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Ji-Sheng Han

Publications and source records attributed to Ji-Sheng Han.

At least 37 records · Page 2Linked to original sources

Repeated peripheral electrical stimulations suppress both morphine-induced CPP and reinstatement of extinguished CPP in rats: accelerated expression of PPE and PPD mRNA in NAc implicated.

Previous studies have shown that peripheral electrical stimulation (PES) can suppress morphine-induced conditioned place preference (CPP) and the reinstatement of extinguished CPP in the rat. The present study was performed to elucidate if preproenkephalin (PPE) and preprodynorphin (PPD) mRNAs in the nucleus accumbens (NAc) play a role in this event. Rats were trained with morphine for 4 days to establish CPP paradigm. They were then given 15-min test once a day for eight consecutive days for extinction trial. Twenty-four hours after the 8th session of extinction trials, rats were given peripheral electrical stimulation (PES) at 2 or 100 Hz once a day for 3 days, then a morphine-priming injection at a dose of 1, 2, or 4 mg/kg to reinstate the extinguished CPP. At the end of the experiment, PPE and PPD mRNA levels in the nucleus acccumbens (NAc) were determined by the semiquantitative RT-PCR technique. The results showed that PES at 2- and 100-Hz administered 30 min a day for 3 days suppressed both the expression of morphine-induced CPP and the reinstatement of extinguished CPP. PES at 2 Hz increased preproenkephalin (PPE) mRNA levels, whereas PES of 100 Hz that of preprodynorphin (PPD) mRNA levels in the NAc. These findings suggest that enkephalin and dynorphin in NAc may play important roles in the mechanisms underlying the inhibitory effect of PES on the expression and reinstatement of morphine-induced CPP in rats.

Analysis of Variance↗

Ketamine potentiates the effect of electroacupuncture on mechanical allodynia in a rat model of neuropathic pain.

Mu-opioid agonists and N-methyl-d-aspartate (NMDA) receptor antagonists have been shown to attenuate mechanical allodynia in neuropathic pain models. We have previously reported that 2Hz electroacupuncture (EA) produced analgesia via releasing endogenous opioid peptides (i.e. beta-endorphin and endomorphin) and the activated micro-opioid receptors. The present study aimed to examine whether ketamine, an NMDA receptor antagonist, can enhance the anti-allodynic effects induced by 2Hz EA in a rat model of neuropathic pain following spinal nerve ligation (SNL). The results are as follows: (1) EA itself or i.p. injection of ketamine reduced mechanical allodynia (i.e. increase in withdrawal threshold). (2) Although injection of ketamine at a low dose (1.0mg/kg) alone did not influence mechanical withdrawal threshold, combination of ketamine at this dose with EA produced more potent anti-allodynic effect than that induced by EA alone. (3) The anti-allodynic effect of EA combined with ketamine could be reversed by i.p. injection of naloxone (2.0 mg/kg). These results suggested that ketamine potentiate the anti-allodynic of EA in rats with spinal nerve ligation, and endogenous opioid system is likely to be involved in this process.

Animals↗

Differential modulation of nociceptive neural responses in medial and lateral pain pathways by peripheral electrical stimulation: a multichannel recording study.

It is well accepted that peripheral electrical stimulation (PES) can produce an analgesic effect in patients with acute and chronic pain. However, the neural basis underlying stimulation-induced analgesia remains unclear. In the present study, we examined the pain-related neural activity modified by peripheral stimulation in rats. The stimulation frequency of pulses applied to needle electrodes in the hindlimb was 2 Hz alternating with 100 Hz, with 0.6 ms pulse width for 2 Hz and 0.2 ms for 100 Hz. The intensity of the stimulation was increased stepwise from 1 to 3 mA with each 1-mA step lasting for 10 min. The nociceptive neural and behavioral responses were examined immediately after the termination of stimulation. Using a multiple-channel recording technique, we simultaneously recorded the activity of many single neurons located in the primary somatosensory and anterior cingulate cortex (ACC), as well as the ventral posterior and medial dorsal thalamus in behaving rats. Our results showed that peripheral electrical stimulation significantly reduced the nociceptive responses in ventroposterior thalamus and somatosensory cortex, indicating an inhibition of nociceptive processing. In contrast, the analgesic stimulation produced a significant increase in mediodorsal thalamus while a less significant decrease in cingulate cortex, reflecting a complicated effect associated with combined antinociceptive activation and nociceptive suppression. These results support the idea that peripheral electrical stimulation can ultimately alter the pain perception by specifically inhibiting the nociceptive transmission in the sensory pathway while mobilizing the antinociceptive action in the affective pathway, thus to produce pain relief.

