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Jian-Tian Qiao

Publications and source records attributed to Jian-Tian Qiao.

At least 19 recordsLinked to original sources
PubMed2006

Promotive action of lysophosphatidic acid on proliferation of rat embryonic neural stem cells and their differentiation to cholinergic neurons in vitro.

Effects of lysophosphatidic acid (LPA), an extracellular phospholipid signal, on the proliferation of rat embryonic neural stem cells (NSCs) and their differentiation into microtubule-associated protein 2 (MAP2)-positive and choline acetyltransferase (ChAT)-positive, i.e. cholinergic-committed neurons, were observed in vitro by [(3)H]-thymidine incorporation, immunocytochemistry, Western blot and other techniques. The results showed that: (1) Lower concentrations of LPA (0.01~1.0 mumol/L) dose-dependently enhanced the uptake of [(3)H]-thymidine by NSCs cultured in specific serum-free medium, indicating a significant promotive action of LPA on the proliferation of NSCs. (2) After fetal bovine serum which induces and commences the differentiation of NSCs, was used in the medium, the lower concentrations of LPA increased the percentages of both MAP2- and ChAT-immunoreactive neurons, with a peak at 0.1 mumol/L LPA in two cases. (3) The promotive effects of LPA on the differentiation of MAP2- and ChAT-positive neurons were also supported by the up-regulation of the expressions of both MAP2 and ChAT proteins detected by Western blot. (4) At the early phase of differentiation of NSCs, the cell migration and neurite extension were enhanced significantly by lower dosages of LPA under phase-contrast microscope. These results suggest that LPA within certain lower range of concentrations promotes the proliferation of NSCs and their differentiation into unspecific MAP2-positive and specific cholinergic-committed neurons, and also strengthens the migration and neurite extension of the newly-generated neuronal (and also glial as reported elsewhere) progenitors.

Animals↗
PubMed2006

Amyloid beta-protein fragment 31-35 suppresses long-term potentiation in hippocampal CA1 region of rats in vivo.

Effects of fragment 31-35 of amyloid beta-protein (AbetaP31-35) on the baseline synaptic transmission, shown as fEPSPs, and the long-term potentiation (LTP) induced by high-frequency stimuli (HFS) were investigated in vivo in the hippocampal CA1 region of rats; a longer fragment of AbetaP, i.e., AbetaP25-35, which had been generally accepted as the active center in AbetaP, was also tested comparatively along with AbetaP31-35. The results showed that: (1) the baseline fEPSPs induced by test stimuli were not changed by i.c.v. injection of AbetaP31-35, while application of either AbetaP31-35 or AbetaP25-35 with the same molar concentration (50 nmol) significantly and similarly suppressed the HFS-induced LTP; (2) higher concentration of AbetaP31-35 or longer time of AbetaP exposure exhibited stronger suppression on LTP, indicating a dose- and time-dependent trends; (3) no significant effects could be found on the paired-pulse facilitation (PPF) following AbetaP31-35 injection; (4) pretreatment with verapamil (2.5 mg/kg, i.p., 1 h prior to HFS), a blocker of L-type Ca2+ channels, did not affect the baseline fEPSPs, while it exhibited a significant suppression on LTP induced by HFS; and (5) surprisingly enough, coapplication with verapamil and AbetaP31-35 exhibited a similar suppression on LTP just as both of these two agents were used alone. These results indicate that: (1) AbetaP31-35, similar to AbetaP25-35, possesses potent suppressive effects on hippocampal LTP in vivo, supporting our proposal that the fragment AbetaP31-35 might be to date the shortest active sequence in full-length of AbetaP molecule; (2) AbetaP31-35-induced LTP suppression is not mediated by affecting the presynaptic processes; and (3) L-type Ca2+ channels might be one of the main pathways by which AbetaP31-35 insults LTP.

Amyloid beta-Peptides↗
PubMed2006

Apolipoprotein E4 suppresses delayed-rectifier potassium channels in membrane patches excised from hippocampal neurons.

