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1.
J Physiol Sci ; 71(1): 6, 2021 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-33546583

RESUMO

Our previous research has shown that galanin plays an antinociceptive effect via binding to galanin receptors (GalRs) in nucleus accumbens (NAc). This study focused on the involvement of GalR2 in galanin-induced antinociceptive effect in NAc of neuropathic pain rats. The chronic constriction injury of sciatic nerve (CCI) was used to mimic neuropathic pain model. The hind paw withdrawal latency (HWL) to thermal stimulation and hind paw withdrawal threshold (HWT) to mechanical stimulation were measured as the indicators of pain threshold. The results showed that 14 and 28 days after CCI, the expression of GalR2 was up-regulated in bilateral NAc of rats, and intra-NAc injection of GalR2 antagonist M871 reversed galanin-induced increases in HWL and HWT of CCI rats. Furthermore, intra-NAc injection of GalR2 agonist M1145 induced increases in HWL and HWT at day 14 and day 28 after CCI, which could also be reversed by M871. Finally, we found that M1145-induced antinociceptive effect in NAc of CCI rats was stronger than that in intact rats. These results imply that the GalR2 is activated in the NAc from day 14 to day 28 after CCI and GalR2 is involved in the galanin-induced antinociceptive effect in NAc of CCI rats.


Assuntos
Galanina/análogos & derivados , Neuralgia/terapia , Núcleo Accumbens/metabolismo , Peptídeos/farmacologia , Receptor Tipo 2 de Galanina/metabolismo , Animais , Galanina/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Masculino , Ratos , Ratos Sprague-Dawley , Receptor Tipo 2 de Galanina/genética , Neuropatia Ciática
2.
Adv Physiol Educ ; 43(3): 345-349, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-31305152

RESUMO

A small private online course (SPOC) supports blended learning on a small scale, enabling students to have a more comprehensive and deeper learning experience. It also provides instructors with a flexible and feasible model to better understand the students' learning needs and to supervise students' learning behaviors. In this study, we adopted SPOC flipped classroom blended teaching in the physiology course for clinical undergraduate students of Kunming Medical University. Compared with the control group [lecture-based learning (LBL)], the SPOC flipped classroom method significantly increased the scores of students in the preclass test (65.13 ± 12.45 vs. 53.46 ± 8.09, SPOC vs. LBL) and postclass test (80.43 ± 14.29 vs. 69.01 ± 12.81, SPOC vs. LBL), which is induced by students' increased interest in self-learning. More importantly, the significant difference between the preclass scores of the two groups suggested that the video lecture-based preview is more effective than the textbook-based preview. The study indicated that the SPOC flipped classroom was effective in enhancing the examination scores of students, reflecting an improved learning efficiency and a deeper understanding of the knowledge. In summary, the flipped classroom based on SPOC improves learning outcomes compared with LBL and has a wide application in the learning of basic medical courses.


Assuntos
Currículo , Educação a Distância/métodos , Fisiologia/educação , Aprendizagem Baseada em Problemas/métodos , Estudantes de Medicina/psicologia , Avaliação Educacional/métodos , Humanos , Programas de Autoavaliação/métodos
3.
Neurosci Lett ; 706: 93-98, 2019 07 27.
Artigo em Inglês | MEDLINE | ID: mdl-31085289

RESUMO

Galanin and galanin receptors (GalRs) play important roles in the transmission and modulation of nociceptive information. Our previous research has shown that the expression of GalR1 is upregulated and that GalR1 activation in the nucleus accumbens (NAc) of rats with neuropathic pain has an antinociceptive effect. However, the antinociceptive effect of NAc galanin in neuralgia remains unclear. The present study aimed to explore the antinociceptive effect induced by galanin in rats with neuropathic pain and the underlying mechanism. The results showed that the intra-NAc injection of galanin induced a dose-dependent increase in hindpaw withdrawal latency (HWL) to noxious thermal and mechanical stimulation in mononeuropathic rats and that this effect was stronger than that in intact rats. The intra-NAc injection of the non-selective GalR antagonist galantide reduced HWL in the rats with neuropathic pain, but there was no influence of galantide on HWL in intact rats. Moreover, galanin expression in the NAc was upregulated after sciatic nerve ligation. All of these results demonstrate that galanin plays a role in antinociception via binding to GalRs in the NAc of rats and that endogenous galanin is involved in the antinociception after peripheral nerve injury.


