16 research outputs found

    Early calcium increase triggers the formation of olfactory long-term memory in honeybees

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    <p>Abstract</p> <p>Background</p> <p>Synaptic plasticity associated with an important wave of gene transcription and protein synthesis underlies long-term memory processes. Calcium (Ca<sup>2+</sup>) plays an important role in a variety of neuronal functions and indirect evidence suggests that it may be involved in synaptic plasticity and in the regulation of gene expression correlated to long-term memory formation. The aim of this study was to determine whether Ca<sup>2+ </sup>is necessary and sufficient for inducing long-term memory formation. A suitable model to address this question is the Pavlovian appetitive conditioning of the proboscis extension reflex in the honeybee <it>Apis mellifera, </it>in which animals learn to associate an odor with a sucrose reward.</p> <p>Results</p> <p>By modulating the intracellular Ca<sup>2+ </sup>concentration ([Ca<sup>2+</sup>]i) in the brain, we show that: (i) blocking [Ca<sup>2+</sup>]i increase during multiple-trial conditioning selectively impairs long-term memory performance; (ii) conversely, increasing [Ca<sup>2+</sup>]i during single-trial conditioning triggers long-term memory formation; and finally, (iii) as was the case for long-term memory produced by multiple-trial conditioning, enhancement of long-term memory performance induced by a [Ca<sup>2+</sup>]i increase depends on <it>de novo </it>protein synthesis.</p> <p>Conclusion</p> <p>Altogether our data suggest that during olfactory conditioning Ca<sup>2+ </sup>is both a necessary and a sufficient signal for the formation of protein-dependent long-term memory. Ca<sup>2+ </sup>therefore appears to act as a switch between short- and long-term storage of learned information.</p

    Exploring the pharmacological properties of insect nicotinic acetylcholine receptors.

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    Insect nicotinic acetylcholine (nACh) receptors are molecular targets of insecticides such as neonicotinoids that are used to control disease-carrying insects and agricultural pests. To date, several insect nACh receptor subunits have been identified, indicating different nACh receptor subtypes and pharmacological profiles. Because of the difficulty in expressing functional insect nACh receptors in heterologous systems, new research tools are needed. Studies on insects resistant to the insecticide imidacloprid and on laboratory-generated hybrid and chimaeric nACh receptors in vitro have provided information about the molecular basis of receptor diversity, neonicotinoid resistance and selectivity. Additionally, recent results indicate that the sensitivity of insect nACh receptors to imidacloprid can be modulated by intracellular phosphorylation mechanisms, which offers a new approach to studying insect nACh receptor pharmacology

    Modulation of Low-Voltage-Activated Inward Current Permeable to Sodium and Calcium by DARPP-32 Drives Spontaneous Firing of Insect Octopaminergic Neurosecretory Cells

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    Identification of the different intracellular pathways that control phosphorylation/dephosphorylation process of ionic channels represents an exciting alternative approach for studying the ionic mechanisms underlying neuronal pacemaker activity. In the central nervous system of the cockroach Periplaneta americana, octopaminergic neurons, called dorsal unpaired median (DUM; DUM neurons), generate spontaneous repetitive action potentials. Short-term cultured adult DUM neurons isolated from the terminal abdominal ganglion (TAG) of the nerve cord were used to study the regulation of a tetrodotoxin-sensitive low-voltage-activated (LVA) channel permeable to sodium and calcium (Na/Ca), under whole cell voltage-and current-clamp conditions. A bell-shaped curve illustrating the regulation of the amplitude of the maintained current vs. [ATP]i was observed. This suggested the existence of phosphorylation mechanisms. The protein kinase A (PKA)inhibitor, H89 and elevating [ cyclic adenosine 3 0, 5 0 monophosphate, cAMP] i, increased and decreased the current amplitude, respectively. This indicated a regulation of the current via a cAMP/PKA cascade. Furthermore, intracellular application of PP2B inhibitors, cyclosporine A, FK506 and PP1/2A inhibitor, okadaic acid decreased the current amplitude. From these results and because octopamine (OA) regulates DUM neuron electrical activity via an elevation of [cAMP]i, we wanted to know if, like in vertebrate dopaminergic neurons, OA receptor (OAR) stimulation could indirectly affect the current via PKA-mediated phosphorylation of Dopamine-and cAMP-regulated Phosphoprotein-32 (DARPP-32) known to inhibit PP1/2A. Experiments were performed using intracellular application of phospho-DARPP-32 and non-phospho-DARPP-32. Phospho-DARPP-32 strongly reduced the current amplitude whereas non-phospho-DARPP-32 did not affect the current. All together, these results confirm that DARPP- 32-mediated inhibition of PP1/2A regulates the maintained sodium/calcium current, which contributes to the development of the pre-depolarizing phase of the DUM neuron pacemaker activity
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