Recent studies show a clear association between Alzheimer's disease (AD) and the apolipoprotein E epsilon 4 allele (APOE4). The mechanisms underlying apoE4-mediated detrimental effects have not been well-clarified. The present study investigates possible effects of apoE4 on the delayed-rectifier potassium (IK) channels in inside-out membrane patches excised from rat hippocampal neurons. Acute application of apoE4 (0.5 microM) to the inside of the membrane patches markedly and reversibly suppressed the single IK channel activities. The average open probability and open frequency of IK channels decreased by (92.6+/-7.1)% and (88.6+/-3.2)%, respectively. The mean open time of IK channels decreased by (81.6+/-6.7)%, and the mean closed-time of them increased by 6.9+/-1.9 fold. Meanwhile, the mean current amplitude of IK channels was not significantly affected. In contrast, application of apolipoprotein A (apoA, 0.5 microM), another member of apolipoprotein family with similar molecular weight and amino acid sequence to apoE4, did not exhibit any effects on IK currents. These results indicate that apoE4 molecules can rapidly suppress the activities of IK channels in hippocampal neurons when they act on the inner side of the neuronal membrane. We propose that the overproduction of apoE4 in neurons may suppress normal IK channel activities and thus be responsible for the late-developed neuronal damages related to the pathogenesis of AD.

Animals↗
PubMed2006

Is protein kinase C (PKC) involved in nociception?

The study was designed to determine whether the protein kinase C (PKC) is involved in nociceptive c-Fos expression and the concomitant signaling processes of endogenous opioid-like substances (OLS) that modulate c-Fos expression in the spinal dorsal horn following formalin injection into the unilateral hindpaw in rats by using immunocytochemical techniques. In the first part of experiments in which rats were pretreated with intrathecal (i.t.) chelerythrine (Chel), an inhibitor of PKC, the nociceptive c-Fos-like immunoreactive (Fos-LI) neurons in the lumbar dorsal horn ipsilateral to the formalin injection were significantly suppressed with a reduction rate of 60.3% (p < .001) as compared to that in the control group with i.t. saline. In the second part of experiments in which rats were pretreated with i.t. naloxone (Nal), the nociceptive Fos-LI neurons were significantly increased by 53.2% (p < .01) as compared to that in the control group; however, when rats were pretreated with combined i.t. Nal + Chel, the nociceptive Fos-LI neurons exhibited a percentage reduction similar to that in group with i.t. Chel alone, although the real number of Fos-LI neurons in group with i.t. Nal + Chel still significantly surpassed that in group with i.t. Chen only. These results suggest that: (1) PKC may play an important role in the induction of nociceptive c-Fos expression; (2) nociceptive c-Fos expression is subject to the modulation of endogenous OLS that suppress the nociceptive responses of the dorsal horn neurons; and (3) PKC may not be involved in the signaling processes by which the endogenous OLS modulate the nociceptive c-Fos expression in the spinal level.

Alkaloids↗
PubMed2005

Spinal glial activation in a new rat model of bone cancer pain produced by prostate cancer cell inoculation of the tibia.

Studies suggest that astrocytes and microglia in the spinal cord are involved in the development of persistent pain induced by tissue inflammation and nerve injury. However, the role of glial cells in bone cancer pain is not well understood. The present study evaluated the spinal glial activation in a novel rat model of bone cancer pain produced by injecting AT-3.1 prostate cancer cells into the unilateral tibia of male Copenhagen rats. The structural damage to the tibia was monitored by radiological analysis. The thermal hyperalgesia, mechanical hyperalgesia and allodynia, and spontaneous flinch were measured. The results showed that: (1) inoculation of prostate cancer cells, but not the vehicle Hank's solution, induced progressive bone destruction at the proximal epiphysis of the tibia from day 7-20 post inoculation; (2) the inoculation also induced progressive thermal hyperalgesia, mechanical hyperalgesia, mechanical allodynia, and spontaneous flinches; (3) astrocytes and microglia were significantly activated in the spinal cord ipsilateral to the cancer leg, characterized by enhanced immunostaining of both glial fibrillary acidic protein (GFAP, astrocyte marker) and OX-42 (microglial marker); (4) IL-1beta was up-regulated in the ipsilateral spinal cord, evidenced by an increase of IL-1beta immunostained astrocytes. These results demonstrate that injection of AT-3.1 prostate cancer cells into the tibia produces progressive hyperalgesia and allodynia associated with the progression of tibia destruction, indicating the successful establishment of a novel male rat model of bone cancer pain. Further, bone cancer activates spinal glial cells, which may release IL-1beta and other cytokines and contribute to hyperalgesia.

Animals↗
PubMed2005

Electroacupuncture suppresses spinal expression of neurokinin-1 receptors induced by persistent inflammation in rats.

