COX-2, a synaptically induced enzyme, is expressed by excitatory neurons at postsynaptic sites in rat cerebral cortex

W E Kaufmann, P F Worley, J Pegg, M Bremer, P Isakson, W E Kaufmann, P F Worley, J Pegg, M Bremer, P Isakson

Abstract

Postnatal development and adult function of the central nervous system are dependent on the capacity of neurons to effect long-term changes of specific properties in response to neural activity. This neuronal response has been demonstrated to be tightly correlated with the expression of a set of regulatory genes which include transcription factors as well as molecules that can directly modify cellular signaling. It is hypothesized that these proteins play a role in activity-dependent response. Previously, we described the expression and regulation in brain of an inducible form of prostaglandin synthase/cyclooxygenase, termed COX-2. COX-2 is a rate-limiting enzyme in prostanoid synthesis and its expression is rapidly regulated in developing and adult forebrain by physiological synaptic activity. Here we demonstrate that COX-2 immunoreactivity is selectively expressed in a subpopulation of excitatory neurons in neo-and allocortices, hippocampus, and amygdala and is compartmentalized to dendritic arborizations. Moreover, COX-2 immunoreactivity is present in dendritic spines, which are specialized structures involved in synaptic signaling. The developmental profile of COX-2 expression in dendrites follows well known histogenetic gradients and coincides with the critical period for activity-dependent synaptic remodeling. These results suggest that COX-2, and its diffusible prostanoid products, may play a role in postsynaptic signaling of excitatory neurons in cortex and associated structures.

References

    1. Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4
    1. Vision Res. 1994 Mar;34(6):709-20
    1. Proc Natl Acad Sci U S A. 1986 Mar;83(5):1536-40
    1. J Histochem Cytochem. 1986 May;34(5):599-605
    1. Nature. 1988 Nov 3;336(6194):68-70
    1. Ann N Y Acad Sci. 1989;559:84-99
    1. Nature. 1989 Oct 26;341(6244):739-42
    1. Neuron. 1990 Apr;4(4):477-85
    1. J Neurochem. 1990 Dec;55(6):1920-7
    1. Biochim Biophys Acta. 1991 May 8;1083(2):121-34
    1. J Biol Chem. 1991 Jul 15;266(20):12866-72
    1. Cold Spring Harb Symp Quant Biol. 1990;55:213-23
    1. Proc Natl Acad Sci U S A. 1992 Jun 1;89(11):4888-92
    1. Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5437-41
    1. Prog Brain Res. 1992;90:477-502
    1. Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7384-8
    1. Vis Neurosci. 1992 Nov;9(5):445-59
    1. Cereb Cortex. 1994 Jan-Feb;4(1):40-51
    1. J Biol Chem. 1994 Jun 10;269(23):16333-9
    1. Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12013-7
    1. Biochem J. 1995 Jan 15;305 ( Pt 2):479-84
    1. Neuron. 1995 Feb;14(2):433-45
    1. Science. 1995 Apr 14;268(5208):239-47
    1. Science. 1995 Apr 14;268(5208):297-300
    1. J Biol Chem. 1995 May 5;270(18):10902-8
    1. J Comp Neurol. 1995 May 1;355(2):296-315
    1. Neuroscience. 1995 Dec;69(3):781-96
    1. Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11543-6
    1. Neuron. 1993 Jan;10(1):31-41
    1. Cell. 1993 Jan;72 Suppl:77-98
    1. Nature. 1993 Feb 4;361(6411):453-7
    1. Neuroscience. 1993 Mar;53(2):327-58
    1. Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):7240-4
    1. Cell. 1993 Aug 13;74(3):565-75
    1. Neuron. 1993 Aug;11(2):371-86
    1. J Biol Chem. 1993 Nov 5;268(31):23448-54
    1. J Neurosci. 1994 Jan;14(1):242-62
    1. Prostaglandins. 1994 Jan;47(1):55-9
    1. Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3228-32
    1. Proc Natl Acad Sci U S A. 1983 Oct;80(19):6126-30

Source: PubMed

Спонсоры и соавторы

Заболевания

Медикаментозные вмешательства

Подписаться