Dissociated behavior of low-frequency responses and high-frequency oscillations after systemic morphine administration in conscious rats.

It has been proposed that high-frequency oscillations (HFOs) and underlying conventional somatosensory-evoked potentials (SEPs) have different brain origins. To further explore the neural mechanism of HFOs, we recorded the SEPs responding to high-intensity electrical stimulation applied to the hind paw of conscious, freely moving rats. We also investigated the effect of systemic morphine on HFOs and the conventional SEPs. HFOs after high-intensity electrical stimulation showed a widespread distribution in frontal and temporal regions of the brain. The amplitude of HFOs was significantly decreased by systemic morphine, whereas the primary conventional SEP components remained unaffected. The different changes in HFOs and primary SEP components after systemic morphine administration provided further evidence for the hypothesis that HFOs and underlying conventional SEP components have different origins.

Impaired neural coordination in hippocampus of diabetic rat.

In vitro electrical neurophysiological and behavioural studies have shown that diabetes mellitus negatively affects hippocampal function. In this study, by using in vivo extracellular recording, the spontaneous neural activity was obtained from hippocampus of anaesthetized rats in both streptozotocin-induced diabetes group and normal control group. Temporal relationship between neuronal firing and slow oscillation (1-4 Hz) of local field potentials (LFPs) in hippocampus was analyzed using coherence and phase locking measurement. Lower coherence value (0.617+/-0.028) was observed in diabetic rats than that in control rats (0.730+/-0.024) (P=0.005). Furthermore, phase-locking measurement using von Mises fitting parameterized by a concentration parameter kappa showed a lower degree (kappa= 0.347+/-0.113) of temporal coordination between neuronal spiking and slow oscillation of LFPs in the hippocampus of diabetic rats than that of normal ones (kappa= 1.174+/-0.134) (P<0.001). Both approaches demonstrated that diabetes can indeed impair the temporal coordination between neuronal spiking and slow oscillation of population activity in hippocampus. This observed neural coordination impairment may serve as a network level mechanism for diabetes-induced memory deterioration.

Dynamic processing of nociception in cortical network in conscious rats: a laser-evoked field potential study.

(1) Field potential study in conscious rats provides a convenient and effective animal model for pain mechanism and pharmacological research. However, the spatial-temporal character of nociception processing in cortex revealed by field potential technique in conscious rats remains unclear. (2) In the present study, multi-channel field potentials evoked by noxious laser stimulation applied to the hind paw of conscious rats were recorded through 12 chronically implanted skull electrodes. Independent component analysis (ICA) was used to remove possible artifacts and to extract the specific nociception-related component. (3) Two fast sharp responses and one slow blunt response were evoked by noxious laser stimulation. Systemic morphine (5 mg/kg, i.p.) preferentially attenuated the amplitude of the slow blunt response while had no significant effect on the first two sharp responses. ICA revealed that those responses came from activities of contralateral anterior parietal area, medial frontal area and posterior parietal area. A movement artifact was also detected in this study. Partial directed coherence (PDC) analysis showed that there were changes of information flows from medial frontal and posterior parietal area to anterior parietal area after noxious laser stimulation. (4) Characterization of the spatio-temporal responses to noxious laser stimulation may be a valuable model for the study of pain mechanisms and for the assessment of analgesia.

[In vivo extracellular neural recording for the study of cortical plasticity].

Neural network plasticity is fundamental for learning and memory. Its abnormal change underlies some neural diseases. Measurement of the plasticity of cortex can help understand the mechanism of plasticity, and provide a quantitative way to observe the neural process of natural aging and neurodegenerative diseases, which may lead to a new approach for evaluation of anti-aging drugs and new medical treatments for neurodegenerative diseases. In this study, a systematic method was established based on whisker pairing (WP) experiment to measure the network plasticity in the barrel cortex in rat. WP experiment is a classical experiment to study the effect of innocuous bias of the flow of sensory activity from the whiskers for certain periods in awake and behaving rats on the receptive field organization in S1 barrel cortex neurons. In the experiment, one pair of adjacent whiskers D2 and D3 remained intact while others were being trimmed throughout a certain period. After that, receptive fields of single cells in the contralateral barrel were analyzed by post-stimulus time histogram after certain days of WP and compared with the controls. In the control group, response magnitudes to surrounding whiskers D1 and D3 deflection were not significantly different. However, after WP, a bias occurred in response to paired surrounding whisker D3 relative to the opposite trimmed surrounding whisker D1. In this study, by comparing the bias degree in rats in different groups after WP, a quantitative method was established to compare cortical plasticity. Example of corical plasticity comparison between adolescent and mature rats was employed in this paper to illustrate our method. The key techniques of this method such as the identification of D2 barrels, supragranular (L2-3) and barrel layer (L4) in real-time were described in details. The feasibility of this approach was further verified by compendious report of results and our previous study regarding cortical plasticity comparison between adolescent and mature rats.

A comparison between spontaneous electroencephalographic activities induced by morphine and morphine-related environment in rats.

Previous studies demonstrated that drug cues could elicit drug-like or withdrawal-like effect, both subjectively and physiologically. However, few studies have compared the central activities induced by a drug-related environment and the drug itself. The aim of this study was to observe and compare electroencephalographic (EEG) changes induced by acute morphine administration and by the morphine-related environment. EEG activities were recorded via twelve skull electrodes scattered on the left and right cortex in conscious, freely moving rats, either after acute morphine administration or after successful training of conditioned place preference. Acute administration of morphine (0.1, 0.5, 1, 5, 10, 20 mg/kg, i.p.) produced an increase in absolute EEG power in the delta, theta, alpha1, alpha2, beta1, and beta2 bands, as well as a decrease in the gamma band. Topographic mapping revealed a maximal increase in the lateral leads in the theta band and a maximal change in the centro-frontal region in the remaining bands. After place conditioning training, the morphine-related environment induced a diffuse decrease in absolute power in the delta, theta, alpha1, alpha2, beta1, and beta2 bands, which was opposite to the changes induced by acute morphine administration. In addition, the changes in relative power induced by the two situations also diverged. These results indicate that the central mechanisms underlying the motivation of morphine-induced place preference may be somehow different from those underlying the reward effects produced by acute morphine administration.