The obtained results indicate that even
The obtained results indicate that even when the impairment of the same forms of memory are present, amnesia can develop in different ways. Impairment of memory reconsolidation in the conditioned food aversion model through both the serotonin receptor antagonist and the antagonist of NMDA glutamate receptor-induced amnesias developing in time. During the early phases (on the 1st and 3rd days after the induction), both amnesias were resistant to different reminding influences. At the same time, repeated training of snails induced formation of conditioned food aversion memory, and memory was forming faster than during the initial training. In previous studies on interneurons related to defensive behavior in snails, we found the gradual reduction of responses to CS for a few days after the impairments of memory reconsolidation by the protein synthesis inhibitor . Repeated training at a late phase (the 10th and 30th days) of serotonin-dependent amnesia led to long-term memory formation, while at a late phase of NMDA-dependent amnesia, long-term memory during the second training was not formed. Differences in amnesias characteristics at its late phases suggest that the processes of their induction involve the specific molecular mechanisms, which ultimately determine what kind of amnesia will be formed, amnesia that is sensitive or insensitive to repeated training. It is important to note that different types of amnesia occur in the case of impairment of two different (parallel) components maintaining conditioned food aversion memory. In particular, we have previously found that a blockade of NMDA glutamate receptors in memory reactivation (reminder) impaired reconsolidation of recent (2 days), but not remote (10 days), memory of the conditioned food aversion [55,65]. Conversely, the inhibition of 5-HT receptors during memory reactivation impaired both recent and remote memory of conditioned food aversion . Different mechanisms describing the involvement of serotonin and glutamatergic systems in the development of long-term memory and amnesia have been published using aplysia, the marine mollusk [35,36,38,39]. In the culture of sensory and motor neurons of the mollusk Trigonelline receptor forming monosynaptic glutamatergic synapses, it was found that these synapses express 2 forms of persisting facilitation: (1) a non-associative form caused by applications of serotonin, which is a cellular analog of long-term sensitization and (2) an associative form caused by the pairings of presynaptic tetanus and a serotonin application. This is a cellular analog of the classical conditioned reflex . Two days after the induction of synaptic facilitation, it was revealed that heterosynaptic reactivation caused by short application of serotonin and combined with application of the protein synthesis inhibitor rapamycin, led to a reversion of non-associative long-term synaptic facilitation . In contrast, homosynaptic reactivation induced by tetanic stimulation of the sensory neuron plus rapamycin induced reversion of associative (but not non-associative) long-term synaptic facilitation. Thus, 2 forms of persisting facilitation are expressed in the same synapse in which each form contributes to different types of learning and memory, becoming labile under different reactivations. Our results extend the current understanding of the mechanisms underlying amnesia and have some practical significance. Currently, attempts are being made to apply the procedure of memory reconsolidation and its impairment by the neurotransmitter receptor antagonists for the pharmacological correction of diseases, such as post-traumatic stress disorder (PTSD), drug addiction, obsessive-compulsive disorder, etc [1,4,88]. The application results of pharmacological agents for treatment of these disorders are contradictory and not always successful. We have found that properties of amnesia can change substantially over time following induction. In this regard, during the early and late phases of amnesia, fundamental differences in effects can exist. These are used to study amnesia mechanisms and memory recovery attempts. Secondly, the impairment of the same memory by different amnestic agents can cause different types of amnesia, differing in the molecular mechanisms and, in particular, involving different receptors to neurotransmitters. Thus, the effectiveness of methods to therapeutic correction and pharmacologic action on neurological pathologies can depend on the types of amnesias, peculiarities of the dynamics of their development, specificity of the involvement of different neurotransmitters, and other molecular regulatory factors. Among the possible analogues of the stable amnesia, we have focused on the phenomenon of anterograde amnesia, which is defined as the inability to form new memory about the facts and events that occurred after the starting of amnesia [89,90]. Anterograde amnesia was described in Korsakov syndrome, alcohol intoxication, the action of benzodiazepines, and the slow phase of sleep [89,91]. Anterograde amnesia (as well as stable amnesia) features the ability to form short-term, but not long-term, memories. The principal difference between stable amnesia and classical anterograde amnesia is that classical amnesia is not specific to certain forms of memory. Nevertheless, it cannot be excluded because mechanisms of anterograde amnesia are related to the mechanisms of stable amnesia that we identified.