RESUMO
BACKGROUND: It is known that epinephrine/norepinephrine inhibit acute pain transmission. However, the role of ß-adrenoceptors is not clear. Thus, we analyzed if beta-1 and/or beta-2 adrenoceptors can modulate acute pain transmission by performing in vivo single unit recordings during painful and non-painful peripheral stimulation in rats. METHODS: Longitudinal study in which we analyzed seven groups of male rats Wistar: control group (n = 11): saline (0.9 %); EPI group (n = 8): epinephrine 100 mcg; beta-1 agonist group (n = 8): dobutamine 125 mcg; beta-1-antagonist group (n = 9): metoprolol 100 mcg; beta-2-agonist group (n = 7): clenbuterol 100 mcg; beta-2-antagonist group (n = 8): butoxamine 100 mcg; beta-1-antagonist + EPI group (n = 10): metoprolol 100 mcg + epinephrine 100 mcg. For the statistical analysis we used ANOVA. RESULTS: Epinephrine significantly reduced the basal firing rate (BFR) in 34.1 % (p < 0.05) and also the evoked response by painful stimulation in 56 % (p < 0.05). No change was observed in the evoked response by non-painful stimulation. ANTß1 was the only beta-adrenoceptor acting drug that significantly reduced the evoked response by painful stimulation in 41 % (p < 0.05). None of the other drugs alone affected either the BFR or the evoked response to non-painful or painful stimulation. CONCLUSIONS: It is the first time that a beta-1-adrenoceptor antagonist (metoprolol) probes to be effective in reducing the response to painful stimulation in WDR neurons.
Introducción: la epinefrina/norepinefrina inhibe la transmisión del dolor agudo; empero, no es claro el papel de los receptores beta-adrenérgicos. Por tanto, analizamos si los fármacos de estos receptores modulan la transmisión del dolor agudo mediante registro electrofisiológico unitario extracelular in vivo durante estimulación periférica dolorosa y no dolorosa en ratas. Métodos: estudio longitudinal en el que se cotejaron siete grupos de ratas: control (n = 11): solución salina (0,9 %); EPI (n = 8): 100 mcg epinefrina; agonista beta-1 (n = 8): 125 mcg dobutamina; antagonista beta-1 (n = 9): 100 mcg metoprolol; agonista beta-2 (n = 7): 100 mcg clembuterol; antagonista beta-2 (n = 8): butoxamina 100 mcg; antagonista beta-1 + EPI (n = 10): 100 mcg metoprolol + 100 mcg epinefrina. Se hizo análisis estadístico por medio de ANOVA. Resultados: La epinefrina redujo significativamente la tasa de disparo basal (RDB) en 34.1 % (p < 0.05) y la respuesta evocada por la estimulación dolorosa en 56 % (p < 0.05). No hubo cambios en la respuesta provocada por la falta de estimulación dolorosa. El antagonista beta-1 fue el único fármaco con acción beta-adrenérgica que redujo significativamente la respuesta evocada por la estimulación dolorosa en 41 % (p < 0.05). Conclusión: por primera vez un antagonista de los receptores beta-1-adrenérgicos (metoprolol) prueba ser eficaz en la reducción de la respuesta a la estimulación dolorosa en las neuronas ARD.
Assuntos
Antagonistas de Receptores Adrenérgicos beta 1/uso terapêutico , Metoprolol/uso terapêutico , Dor/tratamento farmacológico , Antagonistas de Receptores Adrenérgicos beta 1/farmacologia , Animais , Fenômenos Eletrofisiológicos/efeitos dos fármacos , Masculino , Metoprolol/farmacologia , Neurônios/efeitos dos fármacos , Neurônios/fisiologia , Estimulação Física , Ratos , Ratos Wistar , Medula EspinalRESUMO
BACKGROUND: Obesity, as an effect of the nutritional transition in developing countries, has become one of México's greatest public health problems. Body image distortion is one of the possible causes of this socially generalized issue. The aim of this study was to obtain three indicators (the representation of the imagined body, the perceived image of the body, and the body mass index -BMI-) to compare them and know the differences between the real image (BMI) and the other two images. METHODS: Inaccuracy of body size estimation was measured through a survey with a ranked scale to determine if the sample (n = 579) had body image distortion, what degree of distortion had, and how body image distortion behaved across age groups from 15 to 69 years old. RESULTS: The age group from 15 to 19 years old was found to be significantly different from all other age groups through a Kruskal-Wallis test. Differences between men and women were found through a Mann-Whitney test. A relation was found between types of body image distortion and the degree of distortion with a multinomial logistic regression model. CONCLUSIONS: Cultural factors could help to explain these findings. If the inaccuracy of body size estimation can be associated to obese and overweight Mexicans in the future, these results will be critical for the analysis of such an epidemic.
