Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.5.4.4 (
adenosine deaminase
)
5,136
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Neurons of the tuberomammillary nucleus (TM) in the rat have previously been shown to contain the enzymes
adenosine deaminase
(
ADA
), histidine decarboxylase (HDC) and glutamate decarboxylase (GAD). Some neurons coextensive with this cell group also exhibit immunoreactivity for the neuropeptide galanin, express monoamine oxidase activity (MAO), or display the ability to accumulate and decarboxylate
5-hydroxytryptophan
(
5-HTP
). Histochemical and immunohistochemical techniques were used to determine the extent to which these neurochemical properties are colocalized in neurons immunoreactive for
adenosine deaminase
. Galanin was found to coexist with
ADA
in about 45% of the neurons in the TM. In addition, a large number of cells immunoreactive for galanin alone were observed in the posterior hypothalamus outside the confines of TM. Neurons displaying MAO activity formed a subpopulation of those immunoreactive for
ADA
; all neurons containing MAO also contained
ADA
whereas only 60% of the
ADA
-immunoreactive cells were reactive for MAO. Approximately 20% of
ADA
-immunoreactive neurons represented nearly all cells having
5-HTP
uptake capability. However, a very few cells in TM showing
5-HTP
uptake capability appeared to be devoid of
ADA
immunoreactivity. These results demonstrate that although neurons of TM are homogeneous with respect to a number of possible neurotransmitters markers and associated enzymes, these neurons are heterogeneous with respect to their expression of galanin, MAO and
5-HTP
uptake. In certain respects the segregation of histochemical properties within TM correlates with previous histochemical work by others, and suggests the possibility of functional diversity of TM.
...
PMID:Neuronal colocalization of adenosine deaminase, monoamine oxidase, galanin and 5-hydroxytryptophan uptake in the tuberomammillary nucleus of the rat. 242 41
Neurons of the posterior hypothalamic magnocellular nucleus (PHMN) in the rat are immunoreactive for
adenosine deaminase
(
ADA
) and cells coextensive with this nucleus show immunoreactivity for serotonin after pretreatment with
5-hydroxytryptophan
(
5-HTP
). The degree to which
ADA
coexists in cells having
5-HTP
uptake capability was analyzed by a new double immunohistofluorescence procedure employing diethylaminocoumarin (DAMC). It was determined that
5-HTP
accumulating cells of the PHMN represent a subpopulation of those immunoreactive for
ADA
. These results add further to the neurochemical characterization of this globally projecting hypothalamic cell group and point out the utility of DAMC as a new immunohistofluorescence marker.
...
PMID:Adenosine deaminase-containing hypothalamic neurons accumulate 5-hydroxytryptophan: a dual-colour immunofluorescence procedure using a new fluorescence marker. 353 35
The role of adenosine A1 receptors (A1R) in reflex-evoked short-circuit current (Isc) indicative of chloride secretion was studied in the guinea pig colon. The A1R antagonist 8-cyclopentyltheophylline (CPT) enhanced reflex-evoked Isc. Adenosine deaminase and the nucleoside transport inhibitor S-(4-nitrobenzyl)-6-thioinosine enhanced and reduced reflex-induced Isc, respectively. The A1R agonist 2-chloro-N6-cyclopentyladenosine (CCPA) inhibited reflex-evoked Isc at nanomolar concentrations, and its action was antagonized by CPT. In the presence of either N-acetyl-5-hydroxytryptophyl-
5-hydroxytryptophan
amide to block the 5-hydroxytryptamine (5-HT)-mediated pathway or piroxicam to block the prostaglandin-mediated pathway, CCPA reduced the residual reflex-evoked Isc. CCPA reduced the response to a 5-HT pulse without affecting the tetrodotoxin-insensitive Isc responses to carbachol or forskolin. Immunoreactivity for A1R was detected in the membrane (10% of neurons) and cytoplasm (90% of neurons) of neural protein gene product 9.5-immunoreactive (or S-100-negative) submucosal neurons, in glia, and in the muscularis mucosa. A1R immunoreactivity in a majority of neurons remained elevated in the cytoplasm despite preincubation with
adenosine deaminase
or CPT. A1R immunoreactivity colocalized in synaptophysin-immunoreactive presynaptic varicose nerve terminals. The results indicate that endogenous adenosine binding to high-affinity A1R on submucosal neurons acts as a physiological brake to suppress reflex-evoked Isc indicative of chloride secretion.
...
PMID:Activation of neuronal adenosine A1 receptors suppresses secretory reflexes in the guinea pig colon. 995 Aug 19