Assuntos
Galanina/farmacologia , Neuralgia/tratamento farmacológico , Nociceptividade/efeitos dos fármacos , Núcleo Accumbens/efeitos dos fármacos , Receptores de Galanina/metabolismo , Animais , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Galanina/uso terapêutico , Masculino , Neuralgia/metabolismo , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Núcleo Accumbens/metabolismo , Medição da Dor , Estimulação Física , Ratos , Ratos Sprague-Dawley
4.
J Neurosci Res ; 93(10): 1542-51, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26104264

RESUMO

It has been reported that galanin and its receptors might be involved in the modulation and transmission of nociception in the central nervous system. Our previous research has also demonstrated that galanin induces antinociception in the nucleus accumbens (NAc) of intact rats. However, the interaction between galanin and its receptors in the NAc and the underlying mechanism of suppressing pain transmission remain unclear. The present study seeks to determine the antinociception induced by galanin receptor (GalR)-1 stimulation in the NAc of rats with neuropathic pain. The left sciatic nerve of rats was ligated to mimic a neuropathic pain model. Western blots showed that the expression of GalR1 was significantly upregulated in the NAc of rats with neuropathic pain. Intra-NAc injection of GalR1 agonist M617 induced a dose-dependent increase in hindpaw withdrawal latency (HWL) to noxious thermal and mechanical stimulations in rats with neuropathic pain. Also, the effect of M617 was attenuated by M35, a GalR1/2 antagonist; at the same time, M35 reduced the galanin-induced antinociception, suggesting that GalR1 mediates antinociception induced by galanin in the NAc of rats with neuropathic pain. Furthermore, we found that M617-induced antinociception in rats with neuropathic pain was stronger than the antinociception in intact rats. We also found that injections of M617 and galanin each induced significant increases in HWL, but the galanin-induced antinociception was stronger than that of M617. All these results suggest that GalR1 plays an important role in antinociception and that other GalRs also are involved in pain modulation induced by galanin in the NAc of rats with neuropathic pain.


Assuntos
Analgésicos/uso terapêutico , Núcleo Accumbens/metabolismo , Receptor Tipo 1 de Galanina/metabolismo , Ciática/patologia , Analgésicos/farmacologia , Análise de Variância , Animais , Bradicinina/análogos & derivados , Bradicinina/farmacologia , Bradicinina/uso terapêutico , Modelos Animais de Doenças , Lateralidade Funcional , Galanina/farmacologia , Galanina/uso terapêutico , Regulação da Expressão Gênica/efeitos dos fármacos , Regulação da Expressão Gênica/genética , Masculino , Núcleo Accumbens/efeitos dos fármacos , Medição da Dor/efeitos dos fármacos , Medição da Dor/métodos , Fragmentos de Peptídeos/farmacologia , Fragmentos de Peptídeos/uso terapêutico , Ratos , Ratos Sprague-Dawley , Receptor Tipo 1 de Galanina/genética , Ciática/tratamento farmacológico
5.
Neurosci Res ; 97: 20-5, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-25819845

RESUMO

This study tested the hypothesis that antinociceptive effects of galanin and its receptors in nucleus accumbens (NAc) of rats with inflammatory pain provoked by subcutaneous injection of 0.1 ml of 2% carrageenin into the sole of the rat's left hindpaw. The hindpaw withdrawal latencies (HWLs) in response to thermal and mechanical stimulation significantly decreased in bilateral hindpaws at 3 and 4 hour after a subcutaneous injection of carrageenin. However intra-NAc injection of 2 and 3 nmol, but not 1 nmol of galanin markedly induced an increase in the HWLs in a dose-dependent way. Western blot also showed, that the expression of galanin receptor 1 (GalR1) and galanin receptor 2 (GalR2) were significantly upregulated in NAc at 3 hour after a subcutaneous injection of carrageenin. In addition, the rats were intra-NAc injected galanin, 5 min later following by intra-NAc injection of galanin receptor antagonist galantide, the galanin-induce antinociceptive effects were suppressed by galantide. The results demonstrated that galanin and its receptors might be involved in antinociception in the NAc of rats with inflammatory pain.