Introducción: la obesidad es un efecto de la transición nutricional en varios países y es uno de los problemas de salud pública más graves en México. La distorsión de la imagen corporal es un posible factor importante en este asunto socialmente generalizado. El objetivo fue obtener tres indicadores (la representación del cuerpo imaginado, la imagen percibida del cuerpo y el índice de masa corporal IMC) para compararlos y conocer las diferencias entre la imagen real (IMC) con respecto a las otras dos imágenes. Métodos: la imprecisión al estimar el tamaño corporal se midió por medio de una encuesta con una escala graduada para determinar si la muestra (n = 579) tenía distorsión de la imagen corporal, qué grado de distorsión tenía y cómo se comportaba esta en los diferentes grupos de edad (15-69 años). Resultados: el grupo de edad de 15 a 19 años difirió significativamente de los demás grupos etarios, lo cual quedó demostrado al emplear una prueba Kruskal-Wallis. Las diferencias entre hombres y mujeres fueron encontradas a través de una prueba Mann-Whitney. Asimismo, se encontró una relación entre tipos de distorsión de imagen corporal y grado de distorsión observada por medio de un modelo de regresión logística multinomial. Conclusión: los factores culturales podrían esclarecer estos hallazgos. Si la imprecisión de la estimación del tamaño corporal puede ser asociada al sobrepeso y la obesidad en el futuro, estos resultados serán relevantes para su consecuente análisis.
Assuntos
Imagem Corporal , Obesidade/psicologia , Adolescente , Adulto , Fatores Etários , Idoso , Estudos Transversais , Feminino , Serviços de Saúde , Humanos , Modelos Logísticos , Masculino , México , Pessoa de Meia-Idade , Sobrepeso/psicologia , Fatores Sexuais , Adulto JovemRESUMO
BACKGROUND: Several studies have demonstrated a higher prevalence of depression among medical students as compared to the general population. On the other hand, psychoeducational interventions have proven its efficacy on diminishing depressive symptoms. The aim of this study is to determine the prevalence of depressive symptoms among medical students in La Salle University and the effect that psychoeducation has on it. METHODS: Students between the first and the eighth semester voluntarily answered the Beck Depression Inventory test in an anonymous way from 2006 to 2007. After determining the prevalence of depressive symptoms the psychoeducational program was established and prevalence of depressive symptoms was measured for two more years (2008-2009). RESULTS: A total of 1958 students answered the test during the four years. In the first two years (2006-2007) the 36.29% of the students scored for positive depressive symptoms. The next two years (2008-2009), after the psychoeducation program, the prevalence of depressive symptoms diminishes in a significant manner, only 25.51% of the students have depressive symptoms (p<.0001). LIMITATIONS: Because the test were answered anonymously, there is no way we can give neither specific attention nor follow-up to the students with depression. Also we can't determine the effect of the mental health group treatment among the medical students. CONCLUSIONS: Even though the medical students have risks factors for developing depression, we prove that a psychoeducation program can be an effective alternative therapy for decreasing the prevalence of depressive symptoms among medical students.
Assuntos
Depressão/epidemiologia , Estudantes de Medicina/psicologia , Adulto , Depressão/terapia , Feminino , Humanos , Masculino , México , Prevalência , Psicoterapia , Psicoterapia de GrupoRESUMO
OBJECTIVES: The objectives of the study were to compare personality features according to age and sex cohorts in a community sample of Mexico City using the Temperament and Character Inventory-Revised (TCI-R) and to examine the TCI-R psychometric properties according to age and sex parameters. METHOD: A total of 2076 adults filled out the Spanish version of TCI-R. RESULTS: Younger subjects exhibited higher novelty seeking. Self-directedness and cooperativeness scores increased with age. Harm avoidance and self-transcendence were lower in younger adults when compared with older subjects. Women scored higher than men in harm avoidance and reward dependence. Men between 26 and 45 years old reported higher novelty seeking. Women older than 25 years scored higher in self-transcendence, and those older than 45 years exhibited higher cooperativeness scores. The identified TCI-R structure corresponded to the original one. Internal consistency of the higher-order dimensions was good in all age cohorts, in men and women, and in the total sample (αs >.80). CONCLUSION: Our results give further support to personality specific dominant features in men and women. Differences in age cohorts may be explained by maturity and personal experiences acquired during life. The TCI-R psychometric properties and score distributions by age and sex cohorts may be useful for future studies with clinical samples and for cross-cultural comparison purposes.
