The disabling conditions of chronic low-back pain continue to cost patient, family, and society. The intricate mechanisms which perpetuate this medical condition often consist of both organic and functional factors. This study evaluated personality and psychosocial variables which may control individual responses to facet denervation, a treatment for chronic lumbar distress. The subjects were 47 chronic pain patients whose symptoms conformed to the facet syndrome. Patient responses to the Minnesota Multiphasic Personality Inventory (MMPI) and the Sixteen Personality Factor Questionnaire were reviewed in an effort to predict statistically symptomatic relief. Also, the patients' involvement in litigation and their accuracy in determining their pain level were studied as possible influencing variables. Results show the litigation factor and two scalesof the MMPI to be most useful in predicting patient response from facet denervation treatment.

As projeções OTérgicas do PVN que se projetam para o tronco cerebral são responsáveis por mediar os ajustes da FC e esses efeitos benéficos induzidos pelo TF são abolidos pela desnervação sinoaórtica (DAS). Iremos determinar o efeito do treinamento e da DAS sobre os neurônios OTérgicos do PVN em SHR e WKY. Os ratos foram submetidos DSA ou SHAM e treinados ou mantidos sedentários por três meses. Realizou-se medidas hemodinâmicas basais seguidas de retirada dos cérebros. Nos ratos SHAM o TF determinou um aumento na capacidade física e no ganho do controle reflexo da FC. O TF reduziu a FC de repouso em ambos os grupos, com uma queda na pressão arterial nos SHR. Houve aumento da expressão de mRNA para OT no PVN e na densidade de OT nos neurônios OTérgicos do PVN. A DSA aboliu a expressão do mRNA de OT no PVN e reduziu drasticamente a densidade de OT no PVN de WKY e SHR. A DSA revela o papel fundamental dos barorreceptores em mediar a plasticidade/atividade dos neurônios OTérgicos do PVN como os efeitos benéficos do treinamento sobre o controle cardiovascular. / The OTergic projections from PVN to the dorsal brainstem mediate training-induced HR adjustments and that beneficial effects of training are blocked by sinoaortic denervation (SAD). We sought now to determine the combined effect of training and SAD on PVN OTergic neurons in SHR and WKY. Rats underwent SAD or SHAM surgery and were trained or kept sedentary for 3 months. After hemodynamic measurements at rest, the brains were removed. In SHAM rats, training improved treadmill performance and increased the gain of baroreflex control of HR. Training reduced resting HR in both groups, with a fall in blood pressure only in SHR rats. These changes were accompanied by marked increases in PVN OT mRNA expression and peptide density in PVN OTergic neurons. SAD abolished PVN OT mRNA expression and markedly reduced PVN OT density in WKY and SHR. Training had no effect on HR, PVN OT mRNA, or OT content following SAD. SAD uncovers the pivotal role of barorreceptor in driving both the plasticity and activity of PVN OTergic neurons and the beneficial effects of training on cardiovascular control.