Assuntos
Galanina/fisiologia , Nociceptividade/fisiologia , Núcleo Accumbens/fisiopatologia , Limiar da Dor/fisiologia , Receptores de Galanina/fisiologia , Animais , Carragenina , Galanina/farmacologia , Inflamação/induzido quimicamente , Inflamação/complicações , Masculino , Nociceptividade/efeitos dos fármacos , Núcleo Accumbens/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores de Galanina/metabolismo
6.
Neurosci Lett ; 526(1): 45-8, 2012 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-22884928

RESUMO

The present study was performed to explore the antinociceptive effects of M617, a selective galanin receptor 1 agonist, in the central nucleus of amygdala (CeA) of rats. Intra-CeA injection of 0.1 nmol, 0.5 nmol and 1 nmol of M617 induced dose-dependent increases in hindpaw withdrawal latencies (HWLs) to noxious thermal and mechanical stimulations in rats. Furthermore, rats received intra-CeA administration of M617 and galanin. The HWL to noxious thermal and mechanical stimulations increased markedly, and there were no significant differences in HWLs of rats received intra-CeA administration of M617 and galanin. The results demonstrated that intra-CeA injection of M617 induced significant antinociceptive effects in CeA of rats, indicating that galanin receptor 1 may be involved in M617-induced antinociception in the CeA of rats.


Assuntos
Tonsila do Cerebelo/efeitos dos fármacos , Analgésicos/farmacologia , Bradicinina/análogos & derivados , Galanina/farmacologia , Dor/tratamento farmacológico , Fragmentos de Peptídeos/farmacologia , Receptor Tipo 1 de Galanina/agonistas , Tonsila do Cerebelo/fisiopatologia , Analgésicos/uso terapêutico , Animais , Bradicinina/farmacologia , Bradicinina/uso terapêutico , Galanina/uso terapêutico , Temperatura Alta , Injeções , Masculino , Dor/fisiopatologia , Medição da Dor , Fragmentos de Peptídeos/uso terapêutico , Estimulação Física , Ratos , Ratos Sprague-Dawley , Tato
7.
Neurosci Lett ; 520(1): 43-6, 2012 Jun 27.
Artigo em Inglês | MEDLINE | ID: mdl-22595465

RESUMO

It has been demonstrated that galanin plays important roles in the modulation of nociceptive information in rats. The present study is performed to investigate the regulating role of galanin in nociception in the nucleus accumbens (NAc) of rats. Intra-NAc administration of galanin induces dose-dependent increases in the hindpaw withdrawal latency (HWL) to noxious thermal and mechanical stimulation in rats. Furthermore, the galanin-induced antinociceptive effects are blocked by following intra-NAc injection of the galanin receptor antagonist galantide. The results demonstrate that galanin induces antinociceptive effects in the NAc of rats, and galanin receptors are involved in the galanin-induced antinociception effects.


Assuntos
Galanina/fisiologia , Núcleo Accumbens/fisiopatologia , Dor/fisiopatologia , Analgésicos/farmacologia , Animais , Galanina/análogos & derivados , Galanina/farmacologia , Temperatura Alta , Injeções Intraventriculares , Masculino , Núcleo Accumbens/efeitos dos fármacos , Dor/metabolismo , Medição da Dor , Estimulação Física , Ratos , Ratos Sprague-Dawley , Tempo de Reação , Receptores de Galanina/antagonistas & inibidores , Substância P/análogos & derivados , Substância P/farmacologia
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