h-89 has been researched along with 8-chloroadenosine-3--5--cyclic-monophosphorothioate* in 2 studies
2 other study(ies) available for h-89 and 8-chloroadenosine-3--5--cyclic-monophosphorothioate
Article | Year |
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Differential cAMP signaling at hippocampal output synapses.
cAMP is a critical second messenger involved in synaptic transmission and synaptic plasticity. Here, we show that activation of the adenylyl cyclase by forskolin and application of the cAMP-analog Sp-5,6-DCl-cBIMPS both mimicked and occluded tetanus-induced long-term potentiation (LTP) in subicular bursting neurons, but not in subicular regular firing cells. Furthermore, LTP in bursting cells was inhibited by protein kinase A (PKA) inhibitors Rp-8-CPT-cAMP and H-89. Variations in the degree of EPSC blockade by the low-affinity competitive AMPA receptor-antagonist gamma-d-glutamyl-glycine (gamma-DGG), analysis of the coefficient of variance as well as changes in short-term potentiation suggest an increase of glutamate concentration in the synaptic cleft after expression of LTP. We conclude that presynaptic LTP in bursting cells requires activation of PKA by a calcium-dependent adenylyl cyclase while LTP in regular firing cells is independent of elevated cAMP levels. Our results provide evidence for a differential role of cAMP in LTP at hippocampal output synapses. Topics: Action Potentials; Analysis of Variance; Animals; Calcium; Colforsin; Cyclic AMP; Electric Stimulation; Excitatory Amino Acid Antagonists; Excitatory Postsynaptic Potentials; GABA Antagonists; Hippocampus; In Vitro Techniques; Isoquinolines; Neurons; Oligopeptides; Patch-Clamp Techniques; Protein Kinase Inhibitors; Pyridazines; Quinoxalines; Rats; Signal Transduction; Sulfonamides; Synapses; Time Factors | 2008 |
Modulation of GABA release during morphine withdrawal in midbrain neurons in vitro.
Chronic treatment with opioids induces adaptations in neurons leading to tolerance and dependence. Studies have implicated the midbrain periaqueductal gray (PAG) in the expression of many signs of withdrawal. Patch-clamp recording techniques were used to examine whether augmentation of adenylyl cyclase signalling produces hyperexcitation in GABAergic nerve terminals within the mouse PAG. Both the rate of mIPSCs and the amplitude of evoked IPSCs during naloxone-precipitated withdrawal was profoundly enhanced in chronically morphine treated mice, compared to vehicle treated controls, in the presence but not the absence an adenosine A(1) receptor antagonist DPCPX. Enhanced GABAergic transmission in the presence of DPCPX was abolished by blocking protein kinase A. Inhibitors of cAMP transport, phosphodiesterase and nucleotide transport mimicked the effect of DPCPX. Coupling efficacy of micro-receptors to presynaptic inhibition of GABA release was increased in dependent mice in the presence of DPCPX. The increased coupling efficacy was abolished by blocking protein kinase A, which unmasked an underlying micro-receptor tolerance. These findings indicate that enhanced adenylyl cyclase signalling following chronic morphine treatment produces (1) GABAergic terminal hyperexcitability during withdrawal that is retarded by a concomitant increase in endogenous adenosine, and (2) enhanced micro-receptor coupling to presynaptic inhibition that overcomes an underlying tolerance. Topics: Action Potentials; Adenosine; Affinity Labels; Animals; Colforsin; Cyclic AMP; Dipyridamole; Dose-Response Relationship, Drug; Drug Interactions; Enkephalins; Enzyme Inhibitors; gamma-Aminobutyric Acid; In Vitro Techniques; Isoquinolines; Male; Mesencephalon; Mice; Mice, Inbred C57BL; Morphine; Morphine Dependence; Naloxone; Narcotic Antagonists; Narcotics; Neural Inhibition; Neurons; Patch-Clamp Techniques; Periaqueductal Gray; Probenecid; Purinergic P1 Receptor Agonists; Purinergic P1 Receptor Antagonists; Substance Withdrawal Syndrome; Sulfonamides; Synaptic Transmission; Thioinosine; Time Factors; Uricosuric Agents; Vasodilator Agents; Xanthines | 2003 |