【Pharmacology】Antiepileptic drugs

Antiepileptic drugs

prevent or control epilepsy commonly known as seizure
seizure is a sudden burst of uncontrolled electrical activity in the brain

occurs when neurons become excessively active
generally classified into two major groups:

Focal seizures: affect initially only a portion of the brain typically one hemisphere

may occur with or without impairment of awareness

Generalized seizures: affect both sides of the brain at the same time

almost always cause loss of consciousness

seizures can be viewed as the result of an imbalance between inhibitory and excitatory processes in the brain

either too little inhibition or too much excitation

Content:

1. Excitatory synapse
2. Basic mechanism underlying seizures
3. Side-effects
4. Reference

1. Excitatory synapse

Excitatory neuron when at rest,

inside is slightly more negative than the outside
an action potential starts when voltage-gated sodium channels open allowing positively charged sodium ions to rush into the cell
thus reversing the polarization of the membrane
consequently membrane depolarization leads to opening of high-voltage-activated calcium channels
allow positively charged calcium ions enter the neuron
triggering release of glutamate from the vesicles into the synaptic cleft
glutamate binds to two types of receptors on the postsynaptic neuron

AMPA receptors: binding of glutamate open and permit entry of sodium ions
NMDA receptors: open and permit entry of calcium ions

calcium may enter through low-voltage-activated calcium channels also known as t-type calcium channels

t-type calcium channels open in response to small depolarizations at or below resting membrane potential

All this influx of positive ions again leads to depolarization and propagation of action potential

If there is too much glutamate, neurons can become hyperexcitable and a seizure may result.

But this normally doesn't happen because we also have inhibitory neurons.

inhibitory neurons release neurotransmitter GABA
GABA binds to GABA-A receptors on the excitatory neuron
causes them to open and allow negatively charged chloride ions to enter
causes the membrane potential to be more negative on the inside
thus limiting the neurons ability to respond to further stimulation
once GABA dissociates from the GABA-A receptor, it becomes removed from the synaptic cleft by reuptake through the GABA-transporter-1 (GAT-1)
degraded by an enzyme gamma-aminobutyric acid aminotransferase (GABA-T)

Hence, with excess of glutamate, too little GABA can also allow neurons to become hyperexcitable which may lead to seizures.

2. Basic mechanism underlying seizures

Main goal of therapeutic interventions: lower neuronal excitability and or enhance neuronal inhibition

Prevent excessive firing of an action potential in neurons👉blocking voltage-gated sodium channels

block sodium channels and thus reduce the amount of sodium that enters the neuron
Drug:

Carbamazepine
Oxcarbazepine
Lamotrigine
Phenytoin
Topiramate
Valproic acid
Zonisamide

Slow down hyperactive neurons👉blocking calcium channels

inhibit high-voltage-activated calcium channels
Drug:

Lamotrigine
Topiramate

inhibit low-voltage-activated t-type calcium channels
Drug:

Valproic acid
Zonisamide

Many of the antiepileptic drugs act on multiple targets

Lamotrigine Topiramate Valproic acid and Zonisamide 👉 inhibit both calcium channels and sodium channels
Topiramate 👉 inhibit excitatory neurotransmission by blocking AMPA receptors

Gabapentin and Pregabalin

interacting with high-voltage-activated calcium channels
bind to an accessory subunit of the high-voltage-activated calcium channel called alpha-2-delta-1

because the presynaptic channels that contain this specific subunit appear to modulate the release of excitatory neurotransmitters, eg, glutamate

Inhibition of alpha-2-delta-1 containing calcium channels speculated to be one of the main reasons for their antiepileptic effect

Levetiracetam

high-voltage-activated calcium channel blocker
its ability to bind to the SV2A protein found in the walls of vesicles that contain glutamate

appears to impair the synaptic release of glutamate
thus decrease neuronal excitability

Felbamate

inhibits excitatory neurotransmission by blocking NMDA receptors

Drugs that act on the GABA system

Benzodiazepines and Barbiturates
work by binding to GABA-A receptor

thus prolonging the opening of the channel
permitting greater influx of negatively charged chloride ions into the neuron

Review: 【Pharmacology】Anxiolytic and hypnotic drugs

Tiagabine

selective inhibitor of the GABA transporter
blocks GABA reuptake

permitting more GABA to be available for receptor binding on the postsynaptic neurons

Vigabatrin

irreversibly inhibits GABA-aminotransferase

the enzyme responsible for catabolism of GABA

effectively increasing the concentrations of GABA in the brain

3. Side-effects

Sedation
Dizziness
Hyponatremia (Carbamazepine and Oxcarbazepine)
Visual field loss (Vigabatrin)
Double vision (Lamotrigine and Phenytoin)
Gingival hyperplasia (Phenytoin)
Hirsutism cognitive problems (Topiramate and Zonisamide)
Weight loss (Topiramate)
Weight gain (Valproic acid)
Peripheral edema (Gabapentin and Pregabalin)
Liver toxicity (Valproic acid and Felbamate)
Aplastic anemia (Felbamate)

4. Reference

https://youtu.be/xFUHE9gX6W8

【Pharmacology】Drugs for Parkinson’s disease

【Pharmacology】Antipsychotics

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