Animals↗

Hyperpolarization-activated, cyclic nucleotide-gated cation channels: roles in the differential electrophysiological properties of rat primary afferent neurons.

The large, medium-sized, and small neurons of the dorsal root ganglion (DRG) have different functions in the processing of various senses. Hyperpolarization-activated, cyclic nucleotide-gated channels (HCN) contribute greatly to neuronal excitability. In the present study, which used whole-cell patch clamp techniques and immunohistochemical staining methods, the electrophysiological properties of DRG neurons were systematically compared, and the roles of HCN-1, -2, and -4 were examined. The main results were as follows. 1) The large neurons had significantly higher V0.5 values (membrane potential at which the HCN channels were half-activated) and shorter time constants (tau) than small or medium-sized DRG neurons. However, large DRG neurons had higher Ih density (HCN neuron current). 2) HCN-1 was found predominantly, but not exclusively, in large and medium-sized DRG neurons; HCN-2 was found in all DRG neurons; and HCN-4 was poorly visualized in all DRG neurons. HCN-1 and HCN-2 were colocalized in large and medium-sized neurons with immunostaining of adjacent sections. In the dorsal horn of the spinal cord, HCN-1, HCN-2, and HCN-4 were all expressed in laminae I-IV, although HCN-1 was not detectable in lamina II. 3) Blockade of Ih current in DRG neurons caused a significant decrease in V0.5, resting membrane potential, and repetitive firing number of action potential and a significant increase in time of rising phase of action potential. These results suggest that the different HCN channels in the three types of DRG neurons might contribute to their differential electrophysiological properties.

Action Potentials↗

Acupuncture and endorphins.

Acupuncture and electroacupuncture (EA) as complementary and alternative medicine have been accepted worldwide mainly for the treatment of acute and chronic pain. Studies on the mechanisms of action have revealed that endogenous opioid peptides in the central nervous system play an essential role in mediating the analgesic effect of EA. Further studies have shown that different kinds of neuropeptides are released by EA with different frequencies. For example, EA of 2 Hz accelerates the release of enkephalin, beta-endorphin and endomorphin, while that of 100 Hz selectively increases the release of dynorphin. A combination of the two frequencies produces a simultaneous release of all four opioid peptides, resulting in a maximal therapeutic effect. This finding has been verified in clinical studies in patients with various kinds of chronic pain including low back pain and diabetic neuropathic pain.

Acupuncture Analgesia↗

Change of vanilloid receptor 1 expression in dorsal root ganglion and spinal dorsal horn during inflammatory nociception induced by complete Freund's adjuvant in rats.

The present study aimed to systematically observe the change of vanilloid receptor 1 (VR1) during inflammatory nociception induced by intraplantar injection of complete Freund's adjuvant (CFA) into the left hind paw in rats. Hot plate latency (HPL) was used to evaluate resulting thermal hyperalgesia and immunohistochemistry to observe VR1 expression in dorsal root ganglion and spinal cord dorsal horn. Results showed that HPL decreased from day 1 to day 28 after CFA injection, with shortest at day 14. VR1 expression correspondingly increased from day 1 to day 21 with peak at day 14, and returning to the control level at day 28. A shift of VRI expression from small to medium DRG neurons over the observation period was seen. These results suggest that VR1 could play an important role in the early stage, but not the late stage, of CFA inflammatory nociception.

Animals↗

Attenuation of mechanical but not thermal hyperalgesia by electroacupuncture with the involvement of opioids in rat model of chronic inflammatory pain.