It has been demonstrated that electroacupuncture (EA) significantly suppresses behavioral hyperalgesia in a rat model of persistent inflammatory pain and that neurokinin-1 (NK-1)/substance P (SP) receptors play important roles in nociception and hyperalgesia at the spinal cord level. The present study investigated spinal NK-1 receptor involvement in EA-produced suppression of hyperalgesia in a rat model of persistent inflammatory pain. The results showed that hind paw inflammation induced a significant increase of NK-1 receptor expression in the spinal dorsal horn and that this effect was significantly suppressed by EA. This suggests that EA-induced suppression of hyperalgesia is involved, at least partly, in the suppression of the spinal NK-1 receptors induced by sustained peripheral nociceptive input.

Animals↗
PubMed2005

Mu opioid receptor-containing neurons mediate electroacupuncture-produced anti-hyperalgesia in rats with hind paw inflammation.

Previous studies showed that electroacupuncture (EA) significantly attenuates inflammatory hyperalgesia in a complete Freund's adjuvant (CFA)-induced inflammatory pain rat model. The present study demonstrates that pretreatment with Derm-sap, a selective toxin for neurons that contain mu opioid receptor (MOR), specifically decreases MOR and blocks EA anti-hyperalgesia. These data suggest that spinal MOR-containing neurons are involved in the processes by which EA produces anti-hyperalgesia.

Analysis of Variance↗
PubMed2005

Neuroprotective effect of lysophosphatidic acid on AbetaP31-35-induced apoptosis in cultured cortical neurons.

It has been reported that lysophosphatidic acid (LPA) at its lower concentrations prevents apoptosis induced by serum-deprivation in cultured cortical neurons when LPA is added into the cultural medium with serum withdrawal. The present study was designed to investigate whether LPA could also block the apoptosis induced by beta-amyloid peptide fragment 31-35 (AbetaP31-35) in cultured cortical neurons by using techniques of DNA fragmentation electrophoresis, HO33342 staining, and TUNEL examinations. The results showed that pretreatment of LPA suppressed the AbetaP31-35-induced apoptosis only when LPA was applied to the cultured neurons with lower concentrations (1-10 micromol/L) and especially, with a preceding time of 12-24 h before the AbetaP31-35 exposure. These facts imply that LPA also acts as a neuroprotective factor against AbetaP31-35-induced apoptosis, though the mechanism underlying the protective action in this case may be more complex than that involved in the serum deprivation-induced apoptosis.

Amyloid beta-Peptides↗
PubMed2005

Effects of pertussis toxin on electroacupuncture-produced anti-hyperalgesia in inflamed rats.

Our previous study showed that electroacupuncture (EA) significantly attenuated hyperalgesia in an animal model of persistent inflammatory pain. The present study was designed to show if Gi/o protein is involved in EA-produced anti-hyperalgesia. Spinal Gi/o-protein function was destroyed by intrathecal pretreatment with pertussis toxin (PTX). Seven days after the placement of an intrathecal PE-10 tube, PTX was injected into the intrathecal space of the lumbar spinal cord of rats. Seven days after PTX, complete Freund's adjuvant (CFA) was injected into the plantar surface of one hind paw of the rat to induce hyperalgesia in the injected paw. EA treatment was given at acupoint GB30 immediately post-CFA and then hyperalgesia was assessed by measuring the degree of decreased paw withdrawal latency (PWL) to a noxious thermal stimulus. The results showed that PTX pretreatment prevented EA-produced anti-hyperalgesia in the CFA inflammatory pain model but did not affect either baseline pain threshold or CFA-induced hyperalgesia. The data suggest that EA-produced anti-hyperalgesia is mediated by PTX-sensitive Gi/o proteins and the relevant signaling pathways.

Animals↗
PubMed2005

Spinal preprodynorphin mRNA expression in neonatal rats following peripheral inflammation.

Spinal nociceptive neural circuits undergo considerable changes during the postnatal period. This study showed that neonatal rats exhibited earlier upregulation and faster recovery of spinal preprodynorphin (PPD) mRNA than did the adults during complete Freund's adjuvant (CFA)-induced peripheral inflammation. These data suggest that the central nervous systems of neonates and adults respond differently to peripheral noxious inputs, a fact that should be considered when selecting pain treatment strategies for neonate populations.