A insuficiência cardíaca (IC) é o estágio final de diversas patologias cardíacas e apresenta alta morbimortalidade. Dentre as causas, estão os efeitos cardiotóxicos em pacientes tratados com doxorrubicina (Dox). A fisiopatologia da IC apresenta aumento da atividade barorreflexa e marcada hiperatividade simpática (HS), estado compensatório à redução do débito cardíaco. Porém, a HS prolongada culmina em alterações deletérias para o sistema cardiovascular (SC) com piora do quadro de sintomas. Atualmente muito se discute sobre o papel dos corpúsculos carotídeos (CC) na fisiopatologia da IC devido ao seu reflexo simpatotônico e a melhora de pacientes portadores de IC após a remoção dos CC. O nosso objetivo foi avaliar a influência do CC na evolução da IC induzida pela DOX. Para tal, 35 ratos Wistar machos foram dispostos em 4 grupos: controle Salina (CSAL; n=7) e Controle Dox (CDOX; n=12), Desnervado Salina (DSAL; n=4) e Desnervado Doxo (DDOX; n=12). A desnervação consistiu na ressecção do nervo sinusal bilateral prévia à administração de Dox; a indução da IC ocorreu através de 6 aplicações de Dox, na dose de 2.5mg/kg, pela via IP a cada 4 dias. Após 15 dias do término da indução, os animais foram avaliados pelo ecocardiograma e canulados para registro de pressão arterial invasiva e avaliação hemodinâmica, autonômica, barorreflexa e quimiorreflexa. A análise dos resultados mostra que o grupo CDOX apresentou redução do peso corporal, da sensibilidade baro e quimiorreflexa, hiperatividade simpática acompanhada de redução vagal, redução da morfologia cardíaca associada à disfunção diastólica e sistólica e redução do peso bruto cardíaco e ventricular. A desnervação não foi capaz de reverter os efeitos deletérios causados pela Dox, inclusive a desnervação acentuou a disfunção diastólica e sistólica induzida pela Dox. Concluiu-se que a desnervação carotídea não foi eficiente em melhorar a insuficiência cardíaca induzida pela Dox no modelo experimental proposto / Heart failure (HF) is the final stage of several cardiac pathologies and results in high morbimortality. Among the causes, we can mention the cardiotoxic effects in patients treated with doxorubicin (Dox). The pathophysiology of HF has increased baroreflex activity and marked sympathetic hyperactivity (HS), a compensatory state to the reduction of cardiac output. However, prolonged HS results in worsening of the symptoms. Currently, the role of carotid corpuscles (CC) in the pathophysiology of HF is discussed due improvement of sympathetic reflex presents in patients with HF after CC removal. The objective of this study was to evaluate the influence of CC on the evolution of HF induced by DOX for this method 35 Male Wistar rats arranged in 4 groups: Salina control (CSAL; n = 7) and Dox Control (CDOX; n = 12) Salina Denerved (DSAL; n = 4) and Dox Denerved (DDOX; n = 12). A denervation consisted of bilateral sinus nerve resection prior to Dox administration, induction of HF through 6 Dox applications at a dose of 2.5mg / kg, via IP every 4 days. After 15 days of the end of the induction, the animals were evaluated by echocardiogram and cannulated to record invasive blood pressure and hemodynamic, autonomic, baroreflex and chemorreflex evaluation. Our experiment demonstrated that the CDOX group had reduction of body weight, baro and chemoreflex sensitivity, sympathetic hyperactivity accompanied by vagal reduction, reduction of cardiac morphology associated with diastolic and systolic dysfunction and reduction of gross cardiac and ventricular weight. The denervation is not able to reverse the deleterious effects caused by Dox, including denervation accentuated by Dox-induced diastolic and systolic dysfunction. Based on our results on a carotid denervation it was not effective in improving heart failure induced by Dox

A lesão nervosa periférica acarreta atrofia do músculo esquelético por ele inervado, levando a perda de função. E estimulação elétrica tem sido usada na prática clínica como recurso terapêutico complementar, embora existam controvérsias na literatura a respeito da sua eficácia na manutenção do trofismo muscular e dos seus efeitos no tecido conjuntivo associado ao tecido muscular. Assim sendo, este trabalho avaliou os efeitos da estimulação elétrica do músculo tibial anterior em um modelo experimental de axonotmese leve ou severa do nervo ciático de ratos. Após a lesão, um grupo de animais foi tratado com estimulação elétrica (3 vezes por semana) com parâmetros obtidos por eletrodiagnóstico, enquanto que outro grupo de animais lesados constituíram o grupo controle. Foram analisados parâmetros biomecânicos (tensão, rigidez e deformação relativa), parâmetros do eletrodiagnóstico e parâmetros histológicos (volume absoluto do músculo, volume absoluto de tecido muscular propriamente dito, volume absoluto do colágeno fibrilar e volume médio do miócito). Os resultados mostram que a estimulação elétrica promove um aumento da tensão e da rigidez nos dois tempos experimentais; em relação ao eletrodiagnóstico, os animais que receberam estimulação elétrica apresentaram valores de reobase, cronaxia, acomodação e coeficiente de acomodação significativamente diferentes dos animais não tratados, com valores que tendem à normalidade. Os parâmetros histológicos mostram que: 1) há uma diminuição do volume absoluto muscular e do tecido muscular nos animais lesados tanto nos animais controles como nos tratados, em relação aos não-lesados; 2) há um