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Adam C Roberts

Publications and source records attributed to Adam C Roberts.

3 recordsLinked to original sources

Synaptic facilitation and behavioral dishabituation in Aplysia: dependence on release of Ca2+ from postsynaptic intracellular stores, postsynaptic exocytosis, and modulation of postsynaptic AMPA receptor efficacy.

Sensitization and dishabituation of the defensive withdrawal reflex in Aplysia have been ascribed to presynaptic mechanisms, particularly presynaptic facilitation of transmission at sensorimotor synapses in the CNS of Aplysia. Here, we show that facilitation of sensorimotor synapses in cell culture during and after serotonin (5-HT) exposure depends on a rise in postsynaptic intracellular Ca(2+) and release of Ca(2+) from postsynaptic stores. We also provide support for the idea that postsynaptic AMPA receptor insertion mediates a component of synaptic facilitation by showing that facilitation after 5-HT offset is blocked by injecting botulinum toxin, an exocytotic inhibitor, into motor neurons before application of 5-HT. Using a reduced preparation, we extend our results to synaptic facilitation in the abdominal ganglion. We show that tail nerve shock-induced facilitation of siphon sensorimotor synapses also depends on elevated postsynaptic Ca(2+) and release of Ca(2+) from postsynaptic stores and recruits a late phase of facilitation that involves selective enhancement of the AMPA receptor-mediated synaptic response. To examine the potential role of postsynaptic exocytosis of AMPA receptors in learning in Aplysia, we test the effect of injecting botulinum toxin into siphon motor neurons on dishabituation of the siphon-withdrawal reflex. We find that postsynaptic injections of the toxin block dishabituation resulting from tail shock. Our results indicate that postsynaptic mechanisms, particularly Ca(2+)-dependent modulation of AMPA receptor trafficking, play a critical role in synaptic facilitation as well as in dishabituation and sensitization in Aplysia.

Animals↗

Learning in Aplysia: looking at synaptic plasticity from both sides.

Until recently, learning and memory in invertebrate organisms was believed to be mediated by relatively simple presynaptic mechanisms. By contrast, learning and memory in vertebrate organisms is generally thought to be mediated, at least in part, by postsynaptic mechanisms. But new experimental evidence from research using a model invertebrate organism, the marine snail Aplysia, indicates that this apparent distinction between invertebrate and vertebrate synaptic mechanisms of learning is invalid: learning in Aplysia cannot be explained in terms of exclusively presynaptic mechanisms. NMDA-receptor-dependent LTP appears to be necessary for classical conditioning in Aplysia. Furthermore, modulation of trafficking of postsynaptic ionotropic glutamate receptors underlies behavioral sensitization in this snail. Exclusively presynaptic processes appear to support only relatively brief memory in Aplysia. More persistent memory is likely to be mediated by postsynaptic processes, or by presynaptic processes whose expression depends upon retrograde signals.

Animals↗

Hematological and blood viscosity changes in tail-suspended rats.

BACKGROUND: Fluid shifts during exposure to microgravity result in a decrease in plasma volume which can lead to a transient increase in hematocrit. This transient increase in hematocrit could result in an increased blood viscosity. Yet, hematocrit returns to near normal values within a matter of hours of microgravity exposure as a result of a reduction in red blood cell mass. Rat tail-suspension models mimic the fluid shifts and hematological changes associated with microgravity exposure. METHODS: Tail-suspended rats were monitored for hematological and hemorheological changes over 4, 24, 72, and 168 h of tail suspension. Additionally, hematological and hemorheological changes were followed during recovery periods of 48, 120, and 192 h following 168 h of tail suspension. RESULTS: Although hematocrit increased significantly by 4 h of suspension, blood viscosity did not differ from controls. However, blood viscosity was significantly greater in the 72-, 168-, and 168/48-h suspension groups relative to controls despite no significant differences in hematocrits between groups. Theoretical calculations of blood viscosity at hematocrits of 50 and 60% (values intended to mimic hematocrits that would occur if red blood cell mass did not decrease) show a significant increase relative to the blood viscosities determined for the actual hematocrits in the experimental groups. CONCLUSIONS: The lowering of hematocrit associated with spaceflight may substantially reduce blood viscosity and thereby maintain the hematocrit at an optimal level for oxygen delivery to tissues.

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