Reduction of high affinity glutamate uptake in rat hippocampus by two polyamine-like toxins isolated from the venom of the predatory waspphilanthus triangulum F

Marle, J. van; Piek, T.; Lind, A.; Weeren-Kramer, J. van

doi:10.1007/bf01952444

Cited by 14 publications

(4 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some purified neurotoxins are directed against essential components of the nervous system, such as glutamate receptors and ion channels (Anis et al ., 1990; Usherwood & Blagbrough, 1991; Blagbrough et al ., 1992; Green et al ., 1996). Acylpolyamines from wasp venom have been shown to inhibit glutamate uptake in insect neuromuscular synapses (van Marle et al ., 1984, 1986) and from a spider venom to increase glutamate uptake (van Marle et al ., 1989). The ω‐agatoxins and the ω‐conotoxins, peptides isolated from Agelenopsis aperta spider venom and Conus marine snail venom, respectively, distinguish some calcium channel subtypes (Olivera et al ., 1990).…”

Section: Introductionmentioning

confidence: 99%

Purification of a neuroprotective component of Parawixia bistriata spider venom that enhances glutamate uptake

Fontana

Guizzo

Beleboni

et al. 2003

British J Pharmacology

View full text Add to dashboard Cite

1 In this study, we examined the effects of crude venom from the spider Parawixia bistriata on glutamate and GABA uptake into synaptosomes prepared from rat cerebral cortex. Addition of venom to cortical synaptosomes stimulated glutamate uptake and inhibited GABA uptake in a concentration-dependent manner. 2 The venom was fractionated using reverse-phase high-performance liquid chromatography on a preparative column. The fraction that retained glutamate uptake-stimulating activity was further purified on a reverse-phase analytical column followed by ion-exchange chromatography. 3 The active fraction, referred to as PbTx1.2.3, stimulated glutamate uptake in synaptosomes without changing the K M value, and did not affect GABA uptake. Additional experiments showed that the enhancement of glutamate uptake by PbTx1.2.3 occurs when ionotropic glutamate receptors or voltage-gated sodium and calcium channels are completely inhibited or when GABA receptors and potassium channels are activated, indicating that the compound may have a direct action on the transporters. 4 In an experimental model for glaucoma in which rat retinas are subjected to ischemia followed by reperfusion, PbTx1.2.3 protected neurons from excitotoxic death in both outer and inner nuclear layers, and ganglion cell layers. 5 This active spider venom component may serve as a basis for designing therapeutic drugs that increase glutamate clearance and limit neurodegeneration.

show abstract

Section: Introductionmentioning

confidence: 99%

Purification of a neuroprotective component of Parawixia bistriata spider venom that enhances glutamate uptake

Fontana

Guizzo

Beleboni

et al. 2003

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Corticosteroids, like prednisolone and dexamethasone, antagonize the inhibitory action of HC-3 both on the rate of choline uptake and the incorporation of choline into ACh in the rat diaphragm by interfering with Na + influx across the plasma membrane [51,52]. While glucocorticoids produce no changes on skeletal muscle twitches triggered by low frequency nerve stimulation, these drugs significantly enhance post-tetanic potentiation and attenuate neuromuscular block produced by antinicotinic muscle relaxants [53][54][55].…”

Section: Discussionmentioning

confidence: 99%

Tetanic Facilitation of Neuromuscular Transmission by Adenosine A<sub>2A</sub> and Muscarinic M<sub>1</sub> Receptors is Dependent on the Uptake of Choline via High-Affinity Transporters

Castellão-Santana¹,

Abiko²,

Ambiel³

et al. 2018

Pharmacology

View full text Add to dashboard Cite

Background/Aims: In this study, we evaluated the functional impact of facilitatory presynaptic adenosine A_2A and muscarinic M₁ receptors in the recovery of neuromuscular tetanic depression caused by the blockage of high-affinity choline transporter (HChT) by hemicholinium-3 (HC-3), a condition that mimics a myasthenia-like condition. Methods: Rat diaphragm preparations were indirectly stimulated via the phrenic nerve trunk with 50-Hz frequency trains, each consisting of 500–750 supramaximal intensity pulses. The tension at the beginning (A) and at the end (B) of the tetanus was recorded and the ratio (R) B/A calculated. Results: Activation of A_2A and M₁ receptors with CGS21680 (CGS; 2 nmol/L) and McN-A-343c (McN; 3 μmol/L) increased R values. Similar facilitatory effects were obtained with forskolin (FSK; 3 μmol/L) and phorbol 12-myristate 13-acetate (PMA; 10 μmol/L), which activate adenylate cyclase and protein kinase C respectively. HC-3 (4 μmol/L) decreased transmitter exocytosis measured by real-time videomicroscopy with the FM4-64 fluorescent dye and prevented the facilitation of neuromuscular transmission caused by CGS, McN, and FSK, with a minor effect on PMA. The acetylcholinesterase inhibitor, neostigmine (NEO; 0.5 μmol/L), also decreased transmitter exocytosis. The paradoxical neuromuscular tetanic fade caused by NEO (0.5 μmol/L) was also prevented by HC-3 (4 μmol/L) and might result from the rundown of the positive feedback mechanism operated by neuronal nicotinic receptors (blocked by hexamethonium, 120 μmol/L). Conclusion: Data suggest that the recovery of tetanic neuromuscular facilitation by adenosine A_2A and M₁ receptors is highly dependent on HChT activity and may be weakened in myasthenic patients when HChT is inoperative.

show abstract

“…Based on the findings, the venom from Philanthus triangulum F. wasps demonstrated potentials as a source of anticonvulsant agents due to its interference with glutamate uptake, a critical factor in epileptogenesis. 43 Besides PTZ-induced seizures, a treatment using wasp venom peptide from Chartegellus communis (Social wasp), Chartergellus-CP1, showed neuroprotective effects in pilocarpine-induced epilepsy. 44 In the study, electroencephalographic abnormalities that are associated with pilocarpine-induced seizures were significantly reduced upon administration of Charthergellus-CP1.…”

Section: Animal Venom As a Potential Source Of Anticonvulsantsmentioning

confidence: 99%

Animal Venoms as Potential Source of Anticonvulsants

Zainal Abidin,

Liew,

Othman

et al. 2024

F1000Res

View full text Add to dashboard Cite

Abstract* Epilepsy affects millions of people worldwide, and there is an urgent need to develop safe and effective therapeutic agents. Animal venoms contain diverse bioactive compounds like proteins, peptides, and small molecules, which may possess medicinal properties against epilepsy. In recent years, research has shown that venoms from various organisms such as spiders, ants, bees, wasps, and conus snails have anticonvulsant and antiepileptic effects by targeting specific receptors and ion channels. This review underscores the significance of purified proteins and toxins from these sources as potential therapeutic agents for epilepsy. In conclusion, this review emphasizes the valuable role of animal venoms as a natural resource for further exploration in epilepsy treatment research.

show abstract

Reduction of high affinity glutamate uptake in rat hippocampus by two polyamine-like toxins isolated from the venom of the predatory waspphilanthus triangulum F

Cited by 14 publications

References 8 publications

Purification of a neuroprotective component of Parawixia bistriata spider venom that enhances glutamate uptake

Purification of a neuroprotective component of Parawixia bistriata spider venom that enhances glutamate uptake

Tetanic Facilitation of Neuromuscular Transmission by Adenosine A<sub>2A</sub> and Muscarinic M<sub>1</sub> Receptors is Dependent on the Uptake of Choline via High-Affinity Transporters

Animal Venoms as Potential Source of Anticonvulsants

Contact Info

Product

Resources

About