PMID- 8748930
OWN - NLM
STAT- MEDLINE
DCOM- 19961022
LR  - 20191101
IS  - 1044-7393 (Print)
IS  - 1044-7393 (Linking)
VI  - 26
IP  - 3
DP  - 1995 Dec
TI  - Motor alterations and neuronal damage induced by intracerebral administration of 
      Ruthenium red: effect of NMDA receptor antagonists and other anticonvulsant 
      drugs.
PG  - 285-99
AB  - The effects of the intracerebroventricular (icv) and the intrahippocampal (ih) 
      microinjection of the inorganic dye Ruthenium red (RuR) on motor activity, and 
      the protective action of excitatory amino acid receptor antagonists and of 
      GABAergic drugs, were studied in the rat. When administered icv, RuR produced 
      intense tonic-clonic convulsions which were refractory to N-methyl-D-aspartate 
      (NMDA) receptor antagonists and to diphenylhydantoin, whereas aminooxyacetic acid 
      (AOA) and valproate only partially protected against seizure activity. The most 
      notable motor effect of the ih RuR administration was the appearance of intense 
      wet-dog shakes (WDS) behavior, which was remarkably attenuated by the icv or 
      intraperitoneal (ip) administration of the NMDA receptor antagonists 
      (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), CGP-37849, and 
      MK-801, but not by their ih coinjection with RuR. Systemic AOA and valproate were 
      also effective in reducing the number of WDS, whereas the non-NMDA receptor 
      antagonist CNQX was ineffective. Light and electron microscopic observations of 
      the RuR-injected brains revealed that the dye was highly concentrated in neuronal 
      somas located in or near the injected areas. In the case of the CA1 region, 
      remarkable damage of the pyramidal neurons was manifested by vacuolization, and 
      5-9 d after the injection notable cell loss and disruption of the CA1 cell layer 
      organization was apparent. The results indicate that RuR penetrates selectively 
      neuronal bodies and damage them, and suggest that the resulting motor alterations 
      involve hyperactivity of glutamatergic neurotransmission.
FAU - Belmar, E
AU  - Belmar E
AD  - Department of Neurosciences, National University of Mexico.
FAU - Garcia-Ugalde, G
AU  - Garcia-Ugalde G
FAU - Tapia, R
AU  - Tapia R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Chem Neuropathol
JT  - Molecular and chemical neuropathology
JID - 8910358
RN  - 0 (Anticonvulsants)
RN  - 0 (Coloring Agents)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 11103-72-3 (Ruthenium Red)
SB  - IM
MH  - Animals
MH  - Anticonvulsants/administration & dosage/*pharmacology
MH  - Coloring Agents/administration & dosage/*toxicity
MH  - Hippocampus/drug effects/pathology
MH  - Injections, Intraventricular
MH  - Male
MH  - Motor Activity/*drug effects
MH  - Neurons/*drug effects/*pathology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors
MH  - Ruthenium Red/administration & dosage/*toxicity
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - 10.1007/BF02815144 [doi]
PST - ppublish
SO  - Mol Chem Neuropathol. 1995 Dec;26(3):285-99. doi: 10.1007/BF02815144.