Evaluation of Opioid Peptide and Muscarinic Receptors in Human Epileptogenic Neocortex: An Autoradiography Study

Ondarza, Rodolfo; Trejo-Martínez, David; Corona-Amézcua, Rodrigo; Briones, Magdalena; Rocha, Luísa

doi:10.1046/j.1528-1157.43.s.5.27.x

Cited by 16 publications

(5 citation statements)

References 29 publications

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“…Neuronal plasticity evidences the response of a circuit, a neurotransmitter or a receptor that is modified as a result of different factors or altered processes. Herein it is shown that muscarinic receptor changed promptly after stimulus (BIC administration), a finding in line with the observation that this receptor is enhanced in the human epileptic focus at early times following seizures through activity-dependent mechanisms [ 35 ].…”

Section: Discussionsupporting

confidence: 77%

Convulsant bicuculline modifies CNS muscarinic receptor affinity

Schneider

Arnaiz

2006

BMC Neurosci

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Background: Previous work from this laboratory has shown that the administration of the convulsant drug 3-mercaptopropionic acid (MP), a GAD inhibitor, modifies not only GABA synthesis but also binding of the antagonist [ 3 H]-quinuclidinyl benzilate ([ 3 H]-QNB) to central muscarinic receptors, an effect due to an increase in affinity without modifications in binding site number. The cholinergic system has been implicated in several experimental epilepsy models and the ability of acetylcholine to regulate neuronal excitability in the neocortex is well known. To study the potential relationship between GABAergic and cholinergic systems with seizure activity, we analyzed the muscarinic receptor after inducing seizure by bicuculline (BIC), known to antagonize the GABA-A postsynaptic receptor subtype.

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Section: Discussionsupporting

confidence: 77%

Convulsant bicuculline modifies CNS muscarinic receptor affinity

Schneider

Arnaiz

2006

BMC Neurosci

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“…Eventually, the irritative zone zone serves as a control condition, compared with the epileptogenic region of the same patient. However, studies indicate that both regions present significant changes, suggesting an increased excitatory influence in the epileptic focus and decreased inhibitory neurotransmission in the irritative zone 132 . Indeed, the irritative zone increases vascularity, microlesions, and marked activation of mitogen‐activated protein kinase and cAMP‐response element‐binding protein (MAPK/CREB, a signaling pathway involved in synaptic plasticity) 133 .…”

Section: Discussionmentioning

confidence: 99%

“…However, studies indicate that both regions present significant changes, suggesting an increased excitatory influence in the epileptic focus and decreased inhibitory neurotransmission in the irritative zone. 132 Indeed, the irritative zone increases vascularity, microlesions, and marked activation of mitogen‐activated protein kinase and cAMP‐response element‐binding protein (MAPK/CREB, a signaling pathway involved in synaptic plasticity). 133 Previous studies that focused on the human brain with epilepsy revealed a high expression of long noncoding RNA (lncRNAs) genes involved in synaptic plasticity, a situation that correlated with the interictal spiking activity.…”

Section: Discussionmentioning

confidence: 99%

Drug‐resistant epilepsy: Drug target hypothesis and beyond the receptors

Fonseca-Barriendos¹,

Frías‐Soria²,

Pérez-Pérez³

et al. 2021

Epilepsia Open

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Epilepsy is a common chronic neurological disorder that affects more than 50 million people worldwide. 1 Antiseizure drug that serves as the first line of treatment is used to control seizures. However, one-third of patients with epilepsy suffer from drug-resistant epilepsy (DRE) because they fail to achieve control of seizures despite the appropriate treatment schemes used (in monotherapy or various combinations). 2 According to the target hypothesis that explains the drug-resistance phenotype in epilepsy, failure to control epileptic activity by antiseizure medication (ASM) results in losing therapeutic efficacy as a consequence of alterations in the structure and/or function of their targets 3 (Figure 1). In this regard, adopting different therapeutic targets in patients with DRE is crucial, which include alterations in voltage-gated sodium channels (VGSCs) and γ-aminobutyric acid (GABA) receptors.Some studies confirm that resected brain tissue obtained from patients with drug-resistant temporal lobe epilepsy (DR-TLE) who have undergone surgery show reduced sensitivity to carbamazepine, a drug that inhibits VGSC. 4,5 Experimental models have not yet reproduced this condition in DRE. However, studies in models of acute seizures and epilepsy have demonstrated induced alterations in VGSC similar to those detected in brain tissue of patients with the DRE. [6][7][8]

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“…The autoradiography experiments were carried out on adjacent sections thaw-mounted on gelatincoated slides according to the procedures described previously. [17][18][19] Experimental conditions for mu, delta and nociceptin autoradiography are summarized in Table 2. The brain sections were initially washed.…”

Section: Tissue Preparation and Histopathologymentioning

confidence: 99%

Opioid receptor binding in parahippocampus of patients with temporal lobe epilepsy: Its association with the antiepileptic effects of subacute electrical stimulation

Rocha¹,

Cuéllar-Herrera²,

Velasco³

et al. 2007

Seizure

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Opioid receptor binding was evaluated in parahippocampal cortex (PHC) obtained from patients with intractable mesial temporal lobe epilepsy (MTLE) with and without subacute high frequency electrical stimulation (HFS) in this brain area. Mu, delta and nociceptin receptor binding was determined by autoradiography in PHC of five patients (ESAE group) with MTLE history of 14.8 +/- 2.5 years and seizure frequency of 11 +/- 2.9 per month, two of them (40%) with mesial sclerosis. This group demonstrated antiepileptic effects following subacute HFS (130 Hz, 450 micros, 200-400 microA), applied continuously during 16-20 days in PHC. Values were compared with those obtained from patients with severe MTLE (history of 21.7 +/- 2.8 years and seizure frequency of 28.2 +/- 14 per month) in whom electrical stimulation did not induce antiepileptic effects (ESWAE group, n = 4), patients with MTLE in whom no electrical stimulation was applied (MTLE group, n = 4) and autopsy material acquired from subjects without epilepsy (n = 4 obtained from three subjects). Enhanced 3H-DAMGO (MTLE, 755%; ESAE, 375%; ESWAE, 693%), 3H-DPDPE (MTLE, 242%; ESAE, 80%; ESWAE, 346%) and 3H-nociceptin (MTLE, 424%; ESAE, 217%; ESWAE, 451%) binding was detected in the PHC of all epileptic groups. However, tissue obtained from ESAE group demonstrated lower opioid receptor binding (3H-DAMGO, 44.5%, p < 0.05; 3H-DPDPE, 47%, p < 0.05; 3H-nociceptin, 39.3%, p < 0.5) when compared with MTLE group. The present results indicate that a high effectiveness to the antiepileptic effects induced by HFS is associated with reduced opioid peptide binding.

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Evaluation of Opioid Peptide and Muscarinic Receptors in Human Epileptogenic Neocortex: An Autoradiography Study

Cited by 16 publications

References 29 publications

Convulsant bicuculline modifies CNS muscarinic receptor affinity

Convulsant bicuculline modifies CNS muscarinic receptor affinity

Drug‐resistant epilepsy: Drug target hypothesis and beyond the receptors

Opioid receptor binding in parahippocampus of patients with temporal lobe epilepsy: Its association with the antiepileptic effects of subacute electrical stimulation

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