 |
Previous Article | Next Article 
The Journal of Neuroscience, June 1, 1999, 19(11):4238-4244
Adenosine: a Mediator of Interleukin-1 -Induced Hippocampal
Synaptic Inhibition
Wah Ping
Luk1, 2,
Yu
Zhang2,
Thomas D.
White6,
Franklin A.
Lue1, 4,
Chiping
Wu2, 5,
Cheng-Gan
Jiang1,
Liang
Zhang2, 3, 5, and
Harvey
Moldofsky1, 4
1 Center for Sleep and Chronobiology,
2 Playfair Neuroscience, Toronto Hospital Research
Institute, Department of Medicine (3 Neurology and
4 Psychiatry), 5 Bloorview Epilepsy Program,
University of Toronto, Toronto, Ontario, Canada, and
6 Department of Pharmacology, Dalhousie University,
Halifax, Nova Scotia, Canada
Interleukin-1 (IL-1) is a pleotrophic cytokine implicated in a
variety of central activities, including fever, sleep, ischemic injury,
and neuromodulatory responses, such as neuroimmune, and neuroendocrine
interactions. Although accumulating evidence is available regarding the
expression pattern of this cytokine, its receptors in the CNS, and its
mechanistic profile under pathological levels, it is unclear whether
this substance modulates central neurons under physiological
concentrations. Further, in light of the functional and spatial overlap
between the adenosine and IL-1 systems, it is not known whether these
two systems are coupled. We report here that, in rat brain slices,
brief application of sub-femtomolar IL-1 causes a profound decrease
of glutamate transmission, but not GABAergic inhibition, in hippocampal
CA1 pyramidal neurons. This decrease by IL-1 is prevented by
pharmacological blockade of adenosine A1 receptors. In
addition, we show that IL-1 failed to suppress glutamate
transmission at room temperature. Because the production and release of
adenosine in the CNS is thought to be metabolically dependent, this
observation suggests that one of the functions of IL-1 is to
increase the endogenous production of adenosine. Together, these data
suggest for the first time that sub-femtomolar levels of IL-1 can
effectively modulate glutamate excitation in hippocampal neurons via an
adenosine-dependent mechanism.
Key words:
adenosine; brain slices; cytokine; electrophysiology; femtomolar; glutamatergic transmission; hippocampus; interleukin-1
Copyright © 1999 Society for Neuroscience 0270-6474/99/19114238-07$05.00/0
This article has been cited by other articles:

|
 |

|
 |
 
R. Serantes, F. Arnalich, M. Figueroa, M. Salinas, E. Andres-Mateos, R. Codoceo, J. Renart, C. Matute, C. Cavada, A. Cuadrado, et al.
Interleukin-1beta Enhances GABAA Receptor Cell-surface Expression by a Phosphatidylinositol 3-Kinase/Akt Pathway: RELEVANCE TO SEPSIS-ASSOCIATED ENCEPHALOPATHY
J. Biol. Chem.,
May 26, 2006;
281(21):
14632 - 14643.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. A. Alt, F. Obal Jr., T. R. Traynor, J. Gardi, J. A. Majde, and J. M. Krueger
Alterations in EEG activity and sleep after influenza viral infection in GHRH receptor-deficient mice
J Appl Physiol,
August 1, 2003;
95(2):
460 - 468.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. Kubota, T. Kushikata, J. Fang, and J. M. Krueger
Nuclear factor-kappa B inhibitor peptide inhibits spontaneous and interleukin-1beta -induced sleep
Am J Physiol Regulatory Integrative Comp Physiol,
August 1, 2000;
279(2):
R404 - R413.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. Wang, Q. Cheng, S. Malik, and J. Yang
Interleukin-1beta Inhibits gamma -Aminobutyric Acid Type A (GABAA) Receptor Current in Cultured Hippocampal Neurons
J. Pharmacol. Exp. Ther.,
February 1, 2000;
292(2):
497 - 504.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
A. Hmadcha, F. J. Bedoya, F. Sobrino, and E. Pintado
Methylation-Dependent Gene Silencing Induced by Interleukin 1{beta} via Nitric Oxide Production
J. Exp. Med.,
December 6, 1999;
190(11):
1595 - 1604.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|

|