ABSTRACT
Hippocampal (HIP) theta power increases during sensory mismatch, which has been suggested to induce motion sickness with autonomic abnormality (Zou et al., 2009 [29]). To investigate relationships between hippocampal theta rhythm and autonomic functions, theta waves in the HIP and electrocardiograms (ECGs) were recorded during sensory mismatch by backward translocation in awake rats. The rats were placed on a treadmill affixed to a motion stage that was translocated along a figure 8-shaped track. The rats were trained to run forward on the treadmill at the same speed as that of forward translocation of the motion stage (a forward condition) before the experimental (recording) sessions. In the experimental sessions, the rats were initially tested in the forward condition, and then tested in a backward (mismatch) condition, in which the motion stage was turned around by 180° before translocation. That is, the rats were moved backward by translocation of the stage although the rats ran forward on the treadmill. In this condition, proprioceptive information indicated forward movements while vestibular and visual information indicated backward movements. The theta (6-9 Hz) power was significantly increased in the backward condition compared with the forward condition. Spectral analysis of heart rate variability indicated that sympathetic nervous activity increased in the backward condition. These data (theta power and sympathetic nervous activity) were positively correlated. Furthermore, electrical stimulation of the HIP at theta rhythm (8 Hz) increased heart rate. These results suggest that sensory mismatch information activates the HIP to induce autonomic alteration in motion sickness.
Subject(s)
Autonomic Nervous System/physiology , Autonomic Pathways/physiology , Hippocampus/physiology , Motion Perception/physiology , Movement/physiology , Theta Rhythm/physiology , Analysis of Variance , Animals , Blood Pressure/physiology , Electric Stimulation/methods , Electrocardiography/methods , Exercise Test , Fourier Analysis , Heart Rate/physiology , Male , Rats , Rats, Wistar , Time Factors , Vestibule, Labyrinth/physiology , Wakefulness , Water Deprivation/physiologyABSTRACT
The distribution of a live attenuated herpes simplex virus (betaH1)-mediated gene delivery into the central nervous system (CNS) was regulated by growth inhibition with ganciclovir (GCV) and the effect of this transgene expression system on the physiologic response was characterized by the acoustic startle response and its prepulse inhibition. We inoculated betaH1 expressing beta-galactosidase (beta-gal) driven by the latency associated transcripts promoter into the right caudate putamen of rats. Histochemical analysis demonstrated that the inoculation of betaH1 in the right caudate putamen resulted in a high level of beta-gal expression in the neurons of the area projecting to the inoculation site. On 14 days after inoculation without GCV-treatment, beta-gal activity localized in the anterior olfactory nucleus, frontal, insular, orbital, parietal, perirhinal, piriform cortices and the temporal region including the amygdala. In contrast, the distribution of beta-gal activity was regulated by the interval between virus inoculation and GCV-treatment and maintained after its cessation without significant alteration. The whole process of transgene expression did not influence the emotional behavior, indicating that this vector system is a suitable model for analyzing the transgene function or applying the gene therapy for the CNS diseases.
