Premium
Inhibition of dopamine and choline acetyltransferase concentrations in rat CNS neurons by rat α 1 ‐ and α 2 ‐macroglobulins
Author(s) -
Hu YiQun,
Liebl Daniel J.,
Dluzen Dean E.,
Koo Peter H.
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980215)51:4<541::aid-jnr14>3.0.co;2-6
Subject(s) - choline acetyltransferase , medicine , striatum , dopamine , endocrinology , dopaminergic , serotonin , neurotransmitter , biology , 5 ht receptor , cholinergic , central nervous system , receptor
Previous studies have implicated human alpha‐2‐macroglobulin (α 2 M) as a potential regulator of neuronal development and function. Rat alpha‐1‐macroglobulin (α 1 M) and acute‐phase alpha‐2‐macroglobulin (α 2 M) are murine homologues of human α 2 M. In this report, we tested the effect of intracranially infused serotonin‐activated rat α 1 M (5HT‐α 1 M) on the concentration of dopamine (DA) in the corpus striatum in vivo and the effect of 5HT‐activated rat α 1 M and α 2 M on the choline acetyltransferase (ChAT) activity upon embryonic basal forebrain neurons in culture. The results show that direct infusion of 0.65 nmole rat 5HT‐α 1 M into the adult rat corpus striatum produced a consistent attenuation upon striatal DA concentrations. This decrease was particularly prominent at 5–7 days post‐infusion. In addition, rat 5HT‐α 1 M and rat 5HT‐α 2 M, like human 5HT‐α 2 M, all significantly inhibited ChAT activity of embryonic rat cerebral cortex neurons. Although normal human α 2 M and rat α 2 M were either marginally or insignificantly inhibitory in this preparation, normal rat α 1 M dose‐dependently inhibited ChAT activity. These results demonstrate that monoamine‐activated α‐macroglobulins from rat depress dopaminergic and cholinergic neurotransmitter systems in the CNS, and this suggests a potential regulatory role of these alpha‐macroglobulins in neurotransmitter metabolism. J. Neurosci. Res. 51:541–550, 1998. © 1998 Wiley‐Liss, Inc.