Again about central metabotropic glutamate receptors of the group I in the honeybee Apis mellifera (original) (raw)
Related papers
Pharmacology Biochemistry and Behavior, 2004
In contrast to vertebrates the involvement of glutamate and N-methyl-D-aspartate (NMDA) receptors in brain functions in insects is both poorly understood and somewhat controversial. Here, we have examined the behavioural effects of two noncompetitive NMDA receptor antagonists, memantine (low affinity) and MK-801 (high affinity), on learning and memory in honeybees (Apis mellifera) using the olfactory conditioning of the proboscis extension reflex (PER). We induced memory deficit by injecting harnessed individuals with a glutamate transporter inhibitor, L-trans-2,4-PDC (L-trans-2,4-pyrrolidine dicarboxylate), that impairs long-term (24 h), but not short-term (1 h), memory in honeybees. We show that L-trans-2,4-PDC-induced amnesia is rescued by memantine injected either before training, or before testing, suggesting that memantine restores memory recall rather than memory formation or storage. When injected alone memantine has a mild facilitating effect on memory. The effects of MK-801 are similar to those of L-trans-2,4-PDC. Both pretraining and pretesting injections lead to an impairment of long-term (24 h) memory, but have no effect on short-term (1 h) memory of an olfactory task. The implications of our results for memory processes in the honeybee are discussed.
Inhibitory neurotransmission and olfactory memory in honeybees
Neurobiology of Learning and Memory, 2008
In insects, c-aminobutyric acid (GABA) and glutamate mediate fast inhibitory neurotransmission through ligand-gated chloride channel receptors. Both GABA and glutamate have been identified in the olfactory circuit of the honeybee. Here we investigated the role of inhibitory transmission mediated by GABA and glutamate-gated chloride channels (GluCls) in olfactory learning and memory in honeybees. We combined olfactory conditioning with injection of ivermectin, an agonist of GluCl receptors. We also injected a blocker of glutamate transporters (L-trans-PDC) or a GABA analog (TACA). We measured acquisition and retention 1, 24 and 48 h after the last acquisition trial. A low dose of ivermectin (0.01 ng/bee) impaired long-term olfactory memory (48 h) while a higher dose (0.05 ng/bee) had no effect. Double injections of ivermectin and L-trans-PDC or TACA had different effects on memory retention, depending on the doses and agents combined. When the low dose of ivermectin was injected after Ringer, long-term memory was again impaired (48 h). Such an effect was rescued by injection of both TACA and L-trans-PDC. A combination of the higher dose of ivermectin and TACA decreased retention at 48 h. We interpret these results as reflecting the involvement of both GluCl and GABA receptors in the impairment of olfactory long-term memory induced by ivermectin. These results illustrate the diversity of inhibitory transmission and its implication in long-term olfactory memory in honeybees.
Antennal tactile learning in the honeybee: Effect of nicotinic antagonists on memory dynamics
Neuroscience, 2005
Restrained worker honeybees (Apis mellifera L.) are able to learn to associate antennal-scanning of a metal plate with a sucrose reinforcement delivered to the mouthparts. Learning occurs reliably in a single association of the two sensory stimuli. The involvement of nicotinic pathways in memory formation and retrieval processes was tested by injecting, into the whole brain through the median ocellus, either mecamylamine (0.6 g per bee) or ␣-bungarotoxin (2.4 ng per bee). Saline served as a control. Mecamylamine injected 10 min before the retrieval test impairs the retention level tested 3 h and 24 h after single-or multi-trial learning. Retrieval tests performed at various times after the injection show that the blocking effect of mecamylamine lasts about 1 h. The drug has no effect on the reconsolidation or extinction processes. Mecamylamine injected 10 min before conditioning impairs single-trial learning but has no effect on fivetrial learning and on the consolidation process. By contrast, ␣-bungarotoxin only impairs the formation of long-term memory (24 h) induced by the five-trial learning and has no effect on medium-term memory (3 h), on single-trial learning or on the retrieval process. Hence, owing to previous data, at least two kinds of nicotinic receptors seem to be involved in honeybee memory, an ␣-bungarotoxin-sensitive and an ␣-bungarotoxin-insensitive receptor.