Opioid peptides have been proven effective in reducing the sign of hyperalgesia associated with inflammation. Electroacupuncture (EA) produces antinociception via release of endogenous opioid peptides in normal rats. Moreover, intrathecal injection of dynorphin has antinociceptive effect in rats. The present study was designed to examine whether EA has effect on the thermal and mechanical hyperalgesia in rat model of complete Freund's adjuvant (CFA)-induced inflammatory pain. The results are the following: (1) single session of 100Hz EA (0.5-1.0-1.5 mA, 10 min for each intensity) at both Zusanli (ST 36) and Sanyinjiao acupoints (SP 6) significantly increased mechanical withdrawal threshold determined by von Frey filaments but not with thermal withdrawal latency that is determined by hot plate (52 +/- 0.2 degrees C); (2) 100 Hz EA applied twice a week for 4 weeks and showed a significant decrease in the mechanical hyperalgesia at the third and fourth week, with no effect on thermal hyperalgesia; (3) naloxone (20 mg kg(-1)) had the ability to reverse the inhibition of the mechanical hyperalgesia produced by a single session of EA. In conclusion, the present results indicate that a single or repetitive EA could reduce mechanical hyperalgesia, but not thermal hyperalgesia, in CFA-inflammatory pain rats, and the opioid system might be involved in these effects.

Animals↗

Adenovirus-mediated delivery of GDNF ameliorates corticospinal neuronal atrophy and motor function deficits in rats with spinal cord injury.

The aim of the present study was to assess the effect of glial cell line-derived neurotrophic factor (GDNF) delivery mediated by a recombinant adenovirus (AdCMVgdnf or AdCMVlacZ) on the functional recovery and central neuronal atrophy in adult rats with spinal cord injury. Bilateral electrolytic lesions were made in the corticospinal tracts at the T10 vertebral level in a rat model. AdCMVgdnf or AdCMVlacZ was injected at the lesion site immediately after operation. After 2-3 weeks the neurological score and the inclined plane angle were significantly higher and the soma size of corticospinal motoneurons was larger in the AdCMVgdnf group compared with the AdCMVlacZ group. These results demonstrated that adenovirus-mediated delivery of GDNF could prevent the retrograde atrophy of corticospinal motoneurons and improve the motor function in rats with spinal cord injury.

Adenoviridae↗

Evidence from brain imaging with fMRI supporting functional specificity of acupoints in humans.

We tested whether the stimulation of acupoints in the same spinal segments could induce different central responses with functional magnetic resonance imaging (fMRI) study. Stimulation of acupoints ST36/SP6 (Zusanli/Sanyinjiao) or GB34/BL57 (Yanglingquan/Chengshan) both activated primary and secondary somatosensory area, insula, ventral thalamus, parietal Brodmann Area 40, temporal lobe, putamen, and cerebellum, while de-activated amygdala. Nevertheless, ST36/SP6 stimulation specifically activated orbital frontal cortex and de-activated hippocampus. Alternatively, stimulation of GB34/BL57 activated dorsal thalamus and inhibited those of primary motor area and premotor cortex. Thus, stimulation of acupoints in the same spinal segments induced distinct though overlapped cerebral response patterns, which indicated the existence of acupoint specificity.

Adult↗

NMDA receptor in nucleus accumbens is implicated in morphine withdrawal in rats.

The purpose of the present study is to elucidate whether ketamine, a non-competitive antagonist of the NMDA receptor, can suppress the morphine withdrawal syndrome in rats at a dose without affecting motor functions and to identify its site of action in the central nervous system. Rats were made dependent on morphine by multiple injections of morphine hydrochloride for 5 days. They were then given ketamine at the following doses and routes of administration: (a) intraperitoneal (i.p.) injections (2-16 mg/kg), (b) intracerebroventricular (i.c.v.) injections (4-100 microg), and (c) intra-nucleus accumbens (NAc) or intra-amygdalar microinjections (0.4-10 microg). Naloxone HCl (1 mg/kg, i.p.) was administered 3 h after the last ketamine injection to precipitate withdrawal syndrome, which was scored within a period of 30 min. Results showed that some of the precipitated withdrawal signs were dose-dependently suppressed by repeated injections of ketamine at 8 and 16 mg/kg, i.p. or 100 microg, i.c.v. Dose-dependent suppression was observed by repeated microinjections (0.4-10 microg) of ketamine to NAc, but not to amygdala. These results indicate that the NMDA receptor antagonist ketamine has the ability to suppress morphine withdrawal syndrome in experimental settings without motor interference, and NAc could be the critical CNS site mediating such effect.