Aging↗
PubMed2005

c-Fos antisense oligodeoxynucleotide offsets behavioral nociceptive responses and both up-regulations of c-Fos protein and dynorphin a (1-8) in dorsal horn: a study using the formalin test in rats.

The formalin test was used to elicit acute and chronic pain in rats, and antisense oligodeoxynucleotide (AS-ODN) was used as a tool to modulate the expression of nociceptive behavioral and neurochemical responses. AS-ODN complementary to c-Fos mRNA was administered intrathecally (i.t.) 4 h before formalin injection in the experimental group. Normal saline or reverse AS-ODN was pre-administered i.t. at the same time in two control groups (saline and reverse AS-ODN). The results showed that the acute phase of nociceptive behavior showed no change by AS-ODN administration, whereas the tonic phase of nociceptive licking and biting behavior was significantly suppressed by AS-ODN as compared with the saline or the reverse AS-ODN group, respectively (p < .05 and p < .01). At the same time, both Fos-like immunoreactive (FLI) neurons and density of dynorphin-like immunoreactivities (DLI) were decreased significantly (p < .05 and p < .01) in the AS-ODN group as compared with that in two control groups. The results indicate that the long-lasting nociceptive responses elicited by sustained noxious inputs are based on the up-regulation of c-Fos gene expression, which in turn induces the upregulation of Dyn A production. It is proposed that intensified Dyn A production in the dorsal horn may be pivotal for the appearance of chronic pain.

Animals↗
PubMed2004

Protein kinase C is partly involved in c-fos protein expression of nocuously-activated neurons but may not in concomitant modulatory action through opioid receptors at the spinal level in rats.

The present study was aimed to examine if protein kinase C (PKC) activation is necessarily involved in both the c-fos protein expression in the nocuously-activated c-fos protein-like immunoreactive (Fos-LI) neurons and the concomitant opioid receptor-mediated modulation in the dorsal horn circuitry of the spinal cord. Formalin was injected into a hindpaw of rats 5 min after the rats were pretreated with intrathecal (i.t.) administration of chelerythrine (Chel), an inhibitor of PKC, naloxone (Nal), combined administration of these two (Chel + Nal), or vehicle (n=5 in each group),respectively. By using immunocytochemical techniques, the formalin-induced Fos-LI neurons in the lumbar dorsal horn were calculated 1 h after formalin injection. The results showed that: (1) i.t. Chel significantly reduced the number of Fos-LI neurons in the dorsal horn of the spinal cord on the side ipsilateral to the formalin injection, showing a decrease by 60.3% (P<0.001) as compared to that observed in the i.t.vehicle group; (2) i.t. Nal significantly increased the number of Fos-LI neurons in the ipsilateral dorsal horn, with an increase of 46.0% (P<0.01) as compared to that in the i.t.vehicle group, the highest percentage increase being found in the deeper laminae of the dorsal horn; and (3) i.t. Chel + Nal also exhibited a significant decrease in Fos-LI neurons in the ipsilateral dorsal horn as compared to i.t. Nal group, showing a reduction of 53.2%, a value similar to that in the i.t. Chel group. These results suggest that: (1) PKC plays a role in the c-fos protein expression only in nearly one half of the Fos-LI neurons in the dorsal horn; and (2) PKC is possibly not involved in the concomitant modulation on the nociception mediated by micro- (and also partly delta-) opioid receptors in the spinal cord.

Animals↗
PubMed2004

Dual action of lysophosphatidic acid in cultured cortical neurons: survival and apoptogenic.

The effect of lysophosphatidic acid (LPA), with a wide range of its different concentrations, upon cultured mouse cortical neurons was assessed by electrophoresis of DNA fragments, HO33342 and TUNEL stainings, and also by ultrastructural examination at times. The results showed that administration of LPA at lower concentrations (0.1-30 micromol/L) dose-dependently protected cortical neurons from apoptosis that was induced by deprivation of serum from the cultural medium, while 50 micromol/L or higher concentrations of LPA failed to show this effect; and moreover, the concentrations higher than 50 micromol/L induced apoptosis in neurons cultured in serum-containing complete medium. These results suggest that a moderate concentration of LPA may play as a survival factor in apoptotic cortical neurons, while an excessive level of LPA induces apoptosis in neurons cultured in complete medium.

Animals↗
PubMed2004

Endogenous and exogenous glucocorticoid suppresses up-regulation of preprodynorphin mRNA and hyperalgesia in rats with peripheral inflammation.

