-synaptic neuron can feed back
  to the presynaptic by retrograde
  neurotransmitter - Nitric Oxide
• Ca2+ entry activates enzyme NO
  synthase leading to the production
  of Nitric Oxide
• NO diffuses and activates guaynyl
  cyclase in the presynaptic terminal
• Guanylyl cyclase produces the
  second messenger cGMP
• signal transduction cascade leads to
  increased glutamate release from
  the synaptic button

Question 18

LTP and Pre-synaptic Neuron:

Answer 18

Question 19

Synaptic Plasticity and Excitotoxicity:

Answer 19

• glutamate, AMPA, NMDA receptors
• ***calcium overload is the essential
  factor in excitotoxicity
• importance of mechanisms that
  counteract the rise in cytosolic free
  Ca2+ efflux pump and indirectly the
  sodium pump
• Mitochondria and ER keep Ca2+
  under control
• Disruption of mitochondrial function
  disrupts ER, no balance, increase of
  Ca2+
• mitochondria might be an essential
  organelle in the control of Ca2+
  mediated toxicity

needed or unneeded?

Question 20

Long-term Depression:

Answer 20

• low frequency stimulation causes
  long term depression and rather
  than getting an increase in EPSP
  amplitude on further stimulation you
  get a decrease
• NMDA dependent
• AMPA receptors are de-
  phosphorylated and removed from
  the membrane
• prolonged low level rises in Ca2+
  activate phosphatases which remove
  the phosphates rather than kinases

Question 21

Long Term Depression

Answer 21

Question 22

NMDA receptor activity in the medulla is essential for both LTP and spatial learning.

True or False?

Answer 22

False

NMDA receptor activity in the hippocampus is essential both LTP and spatial learning

Question 23

Experimental evidence for the role of LTP in memory formation and learning:

Answer 23

• AP5 is NMDA receptor
• blocks hippocampal LTP
• rat is unable to learn how to get out
  of the maze
• London taxi drivers have an
  increased volume of grey matter in
  hippocampus due to short-term
  memory and spatial navigation
• learning a second language
  increases density of grey matter in
  the left inferior parietal cortex
• playing video games for 30mins a
  day increases brain matter in the
  cortex, hippocampus and cerebellum
• new connections in sites controlling
  spatial navigation, planning and
  decision-making

Question 24

Alcohol and Learning/Memory:

Answer 24

• NMDA antagonist
• blackouts and amnesia
• blocking normal LTP processes
• disrupts short term memory
• chronic alcoholism and associated
  nutritional deficiency can result in
  Korsakoff syndrome or psychosis:
  loss of recent memory, tendency to
  fabricate accounts of recent events

Question 25

Benzodiazepine and Learning/Memory:

Answer 25

- modulators of GABA a receptor - can lead to anterograde amnesia

Question 26

Cholinergics/Anticholinergics and Learning/Memory:

Answer 26

- role of ach in learning and memory - muscarinic antagonist seems to impair spatial learning - use of acetylcholinesterase inhibitors for alzheimers

Question 27

Reduced sensitivity of mu opiod receptor with long termmorphine can result in

Answer 27

abnormal synaptic plasticity

Question 28

Increased numbers of specific nicotinic receptor subunits in the brains of smokers can result in

Answer 28

abnormal synaptic plasticity

Question 29

Addiction can perceives in part as a

Answer 29

pathological form of learning and memory