synaptic excitation and inhibition:epilepsy Flashcards Preview

Neuroscience > synaptic excitation and inhibition:epilepsy > Flashcards

Flashcards in synaptic excitation and inhibition:epilepsy Deck (24)
Loading flashcards...
1
Q

what is the brain’s major excitatory neurotransmitter?

A

50-80% of nerons are glutamatergic - glutamate

2
Q

what are the two groups of glutamate receptors?

A
  1. ionotropic = fast synaptic transmission
    1. NMDA , AMPA, Kainate
    2. gated Na+ and Ca2+ channels
  2. Metabotropic = slow syaptic transmitsion
3
Q

what Are the two types of GABA receptor ?

A

GABA A = post synaptic, ionotropic ligand-gated, linked to Cl - channels

GABA B= pre-synaptic autoreceptors, metabotropic, linked to K+ channels

4
Q

What type of nerotransmitter is GABA?

A

it is a major inhibitory neurotransmitter

5
Q

do neurons fire in sync? or do they stagger?

A

they do not syncronize, they all send signals at different rates

6
Q

describe the mechansim of excitation and inhibition

A

Excitation = to much

  • ionic current - inward Na+ and Ca 2+
  • neurotransmitters - glutamate and aspartate

Inhibition = too little

  • ionic currents - inward Cl - , outward K+
  • neurotransmitter GABA
7
Q

How do most anti-convulsants work?

A

they work by promoting GABA function

  • GABA antagonsits trigger seizures- glutamate antagonists stop seizures

Mutation of genes encoding voltage/ligand-gated channels cuase brain hyperexcitability

8
Q

Describe how gene mutations could effect the excitabiltiy of neurons

A
9
Q

how could damage to one excitatory neuron effect the activity of another neuron?

A

unbalanced excitation/inhibition = seizures

10
Q

damage to glial cells can lead to what?

A

hyperexcitability - they play a role in the taking up the neurotransmitters when they are done, so damage to glial cells could lead to prolonged neurotransmitter time in the synapse = prolonged signal

11
Q

what is epilepsy characterized by?

A

by abnormal and excessive firing/synchronizaiton of a population of neurons leading to recurrent seizures

12
Q

describe how neurons firing in normal brain function differs from neuron firing in a seizure

A

in an epileptic brain

  • sudden abnormal hyper-synchronous electrical neuronal activity that temporarily interrupts normal brain function
13
Q

describe focal vs. generalized onset

A

focal = seizure orignates in one or more foci

  • simple: patient remains conscious
  • complex: patients loses consciousness

generalized onset = seizure beings simultaneiously in both hemispheres

  • non-motor: brief loss of consciousness without loss of postural tone
  • motor: tonic-clonic= convulsions/loss of consciouness $
14
Q

what tool do you use to diagnose a seizure?

A

electroencephalogram ( EEG) - records weak electrical activity generated by the brain - it records the collective activity within the region -

ther is good resolution in time, but poor spatial resolution

15
Q

what would you see on an EEG in the event of a seizure?

A
16
Q

when is epilepsy normally diagnosed?

A

between seizures - transient abnormalities/discharges

like spikes and sharp waves, as well as slowing of the brain waves which is not consistant with behavioural state example in picture shown

17
Q

what is the difference between generalized and focal seizures upon EEG?

A

generalized = begins simultaneously in both hemispheres

focal = starts in one or more foci/locations in the brain and then spreads to the rest of the brain

18
Q

what are pseudo seizures?

A

psychogenic non-epileptic seizures

  • often manifestations of psychiatric disturbance ( patient may or may not be aware)

distinguish psychogenic from real seizure with an EEG

19
Q

what sort of anti-peileptic drugs do we use?

A
  • phenytoin
  • carbamazepine
  • valproate
  • lamotrigine
  • gabapentin
20
Q

what drugs do we do to terminate acute seizures?

A

lorazepam and barbiturates

“flood brain with GABA”

21
Q

what effect do epileptic seizures have on the brain?

A
  • altered gene expression
  • promotes neurogenesis
  • remodelling of synapses
  • cell death (potentially)
  • gliosis- reactivity of glial cells
  • angiogenesis, vascular remodelling
  • inflammation
  • more seizures (Gower’s hypothesis - seizures increase liklihood of another)
22
Q

what is status epilepticus?

A

a severe, continous seizure without recovery - normal seizure self-termination mechanisms fail - medical emergency as significant morbitiy can result -

23
Q

what can status epilepticus cause?

A

seizures cause prlonged opening of glutamate receptor channels - could result in swelling/rupture due to Na+ and H2O entry - necrosis

“toxic” buildup of intracellular Ca2+

decreased energy, disruption of intracellular organelle function

over-activation of Ca2+ activated proteases

activation of programmed cell death pathways

24
Q

What would we see on EEG in the even to of a focal seizure?

A

starts in one or more areas and spreads to all areas