Polyamine Regulation of N-Methyl-D-Aspartate Receptor Channels

Rock, D. M.

doi:10.1146/annurev.pharmtox.35.1.463

Cited by 23 publications

(34 citation statements)

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“…Because many recent reports have also shown that PAs have effects on membrane proteins such as ion channels and receptors (Schuber 1989;Ficker et al 1994;Rock and Macdonald 1995;Williams 1997), PAs may not be restricted to the ribosomes in cells, as stated in the present study. We are now undertaking a further immunoelectron microscopic investigation into PA localization in neurons employing experimental models of cerebral ischemia in rats.…”

Section: Discussionsupporting

confidence: 61%

“…This may indicate an important role of PAs in cell proliferation and growth (Janne et al 1978;Goyns 1982;Tabor and Tabor 1984;Pegg 1986), in addition to their biological effects on membrane structure and function (for reviews see Schuber 1989;Rock and Macdonald 1995;Williams 1997).…”

Section: Discussionmentioning

confidence: 99%

“…However, the possibility that PAs are located in sites other than the ribosomes in cells could not be excluded, because it is known that PAs have effects on membrane proteins such as ion channels and receptors (for reviews see Schuber 1989;Rock and Macdonald 1995;Williams 1997).…”

mentioning

confidence: 99%

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Immunoelectron Microscopic Study for Polyamines

Fujiwara

Bai²,

Kitagawa³

et al. 1998

J Histochem Cytochem.

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SUMMARYThe polyamines (PAs) are ubiquitous polycationic metabolites in eukaryotic and prokaryotic cells and are believed to be intimately involved in the regulation of DNA, RNA, and protein biosynthesis, the exact function of which remains unclear, mainly because of a lack of knowledge of PA subcellular localization. In this study, using immunoelectron microscopy, we have demonstrated that PAs are predominantly located on free and attached ribosomes of the rough endoplasmic reticulum in the neurons of the lateral reticular nucleus of rat medulla oblongata. The nuclei, axons, and nerve endings were devoid of PA. This suggests that PAs are one of the components of biologically active ribosomes, being closely involved in the translation processes of protein biosynthesis.

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

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Immunoelectron Microscopic Study for Polyamines

Fujiwara

Bai²,

Kitagawa³

et al. 1998

J Histochem Cytochem.

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“…Finally, endogenous polyamines such as spermidine and spermine modulate NMDA receptors. Polyamines can cause voltage-dependent inhibition, glycine-dependent potentiation, as well as voltage-and glycine-independent inhibitions (Rock & Macdonald, 1995). 4.3.5.…”

Section: N-methyl-d-aspartic Acid Receptors-thementioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

258

286

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Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca 2+ ] i and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage -an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca 2+ ] i are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca 2+ ] i and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.

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“…Physiological polyamines (putrescine, cadaverine, spermidine, and spermine), the naturally occurring di, tri-, and tetra amines, are closely related to neuronal cell biochemical activity in the brain, including interaction with neurotransmitter receptors such as the Nmethyl-D-aspartate receptor, regulation of substances in degenerating cells, ion channels such as K + and protection of neuronal cells from oxidative damage [5][6][7][8][9][10]. Additionally, administration of spermine reduces infarction in cerebral ischemic rat models [11], although the systemic role of altered PAs has not been well studied.…”

Section: Introductionmentioning

confidence: 99%