vasoactive-intestinal-peptide has been researched along with 1-3-dipropyl-8-cyclopentylxanthine* in 3 studies
3 other study(ies) available for vasoactive-intestinal-peptide and 1-3-dipropyl-8-cyclopentylxanthine
| Article | Year |
|---|---|
A1 and A2A receptor activation by endogenous adenosine is required for VIP enhancement of K+ -evoked [3H]-GABA release from rat hippocampal nerve terminals.
Vasoactive intestinal peptide (VIP) modulates GABA release from hippocampal nerve terminals and enhances hippocampal synaptic transmission through a pathway dependent on GABAergic transmission. Since VIP modulation of hippocampal synaptic transmission is dependent on the tonic actions of adenosine we investigated if endogenous adenosine could influence VIP enhancement of GABA release from isolated hippocampal nerve endings, and which adenosine receptors could be mediating this influence. When extracellular endogenous adenosine was removed using adenosine deaminase (ADA, 1U/ml), the enhancement (57.2+/-3.7%) caused by VIP on GABA release was prevented. Blockade of adenosine A(1) receptors with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10nM) or of A(2A) receptors with ZM241385 (50nM) abolished the effect of VIP. In the presence of ADA, selective A(2A) receptor-activation with CGS21680 (10nM) readmitted most of the enhancement caused by VIP on GABA release (50.7+/-5.3%). Also in the presence of ADA, A(1) receptor activation with N(6)-cyclopentyladenosine (CPA, 50nM) partially readmitted that effect of VIP (32.6+/-3.8%). In conclusion, the enhancement of GABA release caused by VIP in hippocampal nerve terminals is dependent on the tonic actions of adenosine on both A(1) and A(2A) receptors, and this action of adenosine is essential to VIP modulation of GABA release. Topics: Adenosine; Adenosine Deaminase; Animals; gamma-Aminobutyric Acid; Hippocampus; Male; Phenethylamines; Potassium; Presynaptic Terminals; Rats; Rats, Wistar; Receptor, Adenosine A1; Receptor, Adenosine A2A; Receptors, Purinergic P1; Synaptic Transmission; Synaptosomes; Tritium; Vasoactive Intestinal Peptide; Xanthines | 2008 |
Tonic adenosine A1 and A2A receptor activation is required for the excitatory action of VIP on synaptic transmission in the CA1 area of the hippocampus.
Adenosine can regulate synaptic transmission through modulation of the action of other neurotransmitters. The influence of adenosine on VIP enhancement of synaptic transmission in hippocampal slices was investigated. Facilitation of fEPSP slope by 1 nM VIP (23.3+/-1.3%) was turned into an inhibition (-12.1+/-3.4%) when extracellular endogenous adenosine was removed using adenosine deaminase (ADA, 1U/ml). Blockade of adenosine A(1) receptors with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 nM) or of A(2A) receptors with ZM241385 (20 nM) attenuated the effect of VIP. When both DPCPX and ZM241385 were present the effect of VIP was abolished. In the presence of ADA, selective A(1) receptor activation with N(6)-cyclopentyladenosine (CPA, 15 nM) or A(2A) receptor-activation with CGS21680 (10 nM) partially readmitted the excitatory effect of VIP on fEPSPs. In contrast, facilitation of PS amplitude by 1 nM VIP (19.1+/-1.2%) was attenuated in the presence of ADA or DPCPX but was not changed by ZM241385. CPA, in the presence of ADA, fully restored the effect of VIP on PS amplitude. In conclusion, VIP facilitation of synaptic transmission to hippocampal pyramidal cell dendrites is dependent on both A(1) and A(2A) receptor activation by endogenous adenosine. VIP effects on PS amplitude are only dependent on A(1) adenosine receptor activation. This differential sensitivity to adenosine modulation might be due to the different VIP circuits contributing to VIP effects on pyramidal cell dendrites and pyramidal cell bodies. Topics: Adenosine; Adenosine Deaminase; Analysis of Variance; Animals; Drug Interactions; Electric Stimulation; Excitatory Postsynaptic Potentials; Hippocampus; In Vitro Techniques; Male; Membrane Potentials; Neuroprotective Agents; Patch-Clamp Techniques; Pyrimidines; Rats; Rats, Wistar; Receptor, Adenosine A1; Receptor, Adenosine A2A; Synaptic Transmission; Triazines; Triazoles; Vasoactive Intestinal Peptide; Xanthines | 2007 |
Studies investigating the possible involvement of adenosine in the antisecretory action of morphine.
1. Fluid secretion was induced in the jejunum of anesthetised rats using vasoactive intestinal peptide. 2. The adenosine antagonist, DPCPX (0.1 mg/kg), suppressed the antisecretory action of morphine (10 mg/kg), but naloxone (80 micrograms/kg) did not inhibit the antisecretory response of the adenosine agonist, NECA (40 micrograms/kg), at a dose previously shown to antagonize the antisecretory response of morphine. 3. NECA (40 (micrograms/kg) reversed secretion in pithed and reserpine-pretreated (5 mg/kg subcutaneously) rats. 4. It is proposed that adenosine acts as a mediator of the morphine antisecretory effect at a site distal to the noradrenergic neurons involved in the action of morphine. Topics: Adenosine; Adenosine-5'-(N-ethylcarboxamide); Animals; Decerebrate State; Female; Intestinal Mucosa; Jejunum; Male; Morphine; Naloxone; Narcotic Antagonists; Norepinephrine; Purinergic P1 Receptor Agonists; Rats; Rats, Wistar; Reserpine; Sympatholytics; Vasoactive Intestinal Peptide; Xanthines | 1997 |