2012
Unravelling the role of neuromessenger processes in learning and memory has long interested researchers. We investigated the effects of an acetylcholinesterase blocker, Methyl Parathion (MeP), on honeybee learning. We used visual and olfactory tasks to test whether MeP had a detrimental effect on the acquisition of new knowledge when this new knowledge contradicts previously acquired one. Our results indicate that treatment with MeP prior to conditioning was significantly detrimental to the acquisition of incongruous (but not irrelevant or congruous) new knowledge due to improved recall. The neurobiological and ecotoxicological consequences of these results are discussed.
Learning and Memory in Honeybees: From Behavior to Neural Substrates
Annual Review of Neuroscience, 1996
Learning and memory in honeybees is analyzed on five levels, using a top-down approach, (a) Observatory learning is applied during navigation and dance communication. (b) Local cues at the feeding site are learned associatively. (c) Classical conditioning of the proboscis extension response to olfactory stimuli provides insight into behavioral, neural, and neuropharmacological mechanisms of associative learning, (d) At the neural level, the pathways coding the conditioned and the unconditioned stimulus are identified. The reinforcing function of the unconditioned stimulus is traced to a particular neuron, (e) At the cellular level, the cAMP pathway is found to be critically involved. Nitric oxide is an essential mediator for the transfer from short-to long-term memory.
Enhanced cholinergic transmission promotes recall in honeybees
2010
The involvement of the cholinergic system in learning and memory in honeybees has been well established using olfactory conditioning. We examined the effect of Methyl Parathion (MeP), an acetylcholinesterase inhibitor of the organophosphate family, on the learning and recall of visual and olfactory discrimination tasks in honeybees. One of our expectations was to observe the effects induced by both the nicotinic and muscarinic systems, as the blocking of acetylcholinesterase should induce an increase in the activity of both systems. We were also interested in knowing whether the type of tasks could influence the results. The visual tasks involved learning to discriminate the orientation of gratings in a Y-maze; the olfactory task involved learning to discriminate odours in a proboscis extension reflex (PER) paradigm. The results indicate that MeP treatment enhances recall of learned tasks in the visual and olfactory domains, but it does not affect the acquisition phase in either domain. Surprisingly, MeP treatment led to muscariniclike effects but failed to mimic the nicotinic-like effects already described in relation to learning phases in honeybees. Implications for the role of cholinergic pathways in learning and memory and the nature of their involvement are discussed, and an hypothesis relating to the organisation of the cholinergic system and the relationship between the nicotinic and muscarinic systems in honeybees is proposed. The results are also discussed in terms of their ecotoxicological consequences.
2012
Unravelling the role of neuromessenger processes in learning and memory has long interested researchers. We investigated the effects of an acetylcholinesterase blocker, Methyl Parathion (MeP), on honeybee learning. We used visual and olfactory tasks to test whether MeP had a detrimental effect on the acquisition of new knowledge when this new knowledge contradicts previously acquired one. Our results indicate that treatment with MeP prior to conditioning was significantly detrimental to the acquisition of incongruous (but not irrelevant or congruous) new knowledge due to improved recall. The neurobiological and ecotoxicological consequences of these results are discussed.
Aversive learning in honeybees revealed by the olfactory conditioning of the sting extension reflex
PLOS One, 2007
Invertebrates have contributed greatly to our understanding of associative learning because they allow learning protocols to be combined with experimental access to the nervous system. The honeybee Apis mellifera constitutes a standard model for the study of appetitive learning and memory since it was shown, almost a century ago, that bees learn to associate different sensory cues with a reward of sugar solution. However, up to now, no study has explored aversive learning in bees in such a way that simultaneous access to its neural bases is granted. Using odorants paired with electric shocks, we conditioned the sting extension reflex, which is exhibited by harnessed bees when subjected to a noxious stimulation. We show that this response can be conditioned so that bees learn to extend their sting in response to the odorant previously punished. Bees also learn to extend the proboscis to one odorant paired with sugar solution and the sting to a different odorant paired with electric shock, thus showing that they can master both appetitive and aversive associations simultaneously. Responding to the appropriate odorant with the appropriate response is possible because two different biogenic amines, octopamine and dopamine subserve appetitive and aversive reinforcement, respectively. While octopamine has been previously shown to substitute for appetitive reinforcement, we demonstrate that blocking of dopaminergic, but not octopaminergic, receptors suppresses aversive learning. Therefore, aversive learning in honeybees can now be accessed both at the behavioral and neural levels, thus opening new research avenues for understanding basic mechanisms of learning and memory.