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Neuroscience > Module B-08 > Flashcards

Module B-08 Flashcards

1
Q

Define: Synaptic Plasticity

A
  • Lingering event-related changes in synaptic efficacy

- variable postsynaptic responses to specific synaptic inputs

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2
Q

Molecular /physiological (cellular changes) representation of a memory is called_______

A

Engram

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3
Q

Role of Hippocampus in memory

A

Consolidating factual information throughout cerebral cortex

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4
Q

What parts of brain are involved in acquisition of motor skills?

A

cerebellum and basal ganglia work in concert with the frontal lobes

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5
Q

How are short term memories encoded?

A

Transient changes in synaptic function through altered metabolism

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6
Q

How are long term memories encoded?

A

permanent alteration of cellular function, with protein expression and even cellular structure being altered

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7
Q

3 types of memories to encode

A
  • Factual
  • Sensory
  • Motor
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8
Q

Acquired pathological deficits of memory are called _______

A

Amnesias

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9
Q

Acquired pathological deficits in memory are caused by either

A

– Losses of engrams (deficit in initial storage)

– Failures in accessing engrams

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10
Q

Region of brain involved in formation and maintenance of long-term memory for FACTS.

A

The hippocampus and surrounding parahippocampal structures

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11
Q

Describe structure of Hippocampus

A

contains a collection of transversely oriented parallel processing units (lamellae).

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12
Q

Describe pathway of Hippocampal neurons

A
  • Efferents of the entorhinal region of the parahippocampal gyrus relay information into the granule cells forming the dentate gyrus.
  • The dentate gyrus then projects to pyramidal cells of CA3, which then project to the pyramidal cells of CA1.
  • CA1 then projects through the subiculum and back to the entorhinal cortex.
  • This largely excitatory feedback system is thus well suited to reverberatory processing of information.
  • CA1 also projects through the fimbria and fornix to the mammillary bodies of the hypothalamus, which communicate with the cerebral cortex via the thalamus
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13
Q

the hippocampus demonstrate synaptic

plasticity in response to electrical stimulation of _______

A

Afferents

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14
Q

2 types of synaptic responses in Hippocampus due to synpatic plasticity

A

1) Long-term potentiation (LTP) - With high-frequency
stimulation
2) Long-term depression (LTD)- following low-frequency electrical stimulation

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15
Q

How do High frequency stimulation of CA1 cause Long term potentiation?

A

1) substantial increase in intracellular [Ca2+]

2) activate kinases that alter the phosphorylation of key proteins for LTP

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16
Q

How do LOW frequency stimulation of CA1 cause Long term depression?

A

1) smaller rise in intracellular [Ca2+].
2) different enzymes, protein phosphatases, are activated
3) dephosphorylation of proteins, including those forming AMPA receptors. LTD results

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17
Q

Which are the receptors in the hippocampus and cortex that mediate Calcium influx?

A

NMDA

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18
Q

Activation of which receptors mediate plasticity in NMDA receptor independent regions?

A

metabotropic glutamate receptors

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19
Q

Which region has synapses that are NMDA receptor independant

A

hippocampal CA3 and the cerebellum

20
Q

What is the Role of Kinases on AMPA receptor in Hippocampus and Cerebellum in synaptic plasticity?

A

1) HIPPOCAMPUS - Phosphorylation of the GluR1 subunit of the AMPA receptor, followed by its delivery to postsynaptic membrane ===> LTP
2) CEREBELLUM - phosphorylation of the GluR2 subunit, which promotes endocytosis of the receptor===>LTD

21
Q

What is the Role of Phosphorylation on AMPA receptor in Hippocampus and Cerebellum in synaptic plasticity?

A

1) HIPPOCAMPUS -dephosphorylation and endocytosis of the GluR1 subunit of the AMPA receptor====> LTD
2) CEREBELLUM -dephosphorylation of the GluR2 subunit, triggering receptor expression ====> LTP

22
Q

What are Paroxysms?

A

Sudden aberrant neurological event, often mediating the expression of seizures

23
Q

What are Seizures?

A

Pathological hypersynchronization of neuronal acitivity

24
Q

Seizures that last longer than 5 mins

A

status epilepticus

25
Q

Average length of Seizure

A

1-2 mins (except with status epilepticus)

26
Q

Why Status epilepticus considered acutely life threatening?