Amygdala↗

Suppression of neuropathic pain by peripheral electrical stimulation in rats: mu-opioid receptor and NMDA receptor implicated.

Peripheral electrical stimulation (PES) has been utilized to manage chronic pain associated with nerve injury. However, the data on clinical effectiveness are conflicting and the neurophysiological mechanism is not well known. This study was designed to assess whether PES relieved neuropathic pain and its possible mechanisms. The neuropathic pain model was made with lumbar 5th (L5) and 6th (L6) spinal nerve ligations in rats. Nociceptive responses of the rats were assessed by the cold plate test (the number and duration of paw lifts that occurred in 5 min on a 5 +/- 1 degrees C cold plate). PES with a frequency of 2 Hz and at increasing strengths was given for 30 min via stainless-steel needles inserted into standard acupoints on the leg and back, respectively. Immunochemistry was used to examine the immunoreactivity of the NMDA receptor 1 (NR1) subunit in the spinal cord dorsal horn. The results are as follows: (1) PES relieved neuropathic pain and the effect was blocked by 1.0 mg/kg naloxone. (2) The effect of one session of PES lasted up to 12 h. (3) Repetitive PES showed a cumulative effect and no tolerance was observed. (4) There was a significant increase of NR1 immunoreactivity in the superficial laminae of the spinal cord of neuropathic pain rats as compared with naive rats. This increase could be reversed by repetitive 2 Hz PES. These results suggest that PES can relieve neuropathic pain, and that mu-opioid receptors and NMDA receptors are involved in the effect of PES.

Animals↗

Triptolide, a Chinese herbal extract, protects dopaminergic neurons from inflammation-mediated damage through inhibition of microglial activation.

Mounting lines of evidence have suggested that brain inflammation participates in the pathogenesis of Parkinson's disease. Triptolide is one of the major active components of Chinese herb Tripterygium wilfordii Hook F, which possesses potent anti-inflammatory and immunosuppressive properties. We found that triptolide concentration-dependently attenuated the lipopolysaccharide (LPS)-induced decrease in [3H]dopamine uptake and loss of tyrosine hydroxylase-immunoreactive neurons in primary mesencephalic neuron/glia mixed culture. Triptolide also blocked LPS-induced activation of microglia and excessive production of TNFalpha and NO. Our data suggests that triptolide may protect dopaminergic neurons from LPS-induced injury and its efficiency in inhibiting microglia activation may underlie the mechanism.

Analysis of Variance↗

Changes of hypothalamic alpha-MSH and CART peptide expression in diet-induced obese rats.

Two hypothalamic peptides, cocaine and amphetamine-regulated transcript (CART) and alpha-melanocyte-stimulating hormone (alpha-MSH), recognized as anorexigenic neuropeptides to suppress the feeding behavior, were monitored in rats fed with a high-fat (HIF) diet for 14 weeks. While half of the rats developed obesity (diet-induced obese, DIO), some did not (diet resistant, DR). Compared to the DR rats and the control rats (fed with standard chow), DIO rats were accompanied by a markedly higher energy intake and a decrease in the number of neurons carrying alpha-MSH and CART peptide in the arcuate nucleus of the hypothalamus. Failure of hypothalamic anorexigenic peptides CART and alpha-MSH to increase their content in response to HIF diet may play a key role for overly high energy consumption, resulting in obesity.

Animals↗

Electroacupuncture facilitates recovery of male sexual behavior in morphine withdrawal rats.

The effect of electroacupuncture (EA) on the sexual behavior of male rats undergoing morphine withdrawal was studied by measuring various parameters of sexual behavior. In addition, the total serum testosterone (TST) concentrations in male rats at different times of morphine administration and abstinence were measured. Acute and chronic administration of morphine severely inhibited the sexual behavior of the rats and lowered their TST concentrations. TST concentrations recovered to normal within 24 h after the last morphine injection, while sexual behavior remained suppressed for at least 7 days. Electroacupuncture (2/100 Hz alternately) administered once daily for 7 days during morphine withdrawal facilitated the recovery of male sexual behavior and increased TST concentrations to above normal. The effect of EA on sexual behavior may involve both neuronal and hormonal pathways.

