ABSTRACT
It is well known that the insular cortex is involved in the processing of painful input. The aim of this study was to evaluate the pain modulation role of the insular cortex during motor cortex stimulation (MCS). After inducing neuropathic pain (NP) rat models by the spared nerve injury method, we made a lesion on the rostral agranular insular cortex (RAIC) unilaterally and compared behaviorally determined pain threshold and latency in 2 groups: Group A (NP + MCS; n = 7) and Group B (NP + RAIC lesion + MCS; n = 7). Also, we simultaneously recorded neuronal activity (NP; n = 9) in the thalamus of the ventral posterolateral nucleus and RAIC to evaluate electrophysiological changes from MCS. The pain threshold and tolerance latency increased in Group A with "MCS on" and in Group B with or without "MCS on." Moreover, its increase in Group B with "MCS on" was more than that of Group B without MCS or of Group A, suggesting that MCS and RAIC lesioning are involved in pain modulation. Compared with the "MCS off" condition, the "MCS on" induced significant threshold changes in an electrophysiological study. Our data suggest that the RAIC has its own pain modulation effect, which is influenced by MCS.
Subject(s)
Cerebral Cortex/physiopathology , Motor Cortex/physiopathology , Neuralgia/physiopathology , Pain Measurement , Pain Threshold/physiology , Animals , Male , Proto-Oncogene Proteins c-fos/metabolism , Rats, Sprague-Dawley , Thalamus/physiopathologyABSTRACT
The fruit of Zizyphus jujuba has been used as a traditional Chinese medicinal herb and considered for thousands of years to affect various physiological functions in the body. We obtained a Z. jujuba extract (ZJE) and observed the neuroprotective effects of ZJE against ischemic damage in gerbils that had received repeated oral administrations of ZJE for 10 days. In the ZJE-treated ischemia group, neuronal nuclei (a marker for neurons)-immunoreactive neurons were abundant (58.4% vs. sham group) in the hippocampal CA1 region 4 days after ischemia/reperfusion compared to those in the vehicle-treated ischemia group (11.3%). In addition, ZJE treatment significantly decreased the reactive gliosis of astrocytes and microglia in the CA1 region compared to that in the vehicle-treated group 4 days after ischemia/reperfusion. Immunoreactivities of Cu,Zn-superoxide dismutase (SOD1) and brain-derived neurotrophic factor in the ZJE-treated ischemia group were higher those in the vehicle-treated ischemia group 4 days after ischemia/reperfusion. In addition, in the ZJE-treated ischemia group, levels of hydroxynonenal, an indicator of lipid peroxidation, were much lower than those in the vehicle-treated ischemia group after ischemia/reperfusion. These results suggest that the repeated supplements of ZJE can protect neurons from ischemic damage via up-regulation of SOD1 and reduction of lipid peroxidation in the ischemic hippocampal CA1 region.
Subject(s)
Antioxidants/administration & dosage , Brain Ischemia/complications , CA1 Region, Hippocampal/drug effects , Plant Extracts/administration & dosage , Reperfusion Injury/drug therapy , Ziziphus/chemistry , Animals , Brain Ischemia/drug therapy , Brain Ischemia/metabolism , CA1 Region, Hippocampal/cytology , CA1 Region, Hippocampal/metabolism , Disease Models, Animal , Gerbillinae , Humans , Lipid Peroxidation/drug effects , Male , Neurons/drug effects , Neurons/metabolism , Neuroprotective Agents/administration & dosage , Reperfusion Injury/metabolism , Superoxide Dismutase/genetics , Superoxide Dismutase/metabolism , Superoxide Dismutase-1ABSTRACT
Neurogenesis is regulated by several factors such as age, stress and pharmacological agents. We observed the effects of (-)-epigallocatechin-3-gallate (EGCG), a major catechin of green tea, on neurogenesis in mice. The animals were orally administered EGCG for 4 weeks. Brain sections were stained using a marker for cell proliferation (Ki67 and BrdU) and neuroblasts (doublecortin, DCX). In all groups, Ki67, BrdU and DCX immunoreaction were observed in the subgranular zone of the dentate gyrus. Oral administration of EGCG significantly increased the number of Ki67-, BrdU- and DCX-immunoreactive cells as well as BrdU/DCX-colabled cells in the subgranular zone when compared to those in the vehicle-treated group. These results indicate that oral administration of EGCG can enhance cell proliferation and increase the number of neuroblasts in mice hippocampal dentate gyrus.
Subject(s)
Catechin/analogs & derivatives , Cell Proliferation/drug effects , Dentate Gyrus/cytology , Neurogenesis , Neurons/drug effects , Administration, Oral , Animals , Catechin/pharmacology , Dentate Gyrus/drug effects , Doublecortin Protein , Male , Mice , Mice, Inbred C57BLABSTRACT
Capsaicin has effects on the adiposity by increasing energy and lipid metabolism, and decreases appetite and fat intake. In the present study, we investigated changes in food intake and body weight after capsaicin treatment. We also observed changes in orexigenic and anorexigenic neuropeptides-agouti-related peptide (AgRP), alpha-melanocyte-stimulating hormone (alpha-MSH), adrenocorticotropic hormone (ACTH) and orexin-immunoreactivities in the rat hypothalamus after capsaicin administration. Only one day after capsaicin treatment, the mean food intake was significantly decreased. There was no significant difference in the mean body weight between vehicle- and capsaicin-treated groups. In addition, after capsaicin treatment, numbers of AgRP- and orexin-immunoreactive ((+)) cells were significantly decreased in the arcuate nucleus (ARC) and lateral hypothalamic area, respectively. In contrast, the number of alpha-MSH(+) and ACTH(+) cells in the ARC of the capsaicin-treated rats was higher than in the vehicle-treated rats. These results indicate that capsaicin reduces food intake, not body weight, transiently, and decreases AgRP and orexin immunoreactivities, whereas it increases alpha-MSH and ACTH immunoreactivities in rat hypothalamic nuclei.
Subject(s)
Capsaicin/pharmacology , Hypothalamus/drug effects , Hypothalamus/metabolism , Neuropeptides/metabolism , Adrenocorticotropic Hormone/metabolism , Agouti-Related Protein/metabolism , Animals , Body Weight/drug effects , Eating/drug effects , Rats , alpha-MSH/metabolismABSTRACT
We observed the changes of body temperature and the cytokine expressions in the hypothalamus of rats to investigate the effect and mechanism of antipyretic action of acupuncture. Lipopolysaccharide (LPS, i.p., 2.5 mg/kg) was injected into rats and manual acupuncture was performed on Shaofu (HT8), Zutonggu (BL66) or Xingjian (LR2), respectively. The results showed that fever induced by LPS-injection was recovered significantly by acupuncture on each acupoint. LPS increased hypothalamic mRNA levels of interleukin-6 and interleukin-1 beta which, on the contrary, were also reduced to normal levels by acupuncture stimulation on BL66. These results suggest that the acupuncture stimulation may be effective for reducing elevated body temperature induced by bacterial inflammation, and part of its action may be mediated through the suppression of hypothalamic production of pro-inflammatory cytokines.