A

Due to Excitotoxicity, which causes elevated release of glutamate, which raises intracellular calcium to toxic levels

27
Q

What is epilepsy?

A

Chronically heightened susceptibility to seizures

28
Q

What is a convulsion?

A

Motoric manifestations of seizure

29
Q

What is epileptogenesis?

A

The functional transformation of a non-epileptic brain into

an epileptic brain

30
Q

what are the 2 categories of epilepsies?

A
  1. Primary (idiopathic, cryptogenic)

2. Secondary (symptomatic)

31
Q

Features of Primary Epilepsies

A

– Lack apparent cause
– There is Family history
– Early onset

32
Q

Generalized Seizures of Primary Epilepsy

A

– Discharge is bilaterally widespread

– Unconsciousness throughout

33
Q

what are the 9 behavioral manifestations of Primary Epilepsies

A

1) Absence: Often brief, frequent and behaviorally unremarkable (immobility, staring, subtle facial twitching)
2) Clonic: Repetitive flexion and extension of limbs or trunk
3) Tonic: Sustained muscular contractions
4) Tonic-clonic
5) Clonic-tonic
6) Tonic-clonic-tonic
7) Opisthotonic: Sustained flexion of the back, neck and legs, causing the back of the head to approach the heels
8) Atonic: Sudden loss of muscle tone
9) Infantile spasms: Jerk followed by brief stiffening of the body,often occurring in series

34
Q

What type of seizures are resultant of Primary Epilepsies

A

Generalized

35
Q

Difference btw Tonic and Clonic

A

Clonic: Repetitive flexion and extension of limbs or trunk
Tonic: Sustained muscular contractions

36
Q

How are Absent behavior in seizures identified

A
  • poor performance in school

- Associated with spike and wave discharge triggered through thalamic circuitry

37
Q

What type of Epileptic potentials are seen in Infantile spasms?

A

hypsarrhythmia

38
Q

What causes secondary epilepsy

A

a circumscribed population of neurons is abnormally
excitable, acting as a source or focus of seizure activity
- usually Limbic structures like the hippocampus and amygdala

39
Q

2 types of seizures seen in secondary epilepsy

A

1) Partial - Discharge spatially restricted(initially only at focus
but may recruit nearby neurons) and
unilateralized
2) Generalized- Bilateralization with loss of consciousness

40
Q

Manifestations of Partial Seizures

A

• Simple partial seizures
– Parietal foci may trigger somatosensory experience
– Frontal foci may trigger focal motor output that may
progress according to the homunculus of
Brodmann’s area 4 (Jacksonian march)
– Autonomic output can accompany focal discharge
from a variety of sites(e.g., unilateral sweating)
• Complex partial seizures – Earliest aberrations from limbic foci generate aura that may warn of looming seizure
» Strong emotions are commonly experienced (e.g.,
fear)
» Patients remain responsive
» Certain behaviors are often expressed in attempts
to suppress seizures
» Mild facial twitching often seen

41
Q

2 Groups of partial seizures

A

1) simple partial seizure

2) complex Partial seizure

42
Q

What is used to detect seizure activity

A

Electroencephalography (EEG)

43
Q

Types of drugs specific for Absence Seizures

A

Blockers of T-type calcium channels

44
Q

3 types of Antiseizure medication

A
  • Sodium channel blockers
  • GABA agonists
  • Calcium channel blockers
45
Q

What is the effect of Na+-blocking agents?

A

Limits repetitive action potentials- stabilize membranes through prolonged inactivation of voltage-gated sodium channels

46
Q

How do GABA agonist enhance GABAergic transmission?

A
  1. Inhibition of GABA transaminase reduces metabolism of the transmitter
  2. Blockage of GABA uptake increases synaptic longevity
  3. Allosteric binding of benzodiazepines or barbiturates to the GABAA
    receptor complex enhances GAGA-dependent conductance of chloride
47
Q

How do Calcium channel blockers work

A

Reduced influx of calcium limits the capacity of pace-making thalamic cells to synchronize widespread cellular populations

Neuroscience (32 decks)

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