Assuntos
Caráter , Inventário de Personalidade , Personalidade , Temperamento , Adolescente , Adulto , Fatores Etários , Análise Fatorial , Feminino , Humanos , Masculino , México , Pessoa de Meia-Idade , Inventário de Personalidade/normas , Psicometria , Fatores Sexuais , Adulto JovemRESUMO
The role of dopamine as a possible central inhibitory mediator of pain processes has been demonstrated. The administration of L-Dopa diminishes pain perception in humans as well as the response to nociceptive stimuli in animals. Also, the intracerebral microinjection of dopamine in inflammatory and neuropathic pain models (formalin test and deafferentation, respectively) reduces nociceptive response. In this sense, the selective activation of dopamine D2 receptors and the blockade of D1 in the insular cortex and spinal cord diminish nociception. Furthermore, the microinjection of dopamine or amantadine (dopamine releaser) in the anterior cingulate cortex (ACC) also reduces chronic nociception. The efficacy of amantadine has been tested in the treatment of neuropathic pain, even when given as a single dose. There is evidence of the role of amantadine as a releaser of dopamine (DA) calcium channel (N type) dependent in the striatum as well as a low affinity non-competitive antagonist of blockade/non-blockade kinetics of the NMDA receptor. This compound has also been described as a DA agonist and an inhibitor of its reuptake. With this background, we decided to test if the effects of systemically given amantadine related to acute nociception, hyperalgesia and neuropathic nociception can be reverted by a dopaminergic blockade (using haloperidol) within the ACC. The experiments were conducted in agreement with the Ethics Committee of the International Association for the Study of Pain and the approval of the Projects Commission of the Instituto Nacional de Psiquiatría Ramón de la Fuente (INPRF). Male Wistar rats (250-300 g) were housed in the INPRF. During the observation period, the animals were maintained in transparent acrylic individual cages with light-dark cycles of 12 X 12 h, with feeding and hydration ad libitum. For all surgical procedures, rats were anaesthetised with halothane 2% mixed with O2 98%. In order to test the dopaminergic effect of amantadine within the ACC in nociception, we used the hyperalgesia model as well as a neuropathic nociception model induced by denervation. In the model of hyperalgesia, carrageenan was injected in the plantar region (50 µl at 1%), followed by a thermonociception test in which paw withdrawal latency was measured. In the neuropathic nociception model, the right sciatic nerve was denervated and chronic nociception was measured as autotomy behaviour. Moreover, in another series of experiments, haloperidol (3 mg/ 200 nl) was microinjected into the ACC before the induction of hyperalgesia and neuropathic nociception. Amantadine was then injected (90 mg/kg i.p.) and the behavioural development was observed in both models. Systemic amantadine was able to reduce both neuropathic nociception and hyperalgesia. Also, the results show, on the one hand, that haloperidol significantly decreases the antinociceptive effect of amantadine measured as paw withdrawal latency. On the other hand, amantadine can reduce nociception when administered systemically and, according to what has been published previously, when administered directly into the ACC. Our results show that amantadine is effective in diminishing hyperalgesia and nociception induced by deafferentation. This suggests that amantadine can be a therapeutic alternative for the treatment and prevention of neuropathic pain such as phantom limb pain or pain due to deafferentation, among others.
