Biomaterial Database

Hippocampal CA3 lesion prevents postconcussive metabolic dysfunction in CA1. 1992

A Yoshino, and D A Hovda, and Y Katayama, and T Kawamata, and D P Becker

Division of Neurosurgery, UCLA School of Medicine 90024-6901.

Immediately following fluid-percussion (F-P) brain injury, the hippocampus exhibits a marked increase in its local CMRglc (LCMRglc; mumol/100 g/min) as determined using [14C]2-deoxy-D-glucose autoradiography. This injury-induced increase in metabolism is followed in 6 h by a subsequent decrease in LCMRglc. These two postinjury metabolic states may be the result of ionic disruptions following trauma via stimulation of glutamate-gated ion channels. To determine if endogenous glutamate innervation to the CA1 region of the hippocampus can provide an anatomical basis for this proposed mechanism, it was removed by kainic-acid-induced destruction of CA3, and the effect on CA1 metabolism following concussive injury was studied. Five days before a lateral F-P injury (3.5-4.5 atm), kainic acid (0.5 microgram) or vehicle was stereotaxically injected into the left ventricle of 65 rats. Histological inspection indicated that kainic acid produced severe cell loss primarily in the CA3 region of the hippocampus ipsilateral to the injection. The metabolic results indicated that immediately following injury, animals with an intact hippocampus exhibited an increase in LCMRglc to 84.6 +/- 5 within the CA1 region, representing a 81.5% increase over controls. However, in the CA3-lesioned animals, CA1 showed no evidence of an injury-induced hypermetabolism, with LCMRglc remaining at control levels (51.4 +/- 3.9). At 6 h postinjury, the intact hippocampus exhibited a reduction of LCMRglc to rates of 40.7 +/- 4.7 within the CA1 region, representing a 17.9% reduction compared with controls. In contrast, CA3-lesioned animals exhibited less of an injury-induced decrease in LCMRglc within the CA1 region, exhibiting a mean rate of 43.4 +/- 4.5, representing only a 12.5% reduction compared with controls. These results indicate that the removal of the CA3 projection to CA1 protects the CA1 cells from the metabolic dysfunction typically seen following injury. This supports our previous work indicating the important role glutamate plays in the ionic flux and subsequent metabolic changes that follow traumatic brain injury.

UI	MeSH Term	Description	Entries
D007608	Kainic Acid	(2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.	Digenic Acid,Kainate,Acid, Digenic,Acid, Kainic
D008297	Male		Males
D001924	Brain Concussion	A nonspecific term used to describe transient alterations or loss of consciousness following closed head injuries. The duration of UNCONSCIOUSNESS generally lasts a few seconds, but may persist for several hours. Concussions may be classified as mild, intermediate, and severe. Prolonged periods of unconsciousness (often defined as greater than 6 hours in duration) may be referred to as post-traumatic coma (COMA, POST-HEAD INJURY). (From Rowland, Merritt's Textbook of Neurology, 9th ed, p418)	Cerebral Concussion,Commotio Cerebri,Concussion, Intermediate,Concussion, Mild,Concussion, Severe,Mild Traumatic Brain Injury,Brain Concussions,Cerebral Concussions,Concussion, Brain,Concussion, Cerebral,Intermediate Concussion,Intermediate Concussions,Mild Concussion,Mild Concussions,Severe Concussion,Severe Concussions
D002250	Carbon Radioisotopes	Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.	Radioisotopes, Carbon
D003847	Deoxyglucose	2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.	2-Deoxy-D-glucose,2-Deoxyglucose,2-Desoxy-D-glucose,2 Deoxy D glucose,2 Deoxyglucose,2 Desoxy D glucose
D004195	Disease Models, Animal	Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.	Animal Disease Model,Animal Disease Models,Disease Model, Animal
D005971	Glutamates	Derivatives of GLUTAMIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the 2-aminopentanedioic acid structure.	Glutamic Acid Derivatives,Glutamic Acids,Glutaminic Acids
D006624	Hippocampus	A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.	Ammon Horn,Cornu Ammonis,Hippocampal Formation,Subiculum,Ammon's Horn,Hippocampus Proper,Ammons Horn,Formation, Hippocampal,Formations, Hippocampal,Hippocampal Formations,Hippocampus Propers,Horn, Ammon,Horn, Ammon's,Proper, Hippocampus,Propers, Hippocampus,Subiculums
D000818	Animals	Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA.	Animal,Metazoa,Animalia
D017207	Rats, Sprague-Dawley	A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.	Holtzman Rat,Rats, Holtzman,Sprague-Dawley Rat,Rats, Sprague Dawley,Holtzman Rats,Rat, Holtzman,Rat, Sprague-Dawley,Sprague Dawley Rat,Sprague Dawley Rats,Sprague-Dawley Rats