PMID- 25582543
OWN - NLM
STAT- MEDLINE
DCOM- 20151230
LR  - 20161125
IS  - 1531-4332 (Electronic)
IS  - 1095-6433 (Linking)
VI  - 184
DP  - 2015 Jun
TI  - Reversible brain swelling in crucian carp (Carassius carassius) and goldfish 
      (Carassius auratus) in response to high external ammonia and anoxia.
PG  - 65-75
LID - S1095-6433(15)00002-1 [pii]
LID - 10.1016/j.cbpa.2014.12.038 [doi]
AB  - Increased internal ammonia (hyperammonemia) and ischemic/anoxic insults are known 
      to result in a cascade of deleterious events that can culminate in potentially 
      fatal brain swelling in mammals. It is less clear, however, if the brains of 
      fishes respond to ammonia in a similar manner. The present study demonstrated 
      that the crucian carp (Carassius carassius) was not only able to endure high 
      environmental ammonia exposure (HEA; 2 to 22 mmol L(-1)) but that they 
      experienced 30% increases in brain water content at the highest ammonia 
      concentrations. This swelling was accompanied by 4-fold increases in plasma total 
      ammonia (TAmm) concentration, but both plasma TAmm and brain water content were 
      restored to pre-exposure levels following depuration in ammonia-free water. The 
      closely related, ammonia-tolerant goldfish (Carassius auratus) responded 
      similarly to HEA (up to 3.6 mmol L(-1)), which was accompanied by 4-fold 
      increases in brain glutamine. Subsequent administration of the glutamine 
      synthetase inhibitor, methionine sulfoximine (MSO), reduced brain glutamine 
      accumulation by 80% during HEA. However, MSO failed to prevent ammonia-induced 
      increases in brain water content suggesting that glutamine may not be directly 
      involved in initiating ammonia-induced brain swelling in fishes. Although the 
      mechanisms of brain swelling are likely different, exposure to anoxia for 96 h 
      caused similar, but lesser (10%) increases in brain water content in crucian 
      carp. We conclude that brain swelling in some fishes may be a common response to 
      increased internal ammonia or lower oxygen but further research is needed to 
      deduce the underlying mechanisms behind such responses.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Wilkie, Michael P
AU  - Wilkie MP
AD  - Department of Biology and Institute for Water Science, Wilfrid Laurier 
      University, Waterloo, Ontario N2L 3C5, Canada; Department of Biosciences, 
      University of Oslo, Oslo, Norway. Electronic address: mwilkie@wlu.ca.
FAU - Stecyk, Jonathan A W
AU  - Stecyk JA
AD  - Department of Biosciences, University of Oslo, Oslo, Norway; Department of 
      Biological Sciences, University of Alaska Anchorage, Anchorage, USA.
FAU - Couturier, Christine S
AU  - Couturier CS
AD  - Department of Biosciences, University of Oslo, Oslo, Norway.
FAU - Sidhu, Sanya
AU  - Sidhu S
AD  - Department of Biology and Institute for Water Science, Wilfrid Laurier 
      University, Waterloo, Ontario N2L 3C5, Canada.
FAU - Sandvik, Guro K
AU  - Sandvik GK
AD  - Department of Biosciences, University of Oslo, Oslo, Norway.
FAU - Nilsson, Goran E
AU  - Nilsson GE
AD  - Department of Biosciences, University of Oslo, Oslo, Norway.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150109
PL  - United States
TA  - Comp Biochem Physiol A Mol Integr Physiol
JT  - Comparative biochemistry and physiology. Part A, Molecular & integrative 
      physiology
JID - 9806096
RN  - 3K9958V90M (Ethanol)
RN  - 7664-41-7 (Ammonia)
SB  - IM
MH  - Ammonia/*administration & dosage
MH  - Animals
MH  - Body Water
MH  - Brain Edema/*etiology
MH  - Carps
MH  - Ethanol/metabolism
MH  - Goldfish
MH  - *Hypoxia
OTO - NOTNLM
OT  - Ammonia toxicity
OT  - Astrocyte
OT  - Brain
OT  - Encephalopathy
OT  - Ethanol
OT  - Glutamine
OT  - Glutamine synthetase
OT  - Hyperammonemia
OT  - Methionine sulfoximine
OT  - Neurotoxicity
EDAT- 2015/01/15 06:00
MHDA- 2015/12/31 06:00
CRDT- 2015/01/14 06:00
PHST- 2014/09/17 00:00 [received]
PHST- 2014/12/30 00:00 [revised]
PHST- 2014/12/31 00:00 [accepted]
PHST- 2015/01/14 06:00 [entrez]
PHST- 2015/01/15 06:00 [pubmed]
PHST- 2015/12/31 06:00 [medline]
AID - S1095-6433(15)00002-1 [pii]
AID - 10.1016/j.cbpa.2014.12.038 [doi]
PST - ppublish
SO  - Comp Biochem Physiol A Mol Integr Physiol. 2015 Jun;184:65-75. doi: 
      10.1016/j.cbpa.2014.12.038. Epub 2015 Jan 9.