PubMed · 3683891
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1987. Transient global amnesia.. https://doi.org/10.1212/wnl.37.12.1889-b
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The effects of dynorphin A-(1-13) on carbon monoxide (CO)-induced amnesia in mice were investigated using a step-down type passive avoidance task. Memory deficiency occurred in mice when training commenced 7 days after CO exposure although it was not produced 1 day after CO exposure. The median step-down latency in the retention test of the CO-exposed group was significantly shorter than that of the control group. Administration of dynorphin A-(1-13) (1.5 nmol/mouse i.c.v.) 15 min before the first training session prolonged the step-down latency in the CO-exposed group. Dynorphin A-(1-13) administered immediately after the first training session or administered 15 min before the retention test also prolonged the step-down latency in the CO-exposed group. To determine whether this effect of dynorphin A-(1-13) was mediated via kappa-opioid receptors, we attempted to block its action using a kappa-opioid receptor antagonist (nor-binaltorphimine). Nor-binaltorphimine (5.44 nmol/mouse i.c.v.) blocked the effect of dynorphin A-(1-13) on delayed amnesia. However, dynorphin A-(1-13) (0.5, 1.5 and 5.0 nmol/mouse) did not facilitate the acquisition of memory in normal mice. These results suggest that dynorphin A-(1-13) modulates the kappa-opioid receptor-mediated opioid neuronal system, and that it ameliorates the disruptive effect of CO on acquisition, consolidation and/or recall of memory.
Arachidonic acid is a putative messenger in synaptic transmission which presumably plays a role in learning and memory. Previous experiments showed that inhibitors of phospholipase A2-dependent release of arachidonic acid cause amnesia in a one-trial passive avoidance task in the chick. To test if arachidonic acid is metabolized to other messengers, the effects of inhibitors of enzymes which metabolize arachidonic acid were tested in the same task. The cyclooxygenase inhibitors indomethacin, naproxen and ibuprofen caused amnestic effects at all concentrations tested when injected intracerebrally before training. Injections were 5 microliters of 5-20 mmolar solutions per hemisphere. The onset of amnestic effects was always 2 h after training, independently of drug type, concentration, and injection time before training. The delay of 2 h after training suggests that the drugs prevent induction of cyclooxygenase synthesis. Post-training injections had no effect. Control tests showed little effect of the drugs on motor control and motivation. Caffeic acid and esculetin, inhibitors of lipoxygenases, and sodium furegrelate, a thromboxane synthase inhibitor, had no effect on performance of chicks in the task at all concentrations or time points tested. The results indicate that cyclooxygenase products, but not lipoxygenase or thromboxane synthase products, play a role in memory consolidation in the chick when learning this task.
Training chicks on a one-trial passive avoidance task results in transient up-regulation of the N-methyl-D-aspartate (NMDA) receptor in the left intermediate medial hyperstriatum ventrale (IMHV) of the forebrain 30 min post-training. Injection of the non-competitive NMDA receptor inhibitor, (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)-cyclohepten 5,10-imine maleate (MK-801), around the time of training renders chicks amnesic for the task. Training also results in enhanced expression of the immediate early gene (IEG) c-fos in the IMHV. To determine the relationship between NMDA receptor up-regulation and IEG induction during memory formation we have examined the expression of Fos, Jun and their related proteins 2 h following training in the presence/absence of the putative amnestic agent MK-801. Western blotting of IMHV samples revealed two protein bands with immunoreactivity to the Fos antibody at 47 and 54 kDa. Using an antibody to Jun, two immunoreactive bands were revealed at 39 and 54 kDa. All bands were enhanced in the left IMHV following passive avoidance training. Post-training intraperitoneal injections of MK-801 (75 mM) produced amnesia in approximately 50% of the birds when tested 1 h after training. Injection of MK-801 significantly attenuated expression of these proteins in birds rendered amnesic, but not in those that recalled the task. We conclude that NMDA receptor activation precedes immediate early gene expression in the memory formation cascade.