Chronic failure in the maintenance of long-term potentiation following fluid percussion injury in the rat

• Published in: Brain research Vol. 861; no. 1; pp. 69 - 76
• Main Authors: Sanders, Matthew J, Sick, Thomas J, Perez-Pinzon, Miguel A, Dietrich, W.Dalton, Green, Edward J
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 07-04-2000; Amsterdam Elsevier; New York, NY
• Subjects: Animals; Biological and medical sciences; Brain Injuries - physiopathology; Brain injury; Excitatory Postsynaptic Potentials - physiology; Fluid percussion; Hippocampus; Hippocampus - physiopathology; Injuries of the nervous system and the skull. Diseases due to physical agents; Learning - physiology; Long-Term Potentiation - physiology; LTP; Male; Medical sciences; Neuronal Plasticity - physiology; Rat; Rats; Rats, Sprague-Dawley; Traumas. Diseases due to physical agents; traumatic brain injury; LTP; Rat; Fluid percussion; Brain injury; Hippocampus; Potentiation; Nervous system diseases; Rodentia; Central nervous system; Electrophysiology; Long term; Trauma; Vertebrata; Chronic; Experimental disease; Mammalia; Synaptic transmission; Animal; Excitatory postsynaptic potential; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(00)01986-7

Traumatic brain injury (TBI) can produce chronic cognitive learning/memory deficits that are thought to be mediated, in part, by impaired hippocampal function. Experimentally induced TBI is associated with deficits in hippocampal synaptic plasticity (long-term potentiation, or LTP) at acute post-injury intervals but plasticity has not been examined at long-term survival periods. The present study was conducted to assess the temporal profile of LTP after injury and to evaluate the effects of injury severity on plasticity. Separate groups of rats were subjected to mild (1.1–1.4 atm), moderate (1.8–2.1 atm), or severe (2.2–2.7 atm) fluid percussion (FP) injury (or sham surgery) and processed for hippocampal electrophysiology in the first or eighth week after injury. LTP was defined as a lasting increase in field excitatory post-synaptic potential (fEPSP) slope in area CA1 following tetanic stimulation of the Schaffer collaterals. The fEPSP slope was measured for 60 min after tetanus. Assessment of LTP at the acute interval (6 days) revealed modest peak slope potentiation values (129–139%), which declined in each group (including sham) over the hour-long recording session and did not differ between groups. Eight weeks following injury, slices from all groups exhibited robust maximal potentiation (134–147%). Levels of potentiation among groups were similar at the 5-min test interval but differed significantly at the 30- and 60-min test intervals. Whereas sham slices showed stable potentiation for the entire 60-min assessment period, slices in all of the injury groups exhibited a significant decline in potentiation over this period. These experiments reveal a previously unknown effect of TBI whereby experimentally induced injury results in a chronic inability of the CA1 hippocampus to
maintain synaptic plasticity. They also provide evidence that sham surgical procedures can significantly influence hippocampal physiology at the acute post-TBI intervals. The results have implications for the mechanisms underlying the impaired synaptic plasticity following TBI.