A COMPARISON OF THE ADENOSINE-MEDIATED SYNAPTIC INHIBITION IN THE CA3AREA OF IMMATURE AND ADULT-RAT HIPPOCAMPUS

Citation
S. Descombes et al., A COMPARISON OF THE ADENOSINE-MEDIATED SYNAPTIC INHIBITION IN THE CA3AREA OF IMMATURE AND ADULT-RAT HIPPOCAMPUS, Developmental brain research, 110(1), 1998, pp. 51-59
Citations number
45
Categorie Soggetti
Neurosciences,"Developmental Biology
ISSN journal
01653806
Volume
110
Issue
1
Year of publication
1998
Pages
51 - 59
Database
ISI
SICI code
0165-3806(1998)110:1<51:ACOTAS>2.0.ZU;2-C
Abstract
We compared the effects of the adenosine Al receptor activation on the postsynaptic potentials (psps) recorded from the CA3 area of immature (postnatal days 10-20) and adult rat hippocampal neurons in vitro. Th e adenosine Al receptor agonist 2-phenyl-isopropyladenosine (PIA, 1 mu M) depressed the stimulus-induced psps less in immature and more in a dult neurons. In the presence of the GABA, receptor antagonist bicucul line methiodide (BMI, 10 mu M), PIA reduced the duration and number of action potentials of the stimulus-induced paroxysmal depolarizations (PDs) in immature neurons, while it blocked PDs in adult neurons. Spon taneous BMI-induced PDs, were blocked by PLA in less than half (5/12) immature and all (6/6) adult neurons. The adenosine Al receptor antago nist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 1 mu M) enhanced the s timulus-induced psps in immature and adult neurons alike; this effect did not lead to stimulus-induced bursting in immature neurons. DPCPX i nduced spontaneous bursts (proconvulsant effect) in only 2/16 immature but in all adult (12/12) neurons. In BMI, DPCPX increased the duratio n and number of action potentials of the stimulus-induced PDs in immat ure and adult neurons alike (by about 30%), but it increased the rates of occurrence of spontaneous PDs in significantly more adult neurons. In conclusion, our results suggest that adenosine, acting via Al rece ptors, is a more effective endogenous anti-epileptic in adult than in immature hippocampus, a fact which may contribute to the susceptibilit y of the latter to epileptogenesis. (C) 1998 Elsevier Science B.V. All rights reserved.