Protective effect of group I metabotropic glutamate receptor activation against hypoxic/hypoglycemic injury in rat hippocampal slices: timing and involvement of protein kinase C

Schröder, Ulrich H.; Opitz, Thoralf; Jäger, Tino; Sabelhaus, Clemens F; Breder, Jörg; Reymann, Klaus G.

doi:10.1016/s0028-3908(98)00180-4

Cited by 45 publications

(28 citation statements)

References 50 publications

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“…Because excessive release of glutamate is an important mechanism underlying the excitotoxic effects of hypoxia and ischemia (Hara et al, 1993;Schroder et al, 1999) and adenosine is produced under such conditions (Rudolphi et al, 1992), our data are consistent with a neuroprotective role for adenosine in the IML. This is important because sympathetic outflow at the level of our recordings in the thoracic spinal cord is mainly to the heart and blood vessels in which abnormal activity could lead to circulatory problems.…”

Section: Source Of the Presynaptic Terminalssupporting

confidence: 80%

Adenosine A1 Receptors Reduce Release from Excitatory But Not Inhibitory Synaptic Inputs onto Lateral Horn Neurons

2001

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Although adenosine is an important neuromodulator in the CNS, its role in modulating sympathetic outflow at the level of the spinal cord has not been studied. Because very little is known about adenosine A1 receptors (A1Rs) in the spinal cord, we determined their location and role with particular reference to the control of sympathetic preganglionic activity and interneuronal activity in the rat. High levels of immunoreactivity for A1Rs were observed throughout the spinal cord. Immunostaining was dense in the intermediolateral cell column (IML) and intercalated nucleus, regions containing retrogradely labeled sympathetic preganglionic neurons (SPNs). Electron microscopy revealed A1R immunoreactivity (A1R-IR) within presynaptic terminals and (to a lesser extent) postsynaptic structures in the IML, as well as the luminal membrane of endothelial cells lining capillaries. Using double-labeling techniques, some presynaptic terminals were observed to synapse onto SPNs. To investigate the effects of activating these A1Rs, visualized whole-cell patch-clamp recordings were made from electrophysiologically and morphologically identified SPNs and interneurons. Applications of the A1R agonist cyclopentyladenosine (CPA) reduced the amplitude of EPSPs elicited by stimulation of the lateral funiculus, an effect blocked by the A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine. These effects were attributable to adenosine acting at a presynaptic site because CPA application increased the paired-pulse ratio. CPA did not affect evoked IPSPs. These data show that activating A1Rs reduces fast excitatory, but not inhibitory, transmission onto SPNs and interneurons in the IML and that A1Rs may play a protective role on neurons involved in the control of sympathetic outflow.

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Section: Source Of the Presynaptic Terminalssupporting

confidence: 80%

Adenosine A1 Receptors Reduce Release from Excitatory But Not Inhibitory Synaptic Inputs onto Lateral Horn Neurons

2001

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“…Excitotoxic effects of hypoxia and ischemia are attributable, in part, to excessive release of glutamate (Hara et al, 1993;Schroder et al, 1999). Under these conditions, the concentration of adenosine available increases and activates A1Rs to reduce excitotoxicity (Fowler, 1989;Simpson et al, 1992;Katchman and Hershkowitz, 1993;Sweeney, 1997).…”

Section: A2 a Rs Enhance Ipsps But Not Epspsmentioning

confidence: 99%

Input-Specific Modulation of Neurotransmitter Release in the Lateral Horn of the Spinal Cord via Adenosine Receptors

Brooke

Deuchars²,

Deuchars³

2004

J. Neurosci.

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“…Still, the former phenomenon might play a signalling role for the induction of long-lasting tolerance. There is evidence that the mechanism of rapid preconditioning is associated with increased excitability of neurons [10][11][12], activation of A1 adenosine receptors [13], moderate increase in intracellular free and bound Ca 2+ levels and activation of phosphoinositide hydrolysis [14,15], and activation of protein kinase C [16,17], to mention only some examples of signal-related rapid responses to short-term anoxia. Nevertheless, the data accumulated so far are incomplete and no postulation of any unitary mechanism of rapid anoxic preconditioning can yet be made.…”

Section: Introductionmentioning

confidence: 99%

Calcium Transients in the Model of Rapidly Induced Anoxic Tolerance in Rat Cortical Slices: Involvement of NMDA Receptors

2002

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In this study, we investigated the effects of NMDA receptor antagonists on calcium transients induced by a single 2-min preconditioning anoxia (PA) in rat olfactory cortical slices, and on the ability of PA to prevent pathological calcium overload induced by subsequent 10-min test anoxia (TA). Relative changes in the intracellular Ca²⁺ concentration (Ca_i) and in the level of Ca²⁺ bound to intracellular hydrophobic domains (Ca_b) were monitored using fura-2 and chlortetracycline, respectively. Our results confirmed that TA induces prominent long-lasting increases in Ca_i and Ca_b, reflecting cellular calcium overload. It was found that PA produces moderate increases in both Ca²⁺ pools and prevents Ca²⁺ overload induced by TA carried out 90 min later. Calcium transients and the protective effects of PA were significantly suppressed in slices treated with NMDA receptor antagonists during and 30 min after PA. These results indicate that moderate activation of the NMDA receptors participates in the mechanism of the PA-induced anoxic tolerance of cortical neurons.

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Protective effect of group I metabotropic glutamate receptor activation against hypoxic/hypoglycemic injury in rat hippocampal slices: timing and involvement of protein kinase C

Cited by 45 publications

References 50 publications

Adenosine A1 Receptors Reduce Release from Excitatory But Not Inhibitory Synaptic Inputs onto Lateral Horn Neurons

Adenosine A1 Receptors Reduce Release from Excitatory But Not Inhibitory Synaptic Inputs onto Lateral Horn Neurons

Input-Specific Modulation of Neurotransmitter Release in the Lateral Horn of the Spinal Cord via Adenosine Receptors

Calcium Transients in the Model of Rapidly Induced Anoxic Tolerance in Rat Cortical Slices: Involvement of NMDA Receptors

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