ABSTRACT
Bilateral aspiration lesions of the fimbria-fornix were performed in 10 male Sprague Dawley rats weighing 240-300 g under chloral hydratenarcose (420 mg/kg). Another 9 animals were operated in the same way, but no aspiration was carried out to constitute a control group. A week after surgery recording and stimulation electrodes were lowered to the dentate gyrus and the perforant path respectively, using the same narcose. After tetanic stimulation (10 trains at 400 Hz) a potentiation of the population spike develops in both groups, but the slope of the excitatory postsynaptic potential showed no potentiation in the lesioned group. Acetylcholinesterase histochemistry confirmed a severe reduction of the cholinergic innervation to the hippocampal formation, suggesting a causal relationship to the deficits seen in long-term potentiation. This impaired potentiation could be related to the memory deficits reported for fimbria-fornix lesioned rats. Such pattern of potentiation deviates from what has been described for aged, memory deficient rats, but closely corresponds to the changes described in infantile rats
Subject(s)
Animals , Dentate Gyrus , Hippocampus , Long-Term Potentiation , Rats , Disease Models, AnimalABSTRACT
Bilateral aspiration lesions of the fimbria-fornix were performed in 10 male Sprague Dawley rats weighing 240-300 g under chloral hydrate narcose (420 mg/kg). Another 9 animals were operated in the same way, but no aspiration was carried out to constitute a control group. A week after surgery recording and stimulation electrodes were lowered to the dentate gyrus and the perforant path respectively, using the same narcose. After tetanic stimulation (10 trains at 400 Hz) a potentiation of the population spike develops in both groups, but the slope of the excitatory postsynaptic potential showed no potentiation in the lesioned group. Acetylcholinesterase histochemistry confirmed a severe reduction of the cholinergic innervation to the hippocampal formation, suggesting a causal relationship to the deficits seen in long-term potentiation. This impaired potentiation could be related to the memory deficits reported for fimbria-fornix lesioned rats. Such pattern of potentiation deviates from what has been described for aged, memory deficient rats, but closely corresponds to the changes described in infantile rats