Phenytoin MOA
GLUTAMATE
- decrease voltage-sensitive Na channel opening -> decreased repetitive firing in depolarised neurones > decrease glut released
- decreased Ca chan opening
- may also have other effects
Carbamazepine MOA
GLUTAMATE
- decrease voltage-sensitive Na channel opening -> decreased repetitive firing in depolarised neurones > decrease glut released
- Antag NMDA and AMPA receptors (post synaptic) > decrease glut binding
Oxcarbazepine MOA
GLUTAMATE
- decrease voltage-sensitive Na channel opening -> decreased repetitive firing in depolarised neurones > decrease glut released
- MAY increase K conductance + modulate Ca channels
Lacosamide MOA
GLUTAMATE
- decrease voltage-sensitive Na channel opening -> decreased repetitive firing in depolarised neurones > decrease glut released
- modulates CRMP-2 (involved in neuronal differentiation and axonal growth), mech unclear
* MAY prevent aberrant synaptic connectivity and/or rearrangements seen in epilepsy.
Zonisamide MOA
GLUTAMATE
- decrease voltage-sensitive Na channel opening -> decreased repetitive firing in depolarised neurones > decrease glut released
- decrease T type Ca channels opening
- antagonism at kainate/AMPA receptor sites
Valproate MOA
GABA (mainly)
- increase GABA synth
- decrease GABA metabolism
GLUTAMATE (to some extent)
- decrease voltage-sensitive Na channel opening
- decrease glut binding to AMPA and NMDA
- inhibits T type Ca channels opening
OTHER
- inhibits GSK-3 (like lithium) - may be neuroprotective
Lamotrigine MOA
Broad spectrum
GABA
- inhibits GABA metabolism
GLUTAMATE
- decrease voltage-sensitive Na and Ca channel opening
- **MAY AGGRAVATE SEIZURES IN PTS WITH SPECIFIC NA CHANNEL MUTATIONS
Topiramate MOA
Broad spectrum
GABA
- enhances GABA binding at GABA-A receptors
GLUTAMATE
- decrease voltage-sensitive Na and Ca channel opening
- antag at kainate/AMPA receptor sites
Felbamate MOA
Broad spectrum
GABA
- enhances GABA binding at GABA-A receptors
GLUTAMATE
- decrease voltage-sensitive Na and Ca channel opening
- antag at kainate/AMPA receptor sites
Levetiracetam MOA
novel drug -potential as add on due to diff moa
SV2A
- main moa
- binds to presyn SV2A protein on memb of synaptic vesicles (thought to control vesicle exocytosis) > decrease exocytotic vesicle release > decrease neurotransmitter release
- *does not alter normal neurotransmitters, only decreases hippocampal excitation during repetitive stimulation
OTHER
- SOME evidence of GABA modulation and decrease Ca chan opening as well
Gabapentin MOA
GLUTAMATE
- binds to alpha2delta subunit of voltage-gated Ca channels > decrease channel opening > decrease Ca influx
**LITTLE GABA activity
Pregabalin MOA
GLUTAMATE
- binds to alpha2delta subunit of voltage-gated Ca channels > decrease channel opening > decrease Ca influx
**NO GABA activity
Tiagabine MOA
GABA
- inhibits GABA reuptake > more GABA available for binding
- *NO glutamate effect
Vigabatrin MOA
GABA
- inhibits GABA transaminase (responsible for inactivating GABA)
Ethosuximide MOA
- inhibits T type Ca channels
* *really only used for absence seizures.