Se ha demostrado el papel de la dopamina como posible mediador inhibitorio central de procesos dolorosos. La administración de L-dopa disminuye la percepción de dolor en los seres humanos, así como la respuesta ante estímulos nociceptivos en los animales. Además, la microinyección intracerebral de dopamina en modelos de dolor inflamatorio y neuropático (prueba de formalina y deaferentación) reduce la respuesta nociceptiva. En este sentido, la activación selectiva de los receptores dopaminérgicos D2 y el bloqueo de los receptores D1 en la corteza insular y la médula espinal disminuyen la nocicepción. La microinyección de dopamina o de amantadina (liberador dopaminérgico) en la corteza anterior del cíngulo (CAC) reduce también la nocicepción crónica. Se ha probado la eficacia de la amantadina en el tratamiento del dolor neuropático, incluso cuando se administra en una sola dosis. También se ha demostrado el papel de la amantadina como liberador de dopamina dependiente del canal del calcio (tipo N) en el estriado, así como el de antagonista no competitivo de baja afinidad de cinética de bloqueo y desbloqueo rápido del receptor de NMDA. Este compuesto también se ha descrito como un agonista de dopamina e inhibidor de su recaptura. Con estos antecedentes decidimos probar si los efectos de la amantadina sistémica relacionados con la nocicepción aguda, la hiperalgesia y la nocicepción neuropática, pueden ser revertidos por el bloqueo dopaminérgico mediante la micro inyección de haloperidol en la corteza anterior del cíngulo. Los experimentos se realizaron de acuerdo con las normas del Comité de Ética de la Asociación Internacional para el Estudio del Dolor y con la aprobación de la Comisión de Proyectos del Instituto Nacional de Psiquiatría Ramón de Fuente (INPRF). Se utilizaron ratas Wistar macho (250-300 g) mantenidas en el bioterio del INPRF. Durante el periodo de observación, los animales se mantuvieron en jaulas individuales de acrílico transparente, con ciclos de luz-oscuridad de 12 X 12 h, con alimentación e hidratación ad libitum. Para todos los procedimientos quirúrgicos, las ratas se anestesiaron con halotano al 2%, mezclado con 98% de O2. Para probar el efecto dopaminérgico de la amantadina en la nocicepción en la corteza anterior del cíngulo, utilizamos un modelo de hiperalgesia y un modelo de nocicepción neuropática inducida por denervación. En el modelo de hiperalgesia, se inyectó carragenina en la región plantar (50 µl al 1%), seguida por una prueba de termonocicepción para posteriormente medir la latencia de retiro de la pata. En el modelo de nocicepción neuropática, se denervó el ciático derecho y se midió la nocicepción crónica mediante la conducta de autotomía. Asimismo, en otra serie experimental se microinyectó haloperidol (3mg/200nl) en la CAC antes de la inducción de la hiperalgesia y de la nocicepción neuropática, y posteriormente se inyectó amantadina (90 mg/kg i.p.) y se observó el desarrollo conductual en ambos modelos. La administración sistémica de amantadina logró reducir tanto la nocicepción neuropática como la hiperalgesia. Además, los resultados muestran, por un lado, que el haloperidol disminuye significativamente el efecto antinociceptivo de la amantadina medido como la latencia de retiro de la pata. Por otro, la amantadina puede reducir la nocicepción cuando se administra sistémicamente y, según lo publicado previamente, directamente en la CAC. Nuestros resultados muestran que la amantadina es efectiva en la reducción de la hiperalgesia y la nocicepción por deaferentación. Este hecho sitúa a la amantadina como una alternativa terapéutica para el tratamiento y prevención del dolor neuropático, como el miembro fantasma doloroso o el dolor por deaferentación.
RESUMO
The rostral agranular insular cortex (RAIC) receives dopaminergic projections from the mesolimbic system, which has been involved in the modulation of nociceptive processes. In this study we determined the contribution of dopamine D(1) and D(2) receptors in the RAIC regarding nociception processing in a neuropathic pain model, as well as inflammatory articular nociception measured as pain-induced functional impairment in the rat (PIFIR). Microinjection of vehicle or substances into the RAIC was performed after the induction of nociception. The groups were treated with: a dopamine D(1) receptor antagonist (SCH-23390), a dopamine D(1) receptor agonist (SKF-38393), a dopamine D(2) receptor agonist (TNPA) and a dopamine D(2) receptor antagonist (spiperone). Chronic nociception, induced by denervation, was measured by the autotomy score in which onset and incidence were also determined. The SCH-23390 and TNPA groups showed a decrease in the autotomy score and a delay on the onset as compared to control, whereas the PIFIR groups did not show statistical differences. This work shows the differential role of dopamine receptors within the RAIC in which the activation of D(2) or the blockade of D(1) receptors elicit antinociception.
