When rats received a brief footshock upon stepping off an elevated platform, and an electroconvulsive shock 30 seconds or 6 hours afterward, amnesia was not observed 24 hours later. If a second footshock (noncontingent) was delivered 0.5 second before the electroconvulsive shock, amnesia was observed. The amnesia was temporary if conditioning was strong and permanent if conditioning was weak.

No abstract

We showed previously that the induction of neural crest (NC) and neural tube (NT) defects is a general property of N-methyl-D-aspartate receptor (NMDAR) antagonists. Since homocysteine induces NC and NT defects and can also act as an NMDAR antagonist, we hypothesized that the mechanism of homocysteine-induced developmental defects is mediated by competitive inhibition of the NMDAR by homocysteine. If this hypothesis is correct, homocysteine-induced defects will be reduced by NMDAR agonists. To test the hypothesis, we treated chicken embryos during the process of neural tube closure with sufficient homocysteine thiolactone to induce NC and NT defects in approximately 40% of survivors or with homocysteine thiolactone in combination with each of a selected set of NMDAR agonists in 0. 05-5000 nmol doses. Glutamate site agonists selected were L-glutamate and N-methyl-D-aspartate. Glycine site agonists were glycine, D-cycloserine, and aminocyclopropane-carboxylic acid. Glycine was the most effective overall, reducing defects significantly at two different doses (each P>0.001). These results support the hypothesis that homocysteine may affect NC and NT development by its ability to inhibit the NMDAR. One potentially important consequence of this putative mechanism is that homocysteine may interact synergistically with other NMDAR antagonists to enhance its effect on development.

A stimulus-control hypothesis is offered to account for recent findings which have been taken to indicate that spreading depression prevents the neural storage of memory traces. 3 general conclusions derived from the spreading depression results are reevaluated: (a) Memory confinement to 1 cerebral hemisphere produced by training under unilateral depression is reinterpreted as a generalization-decrement phenomenon, (b) Memory transfer between cerebral hemispheres produced by a few reinforced responses with neither hemisphere depressed is reinterpreted as a stimulus-generalization phenomenon, (c) Memory storage prevented by spreading depression is reinterpreted as memory storage displaced by spreading depression from the depressed areas in the cortex to the nondepressed areas in the subcortex. Several new experiments suggested by the stimulus-control hypothesis are discussed and several old results at variance with the memory interpretations are reexamined in terms of the stimuluscontrol hypothesis.

The opiate-receptor antagonist naloxone was administered to rats after passive-avoidance training either alone or in combination with forced-swim stress. A retention test revealed that while naloxone enhanced retention when administered alone, it impaired retention when administered in combination with forced-swim stress. The findings provide evidence for a “protective” endogenous opioid-based system that, when not blocked pharmacologically, limits enhancement or impairment of retention under conditions of mild and intense stress, respectively.