Jun 1, 1981

Cyclic AMP-generating systems in rat hippocampal slices

Brain Research
M SegalR Hofstein

Abstract

Properties of the norepinephrine (NE) stimulated, cAMP-generating system were studied in rat hippocampal slices. NE but not other putative neurotransmitters, caused a 3--4-fold rise in cAMP levels in the slices. All 3 main subdivisions of the hippocampus (HPC), the dentate gyrus, areas CA3 and CA1, possessed the capacity to produce cAMP. The latency to the NE stimulation of cAMP formation was about 20 sec but maximal stimulation was reached only after 5--10 min of incubation. Intrahippocampal injection of kainic acid (KA) caused a nearly complete destruction of hippocampal neurons and a marked increase in number of glial cells. NE caused a 12--15-fold rise in cAMP levels in KA-treated HPC. Compared to normal HPC where potency order of noradrenergic agonists indicated activation of a beta-1 receptor type, the pattern for the KA-treated HPC indicated the dominance of beta-2 receptors. The beta-1 antagonist, practolol, and the beta-2 antagonist, H35/25, were about equipotent in blocking the NE-stimulated cAMP formation in normal HPC. In KA-treated HPC, on the other hand, H35/25 was much more potent than practolol in inhibiting NE-stimulated cAMP formation. It is suggested that in the HPC beta-1 adrenergic receptors are primarily n...Continue Reading

Mentioned in this Paper

Practolol
Neurons
Antagonist Muscle Action
Kainic Acid
Cyclic AMP
Neuroglia
Norepinephrine, (+, -)-Isomer
Cyclic Adenosine Monophosphate Measurement
Genus Hippocampus
Structure of Hippocampal Formation

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