Effect of Sub-lethal Doses of Imidacloprid on Learning and Memory Formation of Indigenous Arabian Bee (Apis mellifera jemenitica Ruttner) Adult Foragers

2018 ◽  
Vol 48 (3) ◽  
pp. 373-380 ◽  
Author(s):  
J Iqbal ◽  
A S Alqarni ◽  
H S A Raweh
2020 ◽  
Vol 64 (1) ◽  
pp. 123-130
Author(s):  
Gordana Glavan

AbstractOrganophosphate insecticides are known to inhibit the activity of enzyme acetylcholinesterase. They affect olfactory learning and memory formation in honeybees. These insecticides cause mushroom body inactivation in honeybees, but their influence on other brain regions involved in olfactory perception and memory is unknown. The goal of this study was to study the effects of organophosphate insecticide diazinon on carnolian honeybee (Apis mellifera carnica) acetylcholinesterase activity in the olfactory brain regions of antennal lobe, mushroom body and lateral procerebrum (lateral horn). The lamina, medulla and lobula of optic lobes were also analyzed. The level of acetylcholinesterase activity was visualized using the histochemical staining method. Densitometric analysis of histochemical signals indicated that diazinon inhibited acetylcholinesterase activity only in the lip of calyces of mushroom body, but not in other analyzed olfactory regions, antennal lobe and lateral procerebrum. The visual brain system optic lobes were also unaffected. This is in accordance with the literature reporting that mushroom body is the main brain center for olfactory learning and memory formation in honeybees.


2006 ◽  
Vol 56 (2) ◽  
pp. 259-278 ◽  
Author(s):  
Dorothea Eisenhardt

AbstractThe honeybee (Apis mellifera) is a model organism for the study of learning and memory formation and its underlying mechanisms. Honeybees have a rich behaviour that can be studied in the field as well as in the laboratory. In the latter case, olfactory conditioning of the proboscis extension response (PER) has been intensively studied with respect to the neuronal and molecular mechanisms underlying acquisition and memory formation. Quite a lot is known about the neuronal pathways of both the unconditioned and the conditioned stimulus, and molecular mechanisms that lead to memory formation have been identified. In particular, the role of the cAMP-protein kinase A pathway in memory formation has been analysed. Present knowledge about the molecular basis of memory formation is outlined here. The role of the cAMP-dependent signalling cascade in memory formation is summarised and the activation of this pathway by non-associative and associative learning is discussed.


MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Sadniman Rahman ◽  
Chaity Modak ◽  
Mousumi Akter ◽  
Mohammad Shamimul Alam

Background: Learning and memory is basic aspects in neurogenetics as most of the neurological disorders start with dementia or memory loss. Several genes associated with memory formation have been discovered. MicroRNA genes miR-1000 and miR-375 were reported to be associated with neural integration and glucose homeostasis in some insects and vertebrates. However, neuronal function of these genes is yet to be established in D. melanogaster. Objective: Possible role of miR-1000 and miR-375 in learning and memory formation in this fly has been explored in the present study. Methods: Both appetitive and aversive olfactory conditional learning were tested in the miR-1000 and miR-375 knockout (KO) strains and compared with wild one. Five days old third instar larvae were trained by allowing them to be associated with an odor with reward (fructose) or punishment (salt). Then, the larvae were tested to calculate their preferences to the odor trained with. Learning index (LI) values and larval locomotion speed were calculated for all strains. Results: No significant difference was observed for larval locomotion speed in mutant strains. Knockout strain of miR-1000 showed significant deficiency in both appetitive and aversive memory formation whereas miR-375 KO strain showed a significantly lower response only in appetitive one. Conclusion: The results of the present study indicate important role played by these two genes in forming short-term memory in D. melanogaster.


2020 ◽  
Vol 20 (6) ◽  
Author(s):  
Heather Christine Bell ◽  
Corina N Montgomery ◽  
Jaime E Benavides ◽  
James C Nieh

Abstract The health of insect pollinators, particularly the honey bee, Apis mellifera (Linnaeus, 1758), is a major concern for agriculture and ecosystem health. In response to mounting evidence supporting the detrimental effects of neonicotinoid pesticides on pollinators, a novel ‘bee safe’ butenolide compound, flupyradifurone (FPF) has been registered for use in agricultural use. Although FPF is not a neonicotinoid, like neonicotinoids, it is an excitotoxic nicotinic acetylcholine receptor agonist. In addition, A. mellifera faces threats from pathogens, such as the microsporidian endoparasite, Nosema ceranae (Fries et al. 1996). We therefore sought 1) to increase our understanding of the potential effects of FPF on honey bees by focusing on a crucial behavior, the ability to learn and remember an odor associated with a food reward, and 2) to test for a potential synergistic effect on such learning by exposure to FPF and infection with N. ceranae. We found little evidence that FPF significantly alters learning and memory at short-term field-realistic doses. However, at high doses and at chronic, field-realistic exposure, FPF did reduce learning and memory in an olfactory conditioning task. Infection with N. ceranae also reduced learning, but there was no synergy (no significant interaction) between N. ceranae and exposure to FPF. These results suggest the importance of continued studies on the chronic effects of FPF.