aumento progressivo do colágeno fibrilar ao longo do tempo tanto nos tratados como nos controles; nos animais tratados a quantidade de fibras de colágeno aos 8 dias é maior quando comparada aos controles, porém aos 30 dias a quantidade de colágeno tecidual é menor nos animais tratados se aproximando mais aos valores encontrados no grupo não-lesado; 3) para lesões severas a estimulação elétrica é capaz de prevenir parcialmente a atrofia da célula, uma vez nestes animais os valores de diâmetro do miócito foi maior nos animais tratados que nos controles. Assim sendo, os dados obtidos sugerem que a estimulação elétrica tem um efeito modulador na deposição do colágeno fibrilar e no trofismo muscular, principalmente nas lesões severas. Os resultados dos testes biomecânicos refletem os achados estruturais. Além disso, os resultados obtidos sugerem que a estimulação elétrica pode atuar positivamente na regeneração neural, pois os parâmetros do eletrodiagnóstico são próximos aqueles de músculos com inervação íntegra. / Peripheral nerve injury results in atrophy of skeletal muscles innervated by it, leading to loss of function. Electrical stimulation has been used in clinical practice as a therapeutic supplement, although there is controversy in the literature regarding its effectiveness in maintaining muscle mass and its effects on the connective tissue associated with the muscle. Therefore, this study evaluated the effects of electrical stimulation of the tibialis anterior muscle in an experimental model of mild or severe axonotmesis of the sciatic nerve of rats for 8 or 30 days. After injury, a group of animals was treated with electrical stimulation (3 times per week) and parameters being obtained by electrodiagnostic, while another group of injured animals was used as controls. We analyzed the biomechanical parameters (tension, stiffness and relative deformation), electrodiagnostic parameters and histological parameters (absolute volume of muscle, the absolute volume of muscle tissue proper, the absolute volume of the fibrillar collagen and average volume of myocytes). The results show that electrical stimulation promotes an increase in tension and stiffness in both experimental times. In relation to electrodiagnostic, animals receiving electrical stimulation showed values of rheobase, chronaxie, accommodation and accommodation coefficient significantly different from untreated animals, with values that tend to normality. The histological parameters show that: 1) there is a decrease in the absolute volume of muscle tissue and muscle proper in the injured animals both in controls and in treated animals, compared to non-injured, 2) there is a progressive increase in fibrillar collagen over time in both treated and controls, in treated animals collagen deposition at 8 days is higher compared to controls, but at 30 days the amount of collagen tissue is lower and more similar to the values found in the non-injured; 3) for severe injuries electrical stimulation is able to partially prevent the atrophy of cells, since higher values of diameter of myocytes was found in treated animals in comparison to controls. Therefore, the data suggest that electrical stimulation has a modulating effect on deposition of fibrillar collagen which can regulate the muscle mass, especially in severe injuries, as evidenced by the results of the biomechanical tests. Moreover, the results suggest that electrical stimulation can play a positive role in neural regeneration, because the electrodiagnostic parameters are similar to those of muscles with intact innervation

Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denervation blocks lipid mobilization; thus, rostral sites in the neuroaxis connected to WAT via the SNS may promote WAT lipid mobilization. The hypothalamic paraventricular nucleus (PVN) may play a role via its descending projections to the intermediolateral horn of the spinal cord. Therefore, the consequences of PVN lesions (PVNx) on WAT mobilization or accumulation were tested. PVNx resulted in increased lipid accumulation, indicated by increases in retroperitoneal (RWAT) , epididymal (EWAT) , and inguinal WAT (IWAT) pad masses, in fed hamsters, but PVNx did not block fasting (56 h)-induced lipid mobilization. Because adrenal medullary catecholamines, especially epinephrine, also play a minor role in lipid mobilization, we tested the contribution of catecholamine release on lipid mobilization through adrenal demedullation (ADMEDx), with and without PVNx, and found fastinginduced lipid mobilization was not blocked. There was, however, a suggestion that distal denervation of IWAT, with and without ADMEDx, partially blocked lipid mobilization. In addition, evidence suggests SNS also may be an important controller of fat cell proliferation. Surgical denervation of WAT triggers increases in fat cell number (FCN), but have not determined if this FCN increase is due to preadipocyte proliferation or differentiation of preadipocytes into mature fat cells. We also have not demonstrated what role sensory innervation may have in regulating white adipocyte proliferation. Therefore, the role of WAT sympathetic or sensory innervation on adipocyte proliferation was tested. The SNS but not sensory denervation triggered bona fide proliferation as indicated by bromodeoxyuridine plus AD3, a specific adipocyte membrane protein, colabeling. These and previous data suggest that the SNS plays a role in regulating adiposity.

