CaMKII knockdown affects both early and late phases of olfactory long-term memory in the honeybee

Abstract

Honeybees are able to solve complex learning tasks and memorize learned information for long time periods. The molecular mechanisms mediating long-term memory (LTM) in the honeybee Apis mellifera are, to a large part, still unknown. We approached this question by investigating the potential function of the calcium/calmodulindependent protein kinase II (CaMKII), an enzyme known as a 'molecular memory switch' in vertebrates. CaMKII is able to switch to a calcium-independent constitutively active state, providing a mechanism for a molecular memory and has further been shown to play an essential role in structural synaptic plasticity. Using a combination of knockdown by RNA interference and pharmacological manipulation, we disrupted the function of CaMKII during olfactory learning and memory formation. We found that learning, memory acquisition and mid-term memory were not affected, but all manipulations consistently resulted in an impaired LTM. Both early LTM (24 h after learning) and late LTM (72 h after learning) were significantly disrupted, indicating the necessity of CaMKII in two successive stages of LTM formation in the honeybee.

Two extended haplotype blocks are associated with adaptation to high altitude habitats in East African honey bees

“…The r9 region contains genes for encoding several isoforms of calcium/calmodulin-dependent Serine protein Kinase enzyme (CASK; LOC411347; isoforms identified with BLAST; Fig 6B). CASK interacts with a second Ca 2+ /calmodulin kinase, CaMKII, in a fundamental pathway for memory formation that is shared between humans, fly and honey bees [54–56]. We therefore hypothesize that one or both of the divergent haplotypes contain changes to genes that underlie adaptive foraging behaviors at high altitudes.…”

“…CASK acts together with CaMKII to affect long-term memory formation in honey bees [56,85]. Differences in these genes could contribute to foraging performance in highland bees.…”

Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death

“…In mammals CaMKII is abundant in the hippocampus, a region of the brain important for memory formulation (Lisman et al, 2002). It has been demonstrated that reduced CaMKII function, via mutation or pharmacological inhibition, leads to impaired learning and long term potentiation in mice (Malinow et al, 1989;Scholl et al, 2015). Drosophila also shows impaired learning and memory following inhibition of CaMKII (Scholl et al, 2015).…”

“…It has been demonstrated that reduced CaMKII function, via mutation or pharmacological inhibition, leads to impaired learning and long term potentiation in mice (Malinow et al, 1989;Scholl et al, 2015). Drosophila also shows impaired learning and memory following inhibition of CaMKII (Scholl et al, 2015). Knockdown with RNA interference and pharmacological inhibition of CaMKII in honey bee was shown to impair both early and late-long-term memory (Scholl et al, 2015).…”

“…Drosophila also shows impaired learning and memory following inhibition of CaMKII (Scholl et al, 2015). Knockdown with RNA interference and pharmacological inhibition of CaMKII in honey bee was shown to impair both early and late-long-term memory (Scholl et al, 2015). Hence, empirical evidence indicates that disruption of CaMKII leads to impaired memory across various vertebrate and invertebrate models.…”