2010 ◽  
Vol 48 ◽  
pp. 263-274 ◽  
Author(s):  
Tania L. Roth ◽  
Eric D. Roth ◽  
J. David Sweatt

Rapid advances in the field of epigenetics are revealing a new way to understand how we can form and store strong memories of significant events in our lives. Epigenetic modifications of chromatin, namely the post-translational modifications of nuclear proteins and covalent modification of DNA that regulate gene activity in the CNS (central nervous system), continue to be recognized for their pivotal role in synaptic plasticity and memory formation. At the same time, studies are correlating aberrant epigenetic regulation of gene activity with cognitive dysfunction prevalent in CNS disorders and disease. Epigenetic research, then, offers not only a novel approach to understanding the molecular transcriptional mechanisms underlying experience-induced changes in neural function and behaviour, but potential therapeutic treatments aimed at alleviating cognitive dysfunction. In this chapter, we discuss data regarding epigenetic marking of genes in adult learning and memory formation and impairment thereof, as well as data showcasing the promise for manipulating the epigenome in restoring memory capacity.


2021 ◽  
Vol 15 ◽  
Author(s):  
Camilla Roselli ◽  
Mani Ramaswami ◽  
Tamara Boto ◽  
Isaac Cervantes-Sandoval

Understanding the nature of the molecular mechanisms underlying memory formation, consolidation, and forgetting are some of the fascinating questions in modern neuroscience. The encoding, stabilization and elimination of memories, rely on the structural reorganization of synapses. These changes will enable the facilitation or depression of neural activity in response to the acquisition of new information. In other words, these changes affect the weight of specific nodes within a neural network. We know that these plastic reorganizations require de novo protein synthesis in the context of Long-term memory (LTM). This process depends on neural activity triggered by the learned experience. The use of model organisms like Drosophila melanogaster has been proven essential for advancing our knowledge in the field of neuroscience. Flies offer an optimal combination of a more straightforward nervous system, composed of a limited number of cells, and while still displaying complex behaviors. Studies in Drosophila neuroscience, which expanded over several decades, have been critical for understanding the cellular and molecular mechanisms leading to the synaptic and behavioral plasticity occurring in the context of learning and memory. This is possible thanks to sophisticated technical approaches that enable precise control of gene expression in the fruit fly as well as neural manipulation, like chemogenetics, thermogenetics, or optogenetics. The search for the identity of genes expressed as a result of memory acquisition has been an active interest since the origins of behavioral genetics. From screenings of more or less specific candidates to broader studies based on transcriptome analysis, our understanding of the genetic control behind LTM has expanded exponentially in the past years. Here we review recent literature regarding how the formation of memories induces a rapid, extensive and, in many cases, transient wave of transcriptional activity. After a consolidation period, transcriptome changes seem more stable and likely represent the synthesis of new proteins. The complexity of the circuitry involved in memory formation and consolidation is such that there are localized changes in neural activity, both regarding temporal dynamics and the nature of neurons and subcellular locations affected, hence inducing specific temporal and localized changes in protein expression. Different types of neurons are recruited at different times into memory traces. In LTM, the synthesis of new proteins is required in specific subsets of cells. This de novo translation can take place in the somatic cytoplasm and/or locally in distinct zones of compartmentalized synaptic activity, depending on the nature of the proteins and the plasticity-inducing processes that occur. We will also review recent advances in understanding how localized changes are confined to the relevant synapse. These recent studies have led to exciting discoveries regarding proteins that were not previously involved in learning and memory processes. This invaluable information will lead to future functional studies on the roles that hundreds of new molecular actors play in modulating neural activity.


2018 ◽  
Vol 107 ◽  
pp. 250-256 ◽  
Author(s):  
Julie A. Mustard ◽  
Valerie Alvarez ◽  
Sofy Barocio ◽  
Jamie Mathews ◽  
Alexander Stoker ◽  
...  

2020 ◽  
Vol 382 (1) ◽  
pp. 161-172 ◽  
Author(s):  
Susanne Meis ◽  
Thomas Endres ◽  
Volkmar Lessmann

Abstract The amygdala is a central hub for fear learning assessed by Pavlovian fear conditioning. Indeed, the prevailing hypothesis that learning and memory are mediated by changes in synaptic strength was shown most convincingly at thalamic and cortical afferents to the lateral amygdala. The neurotrophin brain-derived neurotrophic factor (BDNF) is known to regulate synaptic plasticity and memory formation in many areas of the mammalian brain including the amygdala, where BDNF signalling via tropomyosin-related kinase B (TrkB) receptors is prominently involved in fear learning. This review updates the current understanding of BDNF/TrkB signalling in the amygdala related to fear learning and extinction. In addition, actions of proBDNF/p75NTR and NGF/TrkA as well as NT-3/TrkC signalling in the amygdala are introduced.


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