As projeções OTérgicas do PVN que se projetam para o tronco cerebral são responsáveis por mediar os ajustes da FC e esses efeitos benéficos induzidos pelo TF são abolidos pela desnervação sinoaórtica (DAS). Iremos determinar o efeito do treinamento e da DAS sobre os neurônios OTérgicos do PVN em SHR e WKY. Os ratos foram submetidos DSA ou SHAM e treinados ou mantidos sedentários por três meses. Realizou-se medidas hemodinâmicas basais seguidas de retirada dos cérebros. Nos ratos SHAM o TF determinou um aumento na capacidade física e no ganho do controle reflexo da FC. O TF reduziu a FC de repouso em ambos os grupos, com uma queda na pressão arterial nos SHR. Houve aumento da expressão de mRNA para OT no PVN e na densidade de OT nos neurônios OTérgicos do PVN. A DSA aboliu a expressão do mRNA de OT no PVN e reduziu drasticamente a densidade de OT no PVN de WKY e SHR. A DSA revela o papel fundamental dos barorreceptores em mediar a plasticidade/atividade dos neurônios OTérgicos do PVN como os efeitos benéficos do treinamento sobre o controle cardiovascular. / The OTergic projections from PVN to the dorsal brainstem mediate training-induced HR adjustments and that beneficial effects of training are blocked by sinoaortic denervation (SAD). We sought now to determine the combined effect of training and SAD on PVN OTergic neurons in SHR and WKY. Rats underwent SAD or SHAM surgery and were trained or kept sedentary for 3 months. After hemodynamic measurements at rest, the brains were removed. In SHAM rats, training improved treadmill performance and increased the gain of baroreflex control of HR. Training reduced resting HR in both groups, with a fall in blood pressure only in SHR rats. These changes were accompanied by marked increases in PVN OT mRNA expression and peptide density in PVN OTergic neurons. SAD abolished PVN OT mRNA expression and markedly reduced PVN OT density in WKY and SHR. Training had no effect on HR, PVN OT mRNA, or OT content following SAD. SAD uncovers the pivotal role of barorreceptor in driving both the plasticity and activity of PVN OTergic neurons and the beneficial effects of training on cardiovascular control.