Assuntos
Córtex Cerebral/fisiologia , Agonistas de Dopamina/farmacologia , Antagonistas de Dopamina/farmacologia , Dopamina/fisiologia , Neuralgia/fisiopatologia , Nociceptores/fisiologia , Dor/fisiopatologia , Receptores de Dopamina D1/fisiologia , Receptores de Dopamina D2/fisiologia , Neuropatia Ciática/fisiopatologia , Automutilação/fisiopatologia , 2,3,4,5-Tetra-Hidro-7,8-Di-Hidroxi-1-Fenil-1H-3-Benzazepina/farmacologia , Vias Aferentes/fisiopatologia , Animais , Apomorfina/análogos & derivados , Apomorfina/farmacologia , Benzazepinas/farmacologia , Doença Crônica , Temperatura Alta/efeitos adversos , Masculino , Microinjeções , Modelos Neurológicos , Ratos , Ratos Wistar , Receptores de Dopamina D1/efeitos dos fármacos , Receptores de Dopamina D2/efeitos dos fármacos , Receptores de N-Metil-D-Aspartato/fisiologia , Espiperona/farmacologiaRESUMO
Taurine is an inhibitory amino-acid which has been proposed as a nociceptive process neuromodulator. The glycine(A) receptor (glyR(A)) has been postulated as a receptor in which taurine exerts its function. Functional image studies have documented the role of the anterior cingulate cortex (ACC) in the affective component of pain. The aim of this study was to investigate the role of taurine as a glycinergic agonist in the ACC using a neuropathic pain model related to autotomy behaviour (AB). In order to test whether glyR(A) is responsible for taurine actions, we microinjected strychnine, a glyR(A) antagonist. We used taurine microinjected into the ACC, followed by a thermonociceptive stimulus and a sciatic denervation. Chronic nociception was measured by the autotomy score, onset and incidence. The administration of taurine 7 days after denervation modifies the temporal course of AB by inhibiting it. Our results showed a decreased autotomy score and incidence in the taurine groups, as well as a delay in the onset. Those experimental groups in which strychnine was microinjected into the ACC, either on its own or before the microinjection of taurine, showed no difference as compared to the control group. When taurine was microinjected prior to strychnine, the group behaved as if only taurine had been administered. Our results evidence a significant neuropathic nociception relief measured as an AB decrease by the microinjection of taurine into the ACC. Besides, the role of the glyR(A) is evidenced by the fact that strychnine antagonises the antinociceptive effect of taurine.
Assuntos
Giro do Cíngulo/fisiologia , Dor/tratamento farmacológico , Dor/etiologia , Doenças do Sistema Nervoso Periférico/complicações , Receptores de Glicina/efeitos dos fármacos , Taurina/uso terapêutico , Animais , Comportamento Animal/fisiologia , Glicinérgicos/administração & dosagem , Glicinérgicos/farmacologia , Masculino , Microinjeções , Dor/psicologia , Medição da Dor/efeitos dos fármacos , Ratos , Ratos Wistar , Receptores de Glicina/antagonistas & inibidores , Estricnina/administração & dosagem , Estricnina/farmacologia , Taurina/administração & dosagemRESUMO
The anterior cingulate cortex (ACC) plays a key role in pain processing. It has been reported that increased activity of glutamatergic projections into the ACC intensifies nociception; whereas dopaminergic projections inhibit it. The aim of this study was to evaluate the role of dopaminergic and NMDA systems of the ACC in the modulation of long-term nociception elicited by sciatic denervation in the rat. Score, onset and incidence of long-term nociception were measured by the autotomy behavior. The effects of a single microinjection into the ACC of different doses of dopamine (100 nM, 100 microM and 100 mM), a NMDA receptor antagonist (MK801 200 nM and 9.34 mM) and amantadine, a dopamine agonist and NMDA receptor antagonist (10, 100 and 1000 microM) were tested on long-term nociception. Dopamine diminished autotomy behavior in an inverse dose-dependent manner, with dopamine 100 nM as most effective concentration. MK801 and amantadine elicited a significant reduction on autotomy score. Prior injections of D1 and D2 receptor antagonists blocked the antinociceptive effects of amantadine on long-term nociceptive behavior. The present study suggests an interaction between dopaminergic and glutamatergic systems within the ACC in the genesis and maintenance of long-term nociception.
