ABSTRACT
Lactate and free fatty acids (FFAs) were extracted from the cortices and hippocampi of rats subjected to sham operation, or mild (1.25 atm) or moderate (2.0 atm) fluid percussion (FP) injury, and their total tissue concentrations were measured. The elevation of lactate in the injured left cortex (IC) and ipsilateral hippocampus (IH) was significantly greater in the moderate-injury than in the mild-injury group at most test times between 5 min and 48 h after injury. Levels of total FFAs were elevated in the IC and IH to a greater extent and for a longer period after injury in the moderate-injury (up to 48 h) than in the mild-injury group (up to 20 min). In general, the extent and duration of the elevation of most of the individual FFAs (palmitic, stearic, oleic, and arachidonic acids) in the IC and IH were also greater in the moderate-injury group than in the mild-injury group. In the contralateral cortex (CC) and hippocampus (CH), the elevation of lactate and total FFAs (and individual stearic and arachidonic acids) were also greater in the moderate-injury group than in the low-injury group at 5 min after injury. The extravasation of Evans blue in the IC and IH from 3 to 6 h after injury was also the greatest in the moderate-injury group. The hippocampal CA3 neuronal cell loss, but not cortical lesion volume, also increased with the severity of injury. These findings suggest that certain neurochemical, physiological (blood-brain barrier permeability), and morphologic responses increase with the severity of FP brain injury, and such relationships are consistent with the increased behavioral deficits observed with the increase of severity of brain injury.
Subject(s)
Blood-Brain Barrier/physiology , Cerebral Cortex/injuries , Extravasation of Diagnostic and Therapeutic Materials/etiology , Fatty Acids, Nonesterified/metabolism , Hippocampus/injuries , Lactic Acid/metabolism , Analysis of Variance , Animals , Cerebral Cortex/metabolism , Cerebral Cortex/pathology , Cerebral Cortex/physiopathology , Coloring Agents , Disease Models, Animal , Disease Progression , Evans Blue , Hippocampus/metabolism , Hippocampus/pathology , Hippocampus/physiopathology , Male , Rats , Rats, Sprague-Dawley , Time Factors , Trauma Severity IndicesABSTRACT
Three experiments investigated the role of response requirements in the Morris water maze for pre- and postweanling rats. Fischer-344N pups were required to locate a hidden platform using extramaze cues in a tank modified for the pups' immature response repertoire. Weanlings (20-22 days) displayed spatial learning in a pool 1/2 the size of the adults' (Experiment 1); by 26-28 days of age, probe performance was comparable to adults' on quadrant preference and platform-crossing measures. Preweanlings (17 days), in a pool 1/3 the original size, significantly reduced escape latencies and displayed quadrant preference and platform-crossing scores indicative of spatial navigation. These results suggest that despite its protracted postnatal development, the preweanling hippocampus allows neural integration of visual-spatial information; however, the capacity to demonstrate such learning is dependent on task parameters and the pup's response repertoire.
Subject(s)
Cues , Maze Learning , Orientation , Space Perception , Age Factors , Animals , Association Learning , Escape Reaction , Female , Male , Rats , Rats, Inbred F344ABSTRACT
Levels of PLCgamma, a phospholipase C (PLC) isozyme, were significantly increased in the cytosol in the injured left cortex (LC) at 5, 30 and 120 min after brain injury. In the same site, although levels of membrane PLCgamma did not alter at 5 and 30 min, they were found to be decreased at 2 h after brain injury. In general, the levels of both cytosolic and membrane PLCgamma were unaltered in the contralateral right cortex (RC), ipsilateral left hippocampus (LH) and contralateral right hippocampus (RH) between 5 and 120 min after brain injury. These results suggest that, in addition to well-proposed excitatory neurotransmitter-receptor systems, increased levels of PLCgamma may also contribute to alterations in PIP2 signal transduction pathway, particularly in the greatest injury site (LC) after lateral FP brain injury.
Subject(s)
Brain Injuries/enzymology , Brain/enzymology , Isoenzymes/metabolism , Type C Phospholipases/metabolism , Animals , Cell Membrane/enzymology , Cerebral Cortex/enzymology , Cytosol/enzymology , Functional Laterality , Hippocampus/enzymology , Male , Organ Specificity , Percussion , Phospholipase C gamma , Rats , Rats, Sprague-Dawley , Reference Values , Time FactorsABSTRACT
Regional activities of phosphoinositide-specific phospholipase C (PLC) were measured after lateral fluid percussion (FP) brain injury in rats. The activity of PLC on phosphatidylinositol 4,5-bisphosphate (PIP2) in the rat cortex required calcium, and at 45 microM concentration it increased PLC activity by about ten-fold. The activity of PLC was significantly increased in the cytosol fraction in the injured (left) cortex (IC) at 5 min, 30 min and 120 min after brain injury. However, in the same site, increases were observed in the membrane fraction only at 5 min after brain injury. In both the contralateral (right) cortex (CC) and ipsilateral hippocampus (IH), the activity of PLC was increased in the cytosol only at 5 min after brain injury. These results suggest that increased activity of PLC may contribute to increases in levels of cellular diacylglycerol and inositol trisphosphate in the IC (the greatest site of injury), and to a smaller extent in the IH and CC, after lateral FP brain injury. It is likely that this increased PLC activity is caused by alteration in either the levels or activities of one or more of its isozymes (PLCbeta, PLCgamma, and PLCdelta) after FP brain injury.
Subject(s)
Brain Injuries/enzymology , Type C Phospholipases/metabolism , Animals , Male , Phosphatidylinositol 4,5-Diphosphate/metabolism , Phosphatidylinositol Diacylglycerol-Lyase , Rats , Rats, Sprague-DawleyABSTRACT
Reminder treatments have been shown to facilitate the retrieval of a variety of conditioned responses. Whether or not similar results would occur with an experimental paradigm which involves primarily memory for a stimulus, i.e., where no particular response is specified, is unclear. Accordingly, using Sprague-Dawley rats, we employed a latent inhibition paradigm with a long (10 days) retention interval between sucrose (CS) preexposure and sucrose-illness pairing (training). The results demonstrated a loss of latent inhibition following the 10-day retention interval suggesting "forgetting" of the CS preexposure. However, placing a single reminder exposure to the CS within the preexposure-to-training interval reinstated the preexposure effect. Controls indicated that in the absence of the initial preexposure the reminder per se did not produce latent inhibition. Thus, a reminder can reinstate a stimulus attribute (flavor representation) and explicit conditioned responses.