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  • The first suggestion that histamine

    2022-06-23

    The first suggestion that histamine may play a role in memory consolidation was from Almeida and Izquierdo (de Almeida & Izquierdo, 1986) who showed that the immediate posttraining intracerebroventricular (i.c.v.) administration of 1–10ng of the drug were found to enhance the retention of one-trial inhibitory avoidance in rats (Table 1). This was then (Gold, 1986) and probably still is now (Izquierdo et al., 2016), the task most widely used for studies of memory mechanisms, particularly memory consolidation (McGaugh, 2004, McGaugh, 2015). It relies on hippocampal CA1 long-term potentiation, as ascertained by measurement of cellular biochemical changes (Izquierdo et al., 2006) and by electrophysiological observations (Whitlock, Heynen, Shuler, & Bear, 2006; see Izquierdo et al., 2016) and is strongly modulated by the basolateral amygdala (McGaugh, 2004, McGaugh, 2015). The trace is stored in parallel in hippocampal CA1 and in basolateral amygdala (Fabbri et al., 2016, Izquierdo et al., 1992, Izquierdo et al., 2016).
    Generalization of the effects to other tasks, including extinction memory consolidation In the thirty-one years that followed the original report on memory facilitation by i.c.v. histamine infusion, many authors explored the effect of the drug by administering it into restricted Deferoxamine areas in several tasks. See Table 1, for a summary of the drug effects. Here we will review only findings obtained in well-designed experiments with appropriate controls (see Izquierdo et al., 2016). They corroborated those of de Almeida and Izquierdo (1986) on memory consolidation and pointed to the hippocampal CA1 subregion and the basolateral amygdala as key sites of action. Clearly, because of its location bordering the cerebral ventricles, the dorsal hippocampus appears a priori to be a better candidate being responsible for the i.c.v. effect of histamine. Indeed, posttraining intra-CA1 (Da Silva, Bonini, Bevilaqua, Izquierdo, & Cammarota, 2006) infusion of histamine was found to enhance the memory consolidation of one-trial inhibitory avoidance, but intra-amygdala histamine administration did it (Benetti & Izquierdo, 2013). The effect of i.c.v. histamine was reversed by the “anti-histamine” drugs used in the 1980s, which were largely H1 receptor blockers (de Almeida & Izquierdo, 1986). The effect of intrahippocampal infusion of histamine was reversed by an H2 blocker (Da Silva et al., 2006). The intra-amygdala effect was mimicked by the histamine N-methyltransferase inhibitor, SKF-91488, was unresponsive to H1 or H2 receptor antagonists; importantly, it was also mimicked by the H3 agonist, imetit and blocked by the H3 receptor antagonist, thioperamide. Thus, it is probably mediated by H3 receptors (Benetti & Izquierdo, 2013) (see Fig. 1). The H3 receptors are presynaptic and are present not only in histaminergic synapses, but also on cholinergic, GABAergic, noradrenergic and serotonergic synapses, where they modulate the release of these neurotransmitters (Luo et al., 2017, Schlicker and Kathmann, 2016, Sors et al., 2016; see Baldi et al., 2005, Cangioli et al., 2002). Thus, in principle the H3-mediated memory facilitation by intra-amygdala histamine could be ascribed to effects on the release of any of a number of neurotransmitters, whose interaction with those of histamine has not been sufficiently studied. When given into CA1 following the first extinction session (i.e., at the time in which extinction learning was presumably being consolidated; Bonini et al., 2011), histamine facilitated the consolidation of extinction. This may argue in favor of a hippocampal location of the mechanism that controls consolidation in general. Other evidence, however, suggests multiple sites for memory consolidation, several for each task (see Izquierdo et al., 2016). The cerebellar vermis, which receives histaminergic innervation (see Gianlorenço, Riboldi, Silva-Marques, & Mattioli, 2015), has been shown to be involved in the control of two forms of inhibitory avoidance: the classic footshock motivated form (Silva-Marques, Gianlorenço, & Mattioli, 2016), which measures fear (Izquierdo et al., 2016), and the avoidance of the open arms of aT-maze (Graeff, Netto, & Zangrossi, 1998), which measures anxiety rather than fear. For differences and relations between fear and anxiety, see Izquierdo et al. (2016). Enhancing histamine H2 receptors activity was shown to be involved in the memory consolidation of both forms of inhibitory avoidance (Gianlorenço et al., 2015, Silva-Marques et al., 2016) (Table 1). The relation of the vermis to the basolateral amygdala and dorsal hippocampus vis-à-vis memory consolidation of this form of learning is not known.