Assuntos
Dopamina/fisiologia , Giro do Cíngulo/fisiologia , Nociceptores/fisiologia , Receptores de N-Metil-D-Aspartato/fisiologia , Amantadina/farmacologia , Animais , Maleato de Dizocilpina/farmacologia , Dopamina/farmacologia , Dopaminérgicos/farmacologia , Antagonistas dos Receptores de Dopamina D2 , Antagonistas de Aminoácidos Excitatórios/farmacologia , Masculino , Nociceptores/efeitos dos fármacos , Ratos , Ratos Wistar , Receptores de Dopamina D1/antagonistas & inibidores , Receptores de Dopamina D1/metabolismo , Receptores de Dopamina D2/metabolismo , Receptores de N-Metil-D-Aspartato/antagonistas & inibidoresRESUMO
The research of chronic nociception using whole animals is an approach plagued with methodological drawbacks within the ethical realm, as well as difficulties in the analysis and interpretation of time dependent results. On this work, we propose an experimental model that displays tonic nociception measured as a quantifiable self-injury behaviour (SIB) produced by the inflammation of soft tissue located in the paw of the rat elicited by carrageenan 1% (CAR) infiltration. We established five categories or levels for the analysis of the self-injury behaviour reflecting the intensity of rat nociception triggered by CAR infiltration. In addition, we determine that this model does not induce inescapable pain by noticing no significant differences when measuring weight gain and sexual behaviour. We propose this nociception model as physiologically and ethically appropriate for the study of long-lasting nociception.
Assuntos
Carragenina/efeitos adversos , Mediadores da Inflamação/efeitos adversos , Medição da Dor/métodos , Dor/induzido quimicamente , Comportamento Autodestrutivo/induzido quimicamente , Animais , Peso Corporal/efeitos dos fármacos , Peso Corporal/fisiologia , Doença Crônica , Modelos Animais de Doenças , Pé/inervação , Pé/fisiopatologia , Inflamação/induzido quimicamente , Inflamação/patologia , Inflamação/fisiopatologia , Masculino , Nociceptores/efeitos dos fármacos , Nociceptores/fisiologia , Dor/fisiopatologia , Medição da Dor/ética , Ratos , Ratos Wistar , Reprodutibilidade dos Testes , Comportamento Autodestrutivo/fisiopatologia , Comportamento Sexual Animal/efeitos dos fármacos , Comportamento Sexual Animal/fisiologiaRESUMO
El presente trabajo analiza las recientes hipótesis acerca de la génesis del miembro fantasma (MF). Este trastorno se caracteriza por la sensación que experimenta la mayoría de las personas a las que se les ha amputado un miembro o que han padecido la ablución de un nervio, que consiste en seguir percibiéndolo con un alto grado de realidad. Los primeros estudios acerca de la génesis del fenómeno se sitúan en un debate, es decir, se genera el fantasma en el muñón del miembro amputado o es un constructo del sistema nervioso central. Una de las primeras hipótesis propone que la evocación del MF se genera a partir de descargas ectópicas en el sitio de la lesión neural o neuroma. Las recientes corrientes de pensamiento sitúan a la génesis del MF como el resultado de un alto grado de encefalización, inclusive como parte de un proceso cognoscitivo afectivo con base en una representación corporal localizada en la corteza y en diversos núcleos cerebrales. Una de las teorías propuesta es la de la neuromatriz, la cual establece que hay una red neuronal distribuida en varias áreas del cerebro, que procesaría información paralela a la entrada somatosensorial y generaría una referencia genéticamente determinada del cuerpo. Otra de las hipótesis es la denominada "cambio del mapa en lo concerniente a las sensaciones referidas", la cual sostiene que la génesis del MF se debe a la reorganización cortical rápida y precisa entre los sitios adyacentes a la representación cortical del sitio desaferentado. Nuestro grupo ha generado una hipótesis que consiste en situar al detonador del MF en el sitio de la amputación, y explica su persistencia mediante la activación de un mecanismo fisiológico básico de potenciación temporal y espacial en las áreas cerebrales.