Naltrexone blocks the enhancing effect of novel experiences on performance in memory tests in humans.

Two experiments were carried out in healthy human volunteers in order to investigate the effect of novel experiences on retrieval, and the influence of naltrexone thereupon. Naltrexone (50 mg) and placebo (50 mg of starch) were given orally using a double blind design. In Experiment 1, the subjects were asked, on two consecutive days, to recall well-known facts or events, and to recall the year in which major events took place. On Day 2, some subjects were, and others were not, exposed to a nonsense text prior to testing, which was viewed as a novel experience by the subjects. Exposure to the text was followed by enhanced scores in both memory tests. The effect was blocked by naltrexone, but not by the placebo, given 1 hr prior to the novel experience; the treatments had no effect of their own in subjects unexposed to the nonsense text. In Experiment 2, the memory tests were the recognition of famous faces, and the dates test (see above); and the novel experience was being taken for 5 min to a room where they had never been before. Again, the novel experience was followed by increased scores in both memory tests in the untreated and placebo groups, but not in the naltrexone treated subjects. These results confirm previous findings on memory enhancement by pre-test exposure to novel experiences, and suggest that endogenous opioid, or at least naltrexone-sensitive, mechanisms are involved in the effect.

Pre-training adrenaline recovers the amnestic effect of Met-enkephalin in demedullated rats.

The intracerebroventricular administration of 25 ng of Met-enkephalin causes retrograde amnesia for a shuttle avoidance task in intact rats. In demedullated rats, this effect of Met-enkephalin was lost. Intraperitoneal injection of 1.2 micrograms/kg adrenaline recovered the amnestic effect of Met-enkephalin. These results confirm the idea that the amnestic effect of Met-enkephalin is centrally mediated and that adrenal enkephalins do not seem to be important to the amnestic effect of Met-enkephalin since adrenaline recovers this effect in demedullated rats.

Intracerebroventricular administration of nanogram amounts of beta-endorphin and Met-enkephalin causes retrograde amnesia in rats.

The intracerebroventricular (icv) administration of 5.0 or 25.0 ng of beta-endorphin or Met-enkephalin causes retrograde amnesia for a shuttle avoidance task ion rats. In both cases, the higher dose was more effective than the lower one. The present results confirm previous similar findings obtained using systemic administrations of these compounds, and suggest that the amnestic effect of beta-endorphin and Met-enkephalin is mediated centrally.

Pure amnestic seizures in temporal lobe epilepsy. Definition, clinical symptomatology and functional anatomical considerations.

Pure amnestic seizures (PAS) sometimes occur in patients with temporal lobe epilepsy. They never represent the only type of seizures in these patients. Pure amnestic seizures are defined as seizures during which the only clinical manifestation is the patients' inability to retain in memory what occurs during the seizure coupled with the preservation of other cognitive functions and the ability to interact normally with their physical and social environment. It is postulated that PAS result from selective ictal inactivation of mesial temporal (MT) structures without isocortical involvement. This occurs most often in patients with neuropsychological and electroencephalographic (EEG) evidence of bilateral dysfunction of MT structures (six out of eight patients in this study). In the few patients without such evidence as well as in some with bilateral MT dysfunction, PAS may result from seizure discharge limited to the MT structures of both temporal lobes. In the light of current anatomical knowledge, contralateral spread of seizure discharge from the MT structures of one side to those of the other through the dorsal hippocampal commissure is the only likely explanation for this situation. One observation with depth electrode stimulation of MT structures supports this view. In patients with evidence for bilateral MT dysfunction, a unilateral seizure may presumably suffice to induce a PAS, the contralateral MT structures being unable to ensure normal memory function. In most instances PAS can be distinguished from episodes of transient global amnesia on clinical grounds.