Animals↗

Nociceptive responses of anterior cingulate cortical ensembles in behaving rats.

OBJECTIVE: To confirm the role of anterior cingulated cortices (ACC) in the coding of pain affect by exploring the neural ensemble coding pattern within the anterior cingulate cortex in behaving rats with a multichannel recording technique. METHODS: In five adult male Sprague-Dawley rats, two arrays of eight stainless steel microwires were bilaterally implanted into ACC. Noxious radiant heat stimulation was applied to the tail, bilateral fore-paws and hind-paws of freely moving rats. Neuroelectric signals were obtained from the microwires and sent to a multichannel recording device via cables and connectors. The time stamps of neuronal activities were stored on a personal computer for off-line analysis. RESULTS: Noxious heat stimuli evoked predominantly excitatory and sustained neural activity within ACC, reflecting the processing of pain unpleasantness; pain-related anticipatory responses could be seen near the stimulation start, indicating the behavioral preparation for escape; ACC neurons had broad receptive fields by showing quite similar pain-related responses to stimuli on either side of the hind-paw, suggesting that they are not eligible for the localization of a stimulus. CONCLUSION: ACC has played a major role in processing the affective-motivational aspect of pain.

Animals↗

[Transcranial magnetic stimulation (TMS): physiology, psychology, brain mapping and clinical applications].

Non-invasive Transcranial Magnetic Stimulation (TMS) can painlessly induce conductive current to excite cortex. This changes physiological processing in the brain. Varying the parameters of TMS, differential physiologic effects, psychological impacts can be examined. Modulation of sensory perception, suppression or facilitation of cognitive capacity and behavioral performance depicts differential modulatory operation in the brain. TMS could be applied in the research of neurological disease, psychiatric disorders, and pharmacological investigation. Stereotaxic and frameless TMS can improve the anatomy-guided TMS and use for navigation in brain surgery. Finally, the principles derived from acupuncture mechanisms can be integrated into the frequency modulation effects on the brain, shared by TMS.

Brain Mapping↗

[Progress in the basic research on neurobiological mechanisms of cancer pain].

Pain shows the most disruptive influence on the quality of the life of cancer patients. However, the basic neurobiology of cancer pain is poorly understood, as no appropriate animal model of cancer pain is available. New insights into these mechanisms are now arising from femur, calcaneus, humerus model of cancer pain in murine and tibia model in rats. Cancer pain has its unique mechanisms such as osteolysis, peripheral sensitization, central sensitization and nerve entrapping, which are all involved in the development and maintenance of cancer pain. Here we summarized the study progress of cancer pain animal models, neurochemical mechanisms and drugs for treatment of cancer pain from recent literatures.

Afferent Pathways↗

Parallel pain processing in freely moving rats revealed by distributed neuron recording.

The present study was designed to examine the possible differential roles of the medial and lateral pain systems in pain perception. We used a microwire array recording technique to record the pain-evoked neural activity of multiple neurons in freely moving rats. Noxious radiant heat was delivered to either hind-paw in a randomized order. A total of 256 single units were recorded in primary somatosensory cortex (SI), anterior cingulate cortex (ACC), and medial dorsal (MD) and ventral posterior (VP) thalamus during the painful stimulation. The results showed that SI neurons displayed a strong pain-related excitatory response with short duration and significant contralateral bias; VP had very similar functional patterns to that of SI. This suggested that SI, together with VP, participate in the processing of the sensory-discriminative aspect of pain. In contrast, ACC and MD shared common characteristics of moderate and longer-lasting increase of neural activity, bilateral receptive fields without contralateral preference, as well as the anticipatory response at the start of a painful stimulus, corresponding to the specific role of ACC and MD in the affective-motivational aspects of pain. The results provide an initial demonstration of distributed activity patterns within different pain systems in awake and freely moving rats, hence, providing confirmation of the existence of the dual pain pathways.

Action Potentials↗