Convulsants That Decrease Inhibition

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Much of our understanding of the cellular basis of epilepsy comes from the application of convulsants to the brain, in whole animal experiments and, more recently, to isolated slices of brain tissue maintained ex vivo. Penicillin, the first widely used convulsant, is a weak antagonist of the recep

Table 1. Widely Used Convulsants and Their Mechanism of Action

Class of Action Target System Mechanism of Action Examples

Table 1. Widely Used Convulsants and Their Mechanism of Action

Class of Action Target System Mechanism of Action Examples

Decrease inhibition:

1.

g-aminobutyric acid

a.

Receptor antagonists

penicillin, bicuculline, picrotoxin,

b.

Synthesis inhibitors

methoxypyridoxine, isoniazid,

3-mecaptoproprionic acid

c.

Benzodiazepine receptor

inverse agonists

d.

Release inhibitors

opioid peptides

2.

Glycine

a.

Receptor antagonists

strychnine

Enhance excitation:

1.

Excitatory amino acids

a.

NMDA receptors

magnesium-free saline

(e.g. glutamate)

b.

non-NMDA receptors

kainic acid

c.

Potassium channel blockers

tetraethylammonium, 4-aminopyridine,

various peptide toxins

2.

Acetylcholine

a.

Receptor agonists

pilocarpine

b.

Cholinesterase inhibitors

soman

Unknown

a.

Neurotoxins

cholera toxin, tetanus toxin

b.

Injury/Trauma

alumina hydroxide, cobalt

b.

CNS Stimulant

p entylenetetrazol

tors for the predominant brain inhibitory neurotransmitter, g-aminobutyric acid (GABA). More potent antagonists, such as bicuculline and the ion channel-blocker picrotoxin, are now more typically used. Seizures and epileptiform discharge can also be elicited by blocking the synthesis or release of GABA. In addition, substances active at modulatory sites on GABA receptors can also exert convulsant activity, such as inverse agonists of the benzodiazepine receptor.

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