BioMed Research International

Review Article

Subunit Composition of Neurotransmitter Receptors in the Immature and in the Epileptic Brain

Table 2

Subunit composition of glutamate and GABA receptors in the brain submitted to seizures.


Author and year	Study design	Substudy features (if applicable)	AMPA	NMDA	GABA

Animal models of seizures and status epilepticus
Brooks-Kayal et al., 1998 [14]	Rats with pilocarpine-induced status epilepticus and subsequent development of spontaneous temporal lobe seizures (compared to control rats). Hippocampus	24 hours after SE			α1 ↓* α3 ↑* α4 ↑* α1/non-α1 ↓* β1 ↓* β3 ↑* δ ↑* ε ↑*
Brooks-Kayal et al., 1998 [14]		1–4 months after SE and with spontaneous temporal lobe seizures			α1 ↓* α4 ↑* α1/non-α1 ↓* δ ↑* ε ↑* β1 ↓* β3 ↑*

Swann et al., 2007 [19]	Rats with tetanus toxin or flurothyl-induced seizures (compared to control rats)	Tetanus toxin-induced seizures at p10 in hippocampus		GluN1 ↓ GluN2A ↓ GluN2B ↓
		Flurothyl-induced seizures in hippocampus		GluN2A ↓
		Flurothyl-induced seizures in neocortex		GluN2A ↓

Rajasekaran et al., 2012 [23]	Rats with pilocarpine-induced status epilepticus (compared to control rats)		GluA2 surface expression ↓

Data from epilepsy surgery performed for refractory epilepsy
Crino et al., 2001 [15]	Individual neurons from dysplastic tissue from epilepsy surgery (compared to nondysplastic tissue from epileptic patients and to autopsy specimens from patients who died from nonneurological causes). Temporal neocortex and dorsolateral frontal neocortex	Dysplastic neurons	GluA1 ↓* GluA4 ↑*	GluN2A ↓* GluN2B ↑* GluN2C ↑*	α1 ↓* α2 ↓* β1 ↓* β2 ↓*
Crino et al., 2001 [15]		Heterotopic neurons	GluA1 ↓*		α1 ↓* α2 ↓* β2 ↓*

Talos et al., 2008 [20]	Patients with tuberous sclerosis complex and epilepsy who underwent epilepsy surgery (compared to patients with epilepsy without tuberous sclerosis and to autopsy cases without neurological diseases)	Tissue from tubers	GluA1 ↑ GluA4 ↑ GluA2 ↓ GluA3 ↓	GluN2B ↑ GluN3A ↑
Talos et al., 2008 [20]		Cortex from epileptic patients without tuberous sclerosis	GluA1 ↑ GluA2 ↓	GluN2B ↑ GluN3A ↑

Talos et al., 2012 [21]	Patients with tuberous sclerosis complex and epilepsy who underwent epilepsy surgery or whose tissue was collected at autopsy and patients with focal cortical dysplasia and epilepsy that underwent epilepsy surgery to resect the epileptogenic tissue (compared to autopsy cases without neurological diseases)	Tubers			α1 ↓ α4/α1 ↑
		Focal cortical dysplasia IIa			α4 ↓ α4/α1 ↓
		Focal cortical dysplasia IIb			α1 ↓ α4/α1 ↑

Finardi et al., 2006 [16]	Patients with malformations of cortical development undergoing epilepsy surgery because of refractory epilepsy (compared to patients with focal epilepsy without underlying malformation and to nonepileptic patients, brain tissue resected next to a tumor)	Focal cortical dysplasia		GluN2B ↑
Finardi et al., 2006 [16]		Periventricular nodular heterotopia		GluN1 ↓ GluN2A ↓ GluN2B ↓

Data from epilepsy surgery performed for refractory status epilepticus
Loddenkemper et al., 2014 [17]	Patients with SE and ESES (compared to epilepsy surgery patients without status epilepticus, EPI, and to autopsy cases)	SE		GluN2B ↑ GluN2B/GluN2A ↑	α2/α1 ↑ α2 ↑*
		ESES	GluA1 ↑ GluA1/GluA2 ↑	GluN2B/GluNA ↑
		EPI	GluA1/Glu2 ↑		α2/α1 ↑ α2 ↑* α2/α1 ↑*

Studies on mRNA.