PubMed · 5890189
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S L Chorover, P H Schiller. 1965-09-24. Retrograde amnesia.. https://pubmed.ncbi.nlm.nih.gov/5890189/
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In the present study, the effects of intra-ventral tegmental area (VTA) injections of morphine on memory retention of a one-trial passive avoidance task have been investigated in morphine-sensitized rats. Retrieval was examined 24h after training and used as memory retention. Sensitization was obtained by subcutaneous (s.c.) injections of morphine, once daily for 3 and 5 days free of the opioid before training. Post-training administration of the both systemic (2.5, 5 and 7.5mg/kg, s.c.) and intra-VTA (5 and 7.5microg/rat) of morphine, dose-dependently decreased memory retention. The response induced by post-training administration of intra-VTA morphine (7.5microg/rat) was significantly reversed in morphine-sensitized rats. The inhibition of morphine-induced amnesia in morphine-sensitized rats was decreased by once daily injections of naloxone (0.5, 1 and 2mg/kg, s.c.), SCH 23390 (0.025, 0.05 and 0.1mg/kg, s.c.) or sulpiride (25, 50 and 100mg/kg, s.c.), during the sensitization. The results suggest that VTA has an important role in morphine-induced amnesia and morphine sensitization affects this process through opioid and dopamine receptors.
It was previously demonstrated that mitogen-activated protein kinase (MAPK) signaling plays a pivotal role in neural plasticity and memory processes both in rodents and mollusks. Although the MAPK pathways are highly conserved, no evidence was found for its participation in memory models in other animal groups. Here we found ERK-like and JNK-like cross-immunoreactivity in the crab brain with phospho-specific antibodies and we estimated ERK and JNK activity during long-term memory consolidation in the context-signal learning paradigm of the crab Chasmagnathus. At 0, 1, 3 and 6h after training ERK and JNK activity was measured. ERK-like activation was found 1h after spaced training in cytosolic but not in nuclear fractions of brain homogenates, while JNK activity remained unchanged in both fractions. Passive (context exposure) and active (continuous stimulation) controls showed cytosolic ERK and JNK activation immediately after training, which decayed 1h later. In coincidence with this time course of activity, an ERK1/2 pathway inhibitor, PD098059, induced amnesia only when administered 45 min after training but not when administered immediately pre- or post-training. These data support that: (1) cytoplasmic but not nuclear ERK substrates must be differentially phosphorylated during memory consolidation, and (2) ERK phosphorylation and consequent activation 1h after training is necessary for long-term memory consolidation in this arthropod model.
Humanin (HN) is a 24-amino acid peptide that protects neuronal cells from death caused by Alzheimer's disease (AD)-related genes and amyloid-beta (Abeta). Multiple studies have revealed its biochemical and neuroprotective characteristics in vitro; however, little has been known regarding whether HN is effective in vivo in AD model systems. We examined the effect of S14G-HN, a 1,000-fold more potent derivative of HN in vitro, on amnesia induced by Abeta25-35 in mice. The Y-maze test revealed that at least 50 pmol of S14G-HN by intracerebroventricular injection prevented Abeta-induced impairment of short-term/spatial working memory; however, 5 nmol of S14A-HN, a neuroprotection-defective mutant in vitro, did not prevent Abeta-induced amnesia. These results are in agreement with the structure-function correlation shown previously in vitro. In the water-finding task, S14G-HN prevented prolongation of finding latency (the time to find water) observed in Abeta-amnesic mice, indicating that S14G-HN also blocked Abeta-induced impairment of latent learning. In accordance with these observations, immunohistochemical analysis showed that S14G-HN sustained the number of cholinergic neurons in the basal forebrain and the striata nearly to the normal level. Furthermore, genistein, a specific inhibitor of tyrosine kinases, blocked recovery from scopolamine-induced amnesia by S14G-HN, suggesting that certain tyrosine kinase(s) are involved in the inhibitory function of S14G-HN in vivo. Taking these findings together, we conclude that S14G-HN has rescue activity against memory impairment caused by AD-related insults in vivo by activating the same intracellular neuroprotective machinery as elucidated previously in vitro.