A insuficiência cardíaca (IC) é o estágio final de diversas patologias cardíacas e apresenta alta morbimortalidade. Dentre as causas, estão os efeitos cardiotóxicos em pacientes tratados com doxorrubicina (Dox). A fisiopatologia da IC apresenta aumento da atividade barorreflexa e marcada hiperatividade simpática (HS), estado compensatório à redução do débito cardíaco. Porém, a HS prolongada culmina em alterações deletérias para o sistema cardiovascular (SC) com piora do quadro de sintomas. Atualmente muito se discute sobre o papel dos corpúsculos carotídeos (CC) na fisiopatologia da IC devido ao seu reflexo simpatotônico e a melhora de pacientes portadores de IC após a remoção dos CC. O nosso objetivo foi avaliar a influência do CC na evolução da IC induzida pela DOX. Para tal, 35 ratos Wistar machos foram dispostos em 4 grupos: controle Salina (CSAL; n=7) e Controle Dox (CDOX; n=12), Desnervado Salina (DSAL; n=4) e Desnervado Doxo (DDOX; n=12). A desnervação consistiu na ressecção do nervo sinusal bilateral prévia à administração de Dox; a indução da IC ocorreu através de 6 aplicações de Dox, na dose de 2.5mg/kg, pela via IP a cada 4 dias. Após 15 dias do término da indução, os animais foram avaliados pelo ecocardiograma e canulados para registro de pressão arterial invasiva e avaliação hemodinâmica, autonômica, barorreflexa e quimiorreflexa. A análise dos resultados mostra que o grupo CDOX apresentou redução do peso corporal, da sensibilidade baro e quimiorreflexa, hiperatividade simpática acompanhada de redução vagal, redução da morfologia cardíaca associada à disfunção diastólica e sistólica e redução do peso bruto cardíaco e ventricular. A desnervação não foi capaz de reverter os efeitos deletérios causados pela Dox, inclusive a desnervação acentuou a disfunção diastólica e sistólica induzida pela Dox. Concluiu-se que a desnervação carotídea não foi eficiente em melhorar a insuficiência cardíaca induzida pela Dox no modelo experimental proposto / Heart failure (HF) is the final stage of several cardiac pathologies and results in high morbimortality. Among the causes, we can mention the cardiotoxic effects in patients treated with doxorubicin (Dox). The pathophysiology of HF has increased baroreflex activity and marked sympathetic hyperactivity (HS), a compensatory state to the reduction of cardiac output. However, prolonged HS results in worsening of the symptoms. Currently, the role of carotid corpuscles (CC) in the pathophysiology of HF is discussed due improvement of sympathetic reflex presents in patients with HF after CC removal. The objective of this study was to evaluate the influence of CC on the evolution of HF induced by DOX for this method 35 Male Wistar rats arranged in 4 groups: Salina control (CSAL; n = 7) and Dox Control (CDOX; n = 12) Salina Denerved (DSAL; n = 4) and Dox Denerved (DDOX; n = 12). A denervation consisted of bilateral sinus nerve resection prior to Dox administration, induction of HF through 6 Dox applications at a dose of 2.5mg / kg, via IP every 4 days. After 15 days of the end of the induction, the animals were evaluated by echocardiogram and cannulated to record invasive blood pressure and hemodynamic, autonomic, baroreflex and chemorreflex evaluation. Our experiment demonstrated that the CDOX group had reduction of body weight, baro and chemoreflex sensitivity, sympathetic hyperactivity accompanied by vagal reduction, reduction of cardiac morphology associated with diastolic and systolic dysfunction and reduction of gross cardiac and ventricular weight. The denervation is not able to reverse the deleterious effects caused by Dox, including denervation accentuated by Dox-induced diastolic and systolic dysfunction. Based on our results on a carotid denervation it was not effective in improving heart failure induced by Dox

A lesão nervosa periférica acarreta atrofia do músculo esquelético por ele inervado, levando a perda de função. E estimulação elétrica tem sido usada na prática clínica como recurso terapêutico complementar, embora existam controvérsias na literatura a respeito da sua eficácia na manutenção do trofismo muscular e dos seus efeitos no tecido conjuntivo associado ao tecido muscular. Assim sendo, este trabalho avaliou os efeitos da estimulação elétrica do músculo tibial anterior em um modelo experimental de axonotmese leve ou severa do nervo ciático de ratos. Após a lesão, um grupo de animais foi tratado com estimulação elétrica (3 vezes por semana) com parâmetros obtidos por eletrodiagnóstico, enquanto que outro grupo de animais lesados constituíram o grupo controle. Foram analisados parâmetros biomecânicos (tensão, rigidez e deformação relativa), parâmetros do eletrodiagnóstico e parâmetros histológicos (volume absoluto do músculo, volume absoluto de tecido muscular propriamente dito, volume absoluto do colágeno fibrilar e volume médio do miócito). Os resultados mostram que a estimulação elétrica promove um aumento da tensão e da rigidez nos dois tempos experimentais; em relação ao eletrodiagnóstico, os animais que receberam estