The site of a motor memory shifts with consolidation.

The basis for the consolidation of memory is a controversial topic, particularly in the case of motor memory. One view is that motor memory is transferred, partially or completely, to a new location during the consolidation process ("systems consolidation"). We investigated this possibility in a primitive motor system, the vestibulo-ocular reflex (VOR). In the simple circuitry of the VOR, there are relatively few possible storage sites for memory. We partially blocked excitatory neurotransmission in the cerebellar cortex of cats with the glutamate antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). If CNQX was injected immediately after 60 min of rotation under conditions that induced a learned decrease in the gain of the VOR, gain was returned to its baseline value. Expression of the new memory could also be disrupted by rotation in darkness, suggesting that consolidation had not taken place; however, after learning had continued for 3 d, expression of the learned change was diminished only slightly by blockade and was unaffected by rotation in darkness. Our interpretation of these results is that learning may take place initially in the cerebellar cortex and that during consolidation, motor memories are converted to a more distributed representation that includes the cerebellar cortex and another site.

Physiological and behavioral responses to an exposure of pitch illusion in the simulator.

BACKGROUND: It has been suggested that a pilot's physiological and behavioral responses during disorientation can provide a real-time model of pilot state in order to optimize performance. We investigated whether there were consistent behavioral or physiological "markers" that can be monitored during a single episode of disorientation. METHODS: An Integrated Physiological Trainer with a closed loop interactive aircraft control and point of gaze/eye-tracking device was employed. There were 16 subjects proficient in maintaining straight and level flight and with procedures in changing attitude who were exposed to yaw rotation and a brief head roll to 35 +/- 2 degrees. On return to upright head position, subjects were required to initiate either an ascent or descent to a prescribed attitude. BP, HR, skin conductance, eye movements, and point of gaze were monitored throughout the onset, duration, and immediately after the disorientation insult. Simultaneously, airspeed and power settings were recorded. RESULTS: Compared with the control condition, a significant increase (p < 0.01) in HR, HR variability, and mean arterial BP was observed during the disorientation. Flight performance decrement was reflected by a significant delay in setting power for attitude change and deviation in maintaining airspeed (p < 0.01). CONCLUSION: Changes in cardiovascular responses appear to be correlated with the onset of disorientation. The correlation of changing eye-tracking behavior and flight performance decrement is consistent with our previous findings. Further study is required to determine whether these findings can be extrapolated to repeated exposures and to other disorientation scenarios.

Failure of cetirizine and fexofenadine to prevent motion sickness.

OBJECTIVE: To determine the effectiveness of 2 second-generation antihistamines in modulating motion sickness induced by Coriolis vestibular cross-coupling stimulation. METHODS: This prospective, randomized, double-blind, crossover, placebo-controlled study was conducted in 18 healthy adults. Subjects were exposed to Coriolis vestibular cross-coupling in the laboratory using the Staircase Profile Test for baseline susceptibility and when under the influence of cetizirine, fexofenadine, and placebo. Subjective evaluation of sickness symptoms was based on the Graybiel diagnostic criteria of acute motion sickness, Golding's scale, and the Coriolis Sickness Susceptibility Index. RESULTS: Repeated measures ANOVA and Friedman nonparametric ANOVA of rank tests revealed that there were significant differences in symptom assessments based on Graybiel's diagnostic criteria (p < or = 0.001), subjective symptoms of motion sickness (p < or = 0.001), and state-anxiety (p < or = 0.001) before and after motion exposure. However, there are no significant differences between the baseline susceptibility to motion sickness and treatment with placebo, cetirizine, or fexofenadine. CONCLUSIONS: The failure of the second-generation antihistamines cetirizine and fexofenadine to prevent motion sickness suggests that the therapeutic actions of this class of antihistamines against motion sickness may be mediated through central versus peripheral receptors. The sedative effect of other antihistamines, such as hydroxyzine, may play a more significant role in alleviating motion sickness than previously thought.