PMID- 7663989
OWN - NLM
STAT- MEDLINE
DCOM- 19951010
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 680
IP  - 1-2
DP  - 1995 May 22
TI  - Activation of glycogen phosphorylase by serotonin and 
      3,4-methylenedioxymethamphetamine in astroglial-rich primary cultures: 
      involvement of the 5-HT2A receptor.
PG  - 9-15
AB  - Neurotransmitters, neuropeptides, and ions regulate glycogen levels in the brain 
      by modulating the activity of glycogen synthase (GSase) and glycogen 
      phosphorylase (GPase). GPase is co-localized with glial fibrillary acidic protein 
      (GFAP), an astroglia-specific marker, suggesting that glycogen is localized in 
      astroglial cells. Additionally, functional serotonin (5-HT) receptors are found 
      in both neurons and glia, and 5-HT is known to stimulate glycogenolysis. It is 
      reported that 3,4-methylenedioxymethamphetamine (MDMA), a drug of abuse, 
      stimulates the release and inhibits the reuptake of 5-HT, and selectively 
      inhibits the activity of MAO-A. These biochemical consequences of MDMA lead to 
      increased extra-cellular 5-HT levels. This study investigates the effects of 
      MDMA(+) and serotonin (5-HT) on glycogen metabolism in the rat brain. A 
      histochemical method was designed to visualize active glycogen phosphorylase 
      (GPase) in an astroglial-rich primary culture. Serotonin activated GPase in a 
      concentration-dependent manner (100 nM-100 microM). Maximal activation by 5-HT 
      was achieved by 50 microM and resulted in a 167% increase in the number of 
      reactive sites (P < 0.001). MDMA(+) (500 nM-50 microM) directly stimulated GPase 
      activity with maximal activation induced by 5 microM, which caused a 70% increase 
      in the number of reactive sites (P < 0.001). The 5-HT2 receptor agonist, 
      1-(2,5-dimethoxy-4-bromophenyl)-2-aminopropane (DOB), also displayed a 
      concentration-dependent increase in the number of GPase reactive sites. Maximal 
      stimulation by DOB occurred at 100 nM which increased the number of reactive 
      sites by 166% (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Poblete, J C
AU  - Poblete JC
AD  - Department of Biology, New York University, NY 10003, USA.
FAU - Azmitia, E C
AU  - Azmitia EC
LA  - eng
GR  - 271-90-7403/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Receptors, Serotonin)
RN  - 0 (Serotonin Antagonists)
RN  - 0 (Serotonin Receptor Agonists)
RN  - 333DO1RDJY (Serotonin)
RN  - 4764-17-4 (3,4-Methylenedioxyamphetamine)
RN  - 9005-79-2 (Glycogen)
RN  - EC 2.4.1.- (Phosphorylases)
SB  - IM
MH  - 3,4-Methylenedioxyamphetamine/*pharmacology
MH  - Animals
MH  - Astrocytes/*enzymology
MH  - Cells, Cultured
MH  - Enzyme Activation
MH  - Glycogen/metabolism
MH  - Osmolar Concentration
MH  - Phosphorylases/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Serotonin/*physiology
MH  - Serotonin/*pharmacology
MH  - Serotonin Antagonists/pharmacology
MH  - Serotonin Receptor Agonists/pharmacology
EDAT- 1995/05/22 00:00
MHDA- 1995/05/22 00:01
CRDT- 1995/05/22 00:00
PHST- 1995/05/22 00:00 [pubmed]
PHST- 1995/05/22 00:01 [medline]
PHST- 1995/05/22 00:00 [entrez]
AID - 0006-8993(95)00201-Z [pii]
AID - 10.1016/0006-8993(95)00201-z [doi]
PST - ppublish
SO  - Brain Res. 1995 May 22;680(1-2):9-15. doi: 10.1016/0006-8993(95)00201-z.