Morphological changes are thought to contribute to the expression of long-term synaptic plasticity, a cellular basis for learning and memory. The mechanisms mediating the initiation and maintenance of the morphological changes are poorly understood. We repeatedly imaged the axonal arbors of mechanosensory neurons of Aplysia as they formed new synaptic varicosities and axonal branches after applications of serotonin that cause long-term synaptic facilitation. New varicosities formed exclusively from preexisting varicosities, by splitting or branch outgrowth. These changes were prevented by cytochalasin D, which blocks actin polymerization and the turnover of actin filaments. The suppression of the morphological changes by cytochalasin D did not impair their expression when cytochalasin D was removed 24 hr after exposure to serotonin. These results imply that serotonin induces persistent effects at preexisting presynaptic varicosities, which enhance actin polymerization, and that this is essential for presynaptic morphological changes of long-term facilitation.

Prism adaptation is a useful paradigm to study the integration and reorganization of various sensory modalities involved in sensory-motor tasks. By prolonging the prismatic aftereffect and well-timed observation, we aimed to dissociate the components and mechanisms involved in human prism adaptation by their differential decay and development time courses. Here, we show that a single session of prism adaptation training, combining small increments of prism strength below the subjects' awareness threshold, during a pointing task with a free walk session with total prism exposure duration of 75 min, generated a surprisingly long-lasting aftereffect. The aftereffect was measured by the magnitude of the proprioceptive shift (assessed by straight-ahead pointing in the dark) for 7 days. An aftereffect was observed, which lasted for more than 6 days, by a single prism adaptation session. The aftereffect did not decay gradually. Unlike previous descriptions, the aftereffect showed two separate time-courses of decay and increase. After a significant initial decay within 6 h, the aftereffect increased again from 1 day up to 3 days. The novel decay and delayed development profile of this adaptation aftereffect suggests two separate underlying neural mechanisms with different time scales. Our experimental paradigms promise to reveal directly the temporal characteristics of early versus late long-term neural plasticity in complex human adaptive behavior.

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After a single adaptation session to prisms with gradually incremented shift magnitude, the prism adaptation aftereffect was measured by open loop mid-sagittal pointing (O) to a visual target without visual feedback. This aftereffect corresponded to the summation of the shift in proprioception, measured by straight ahead pointing without vision (S), and the visual straight ahead judgement (V), measured by verbal stopping of an LED moving from two opposite directions. However, the measurement of the aftereffects made over a period of 7 days revealed significantly different decay curves in V, O and S. Surprisingly the S shift was still present up to 7 days after the training, while V had returned to the original level by 2 h, which was the first measurement after subjects returned to a normal visual environment. O had returned to pre-test level after 1 day. After 3 days Wilkinson's (J Exp Psychol 89:250-257, 1971) additive hypothesis (O=S-V) no longer fit the data. Rather "O=Pl-V", where Pl (Pr) is the shift in proprioception measured by passive lateral arm movements from left (right), fitted better during the whole 7 days of aftereffect in our study. Therefore, the aftereffect of our strong prism adaptation revealed, firstly, that classical open loop pointing consisted of aftereffect shifts equal to the summation of the shifts in the two passively measurable aftereffect components, vision (V) and proprioception (Pl), rather than with active straight ahead pointing (S). Secondly, the decay of the shift in visual perception and in passively measurable proprioception is independent. The former decays fast, and the latter decays slowly with two separate waves. Thirdly, we suggest that the use of visual perception-dependent spatial codes for visual-manual transformation and the vision-independent internal egocentric reference frame are mutually exclusive. We proposed a model to explain these possible mechanisms.

We aimed to dissociate components in prism adaptation and its aftereffect by using prism adaptation training in healthy humans. Arm proprioceptive aftereffects are usually measured by indicating the subjective straight ahead direction with eyes closed (S). This measure however could be affected by other components besides proprioception, such as an efferent motor component and internal egocentric reference frame. Here we report a very long lasting proprioceptive shift, detected by two measuring methods, that is a component of the adaptation aftereffects to left wedge prism glasses. In order to minimize possible active motor components, arm passive proprioceptive midsagittal judgment was measured (P). The subject's arm was passively brought from the right or left lateral position, and stopped by subjects' verbal order. The results from these different measurements of midsagittal judgment were compared for 7 days after prism adaptation. Surprisingly, we found two distinctly separate aftereffects of proprioceptive shift depending on the directions of the passive arm movement. The shift of the midsagittal plane appeared only when tested from the left (Pl). This indicates that our strong prism adaptation procedure affected proprioception in a directionally biased way and not a spatially ubiquitous way. Further, the early aftereffect seen in active straight ahead pointing (S) was mostly similar to this biased shift in proprioception (Pl). However the long lasting aftereffect in straight ahead pointing was independently maintained up to day 7, when the passive proprioception had returned to pretest level. These results indicate that active straight ahead pointing (S) involves other components in addition to the passively measurable proprioceptive component. We suggest a late onset shift in the internal egocentric reference frame is involved in S. Possible neural mechanisms for these phenomena are discussed.

We have used carbocyanine dyes (DiI and DiO) to generate fate maps for the epiblast layer of the chick embryo between stage X and the early primitive streak stage (stages 2–3). The overall distribution of presumptive cell types in these maps is similar to that described for other laboratory species (zebrafish, frog, mouse). Our maps also reveal certain patterns of movement for these presumptive areas. Most areas converge towards the midline and then move anteriorly along it. Interestingly, however, some presumptive tissue types do not take part in these predominant movements, but behave in a different way, even if enclosed within an area that does undergo medial convergence and anterior movement. The apparently independent behaviour of certain cell populations suggests that at least some presumptive cell types within the epiblast are already specified at preprimitive streak stages.

The hypoblast is generally thought to be responsible for inducing the mesoderm in the chick embryo because the primitive streak, and subsequently the embryonic axis, form according to the orientation of the hypoblast However, some cells become specified as embryonic mesoderm very late in development, towards the end of the gastrulation period and long after the hypoblast has left the embryonic region. We argue that induction of embryonic mesoderm and of the embryonic axis are different and separable events, both in amniotes and in amphibians. We also consider the relationships between the dorsoventral and anteroposterior axes in both groups of vertebrates.