Glucocorticoids (GC) play important roles in response to stressful stimuli, including pain. This study examined the effects of bilateral adrenalectomy (ADX) and dexamethasone (DEX) replacement on the hyperalgesia and spinal preprodynorphin (PPD) mRNA expression induced by injecting complete Freund's adjuvant (CFA) into rats' hind paws. The results demonstrated that CFA induced more intense hyperalgesia and up-expression of spinal PPD mRNA in ADX rats than in control rats, while both of these intensified reactions could be significantly suppressed by subcutaneous pretreatment with DEX. This leads to the conclusion that both exogenous (pharmacological) and endogenous (physiological) GC suppresses the behavioral hyperalgesia and the up-regulation of spinal PPD mRNA induced by sustained peripheral inflammation. The results also suggest that spinal PPD mRNA suppression may partially underlie the inhibition of behavioral hyperalgesia.

Animals↗
PubMed2004

Amyloid beta-protein fragment 31-35 suppresses delayed rectifying potassium channels in membrane patches excised from hippocampal neurons in rats.

To clarify the early initial mechanism underlying the neurotoxicity of amyloid beta-protein (AbetaP) and the shorter essential active sequence in native AbetaP molecules, the effects of AbetaP31-35 and AbetaP25-35 on delayed rectifier K+ current (Ik) were investigated in the inside-out membrane patches excised from hippocampal neurons of rats. The results showed that: 1) After application of AbetaP31-35 (5 microM) to the inside of patches, the average open frequency and open probability of Ik channels reversibly decreased by 70.45 +/- 35.75% and 86.9 +/- 11.13%, respectively; the mean open time decreased by 47.1 +/- 38.8%, while the mean current amplitude of Ik channels was not significantly affected. 2) Application of AbetaP25-35 at the same concentration showed similar effects as did the AbetaP31-35 application. It has generally been accepted that AbetaP25-35 acts as a full-length AbetaP molecule does, so our findings suggest that the neurotoxicity of AbetaP may be initiated by the functional suppression of Ik channels and the sequence of 31-35 might be the shorter active sequence in AbetaP responsible for its neurotoxicity.

4-Aminopyridine↗
PubMed2004

Effects of aging on hyperalgesia and spinal dynorphin expression in rats with peripheral inflammation.

The aging process is associated with various morphological and biochemical changes in the nervous system that may affect the processing of noxious inputs. This study showed greater hyperalgesia and up-regulation of spinal dynorphin (DYN) expression in aging than in young adult rats during CFA-induced peripheral inflammation. These data indicate that nociception is regulated differently in aging individuals, a fact that should be considered when selecting treatment strategies for aging populations with persistent pain.

Aging↗
PubMed2004

Serotonin modulates hypothalamic neuronal activity.

Effects of serotonin (5-HT) on electrophysiological activities of single hypothalamic arcuate neurons in rat brain slices were observed by extracellular recording. The results showed that (1) of 385 arcuate neurons observed, the patterns of spontaneous firing were divided into 3 categories: "slow irregular" (46.0%), "fast continuous" (22.6%), and "bursting" firing (31.4%); (2) of 149 neurons tested for 5-HT, most (55.0%) responded to the drug by decreasing firing rate, 22.2% by increasing firing rate, 11.4% exhibit biphasic pattern, and 11.4% did not respond to 5-HT application; (3) substitution of low Ca2-high Mg2+ artificial cerebrospinal fluid (ACSF) for normal ACSF did not abolish the 5-HT-induced excitatory effect while it did abolish the 5-HT-induced inhibitory effect, suggesting the effect in latter cases was elicited by a Ca2+-dependent release of neuroactive substances; (4) cyproheptadine, a non-selective 5-HT receptor antagonist, antagonized the 5-HT-induced excitatory effect in all neurons tested, while pindolol, a 5-HT1A/1B receptor antagonist, antagonized the 5-HT-induced excitatory effect in 50% of neurons tested; (5) both cyproheptadine and pindolol antagonized the 5-HT-induced inhibitory effect; and (6) bicuculline, a GABAA receptor antagonist, antagonized the 5-HT-induced inhibitory effect. These results suggest that 5-HT may exert its excitatory effects directly through 5-HT1A/1B and other subtypes of 5-HT-receptors located on the surface of the neurons recorded, while its inhibitory effects are mediated indirectly through the activation of a local inhibitory GABAergic interneuron.

Action Potentials↗