PMID- 16382345
OWN - NLM
STAT- MEDLINE
DCOM- 20060208
LR  - 20181113
IS  - 0885-7490 (Print)
IS  - 0885-7490 (Linking)
VI  - 20
IP  - 4
DP  - 2005 Dec
TI  - Altered modulation of motor activity by group I metabotropic glutamate receptors 
      in the nucleus accumbens in hyperammonemic rats.
PG  - 347-58
AB  - One of the neurological complications in hepatic encephalopathy is the impairment 
      of motor coordination and function. Clinical signs of basal ganglia, 
      cortico-spinal and cerebellar dysfunction have been commonly detected in these 
      patients. We are studying the molecular bases of the alterations in motor 
      coordination and function in hepatic encephalopathy. Hyperammonemia is considered 
      the main factor responsible for the neurological alterations in patients with 
      hepatic encephalopathy. Activation of metabotropic glutamate receptors (mGluRs) 
      in the nucleus accumbens (NAcc) induces locomotion in rats. Asa first step in our 
      studies on the alterations in motor co-ordination and function in hyperammonemia 
      and hepatic encephalopathy we studied whether the control of motor function by 
      mGluRs in the NAcc is altered in hyperammonemic rats. The locomotor activity 
      induced by injection into the nucleus accumbens (NAcc) of DHPG, an agonist of 
      group I mGluRs was significantly increased in hyperammonemic rats. Injection of 
      DHPG increased extracellular dopamine but not glutamate in the NAcc of control 
      rats. In hyperammonemic rats DHPG-induced increase in dopamine was significantly 
      reduced, and extracellular glutamate increased 6-fold. The content of mGluR 1 but 
      not mGluR 5, is increased in the NAcc of hyperammonemic rats. Blockade of mGluR 1 
      completely prevented motor and neurochemical effects induced by DHPG. These 
      results show that modulation of both motor function and extracellular 
      concentration of neurotransmitters by mGluRs in the NAcc is altered in 
      hyperammonemia. This may contribute to the alterations in motor function in 
      hepatic encephalopathy.
FAU - Cauli, Omar
AU  - Cauli O
AD  - Laboratory of Neurobiology, Fundacion Valenciana de Investigaciones Biomedicas, 
      Valencia, Spain. weisseborn.kain@mh-hannover.de
FAU - Llansola, Marta
AU  - Llansola M
FAU - Rodrigo, Regina
AU  - Rodrigo R
FAU - El Mlili, Nisrin
AU  - El Mlili N
FAU - Errami, Mohammed
AU  - Errami M
FAU - Felipo, Vicente
AU  - Felipo V
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Metab Brain Dis
JT  - Metabolic brain disease
JID - 8610370
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, Glutamate)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Dopamine/physiology
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Genes, fos/genetics
MH  - Hyperammonemia/*metabolism/*psychology
MH  - Immunohistochemistry
MH  - Motor Activity/*drug effects/physiology
MH  - Nucleus Accumbens/*metabolism
MH  - Rats
MH  - Receptors, Glutamate/drug effects/*metabolism
RF  - 84
EDAT- 2005/12/31 09:00
MHDA- 2006/02/09 09:00
CRDT- 2005/12/31 09:00
PHST- 2005/12/31 09:00 [pubmed]
PHST- 2006/02/09 09:00 [medline]
PHST- 2005/12/31 09:00 [entrez]
AID - 10.1007/s11011-005-7918-0 [doi]
PST - ppublish
SO  - Metab Brain Dis. 2005 Dec;20(4):347-58. doi: 10.1007/s11011-005-7918-0.