Memory impairment induced by cholinergic antagonists injected into the mushroom bodies of the honeybee.

The role of honeybee central brain structures, suspected to be cholinergic, has been studied in learning and memory. The nicotinic antagonist mecamylamine and the muscarinic antagonist scopolamine were locally injected into the calyces and the alpha-lobes of mushroom bodies, and their effects on memory acquisition and retrieval were investigated using one-trial olfactory conditioning of the proboscis extension reflex. A strong impairment of the olfactory learning was noticed following mecamylamine injection into the mushroom body calyces. Mecamylamine and scopolamine disturbed retrieval processes when injected into the alpha-lobes of mushroom bodies but remain without effect on these processes when injected into the mushroom body calyces. These results emphasise the role of the cholinergic networks of the mushroom bodies in the formation and recall of memory in the honeybee. They suggest that the role of the brain structures in these processes is sequential. Mushroom body calyces involved in the associative process of olfactory learning could be relayed by the alpha-lobes for information retrieval.

Mecamylamine-induced impairment of acquisition and retrieval of olfactory conditioning in the honeybee.

Mecamylamine, a nicotinic receptor antagonist, was injected into the honeybee brain haemolymph. The effects of the drug were investigated on Pavlovian conditioning of the proboscis extension reflex. The conditioned response was acquired after a one-trial learning session, consisting of an olfactory-conditioned stimulus combined with a gustatory antennal unconditioned stimulus. The drug was injected at different times before or after the learning session in order to dissociate its effects on acquisition, consolidation and retrieval processes. The performance was evaluated in short-delayed recall tasks. To control potential effects on sensory-motor activity, the effects of the drug were also investigated on sensory processes (through olfactory and gustatory functions) and on motor processes of proboscis extension. The results of conditioning experiments showed that pretrial injection induced a decrease of retention performance 1 h after the learning trial. Mecamylamine injected 20 min after the learning session induced a time-dependent impairment of retention performance, as has been shown by the performance level registered from 10 to 80 min after injection. A 5-min post-trial injection had no effect on retention performance. Control experiments did not reveal any effect of mecamylamine on the response reflex of proboscis extension and on responsiveness to olfactory stimuli (geraniol, lavender and vanillin). The absence of effects on sensory perception combined with the amnestic effect induced by pre- or late post-trial injections lead us to conclude that mecamylamine specially impaired acquisition and retrieval processes. The involvement of nicotinic-like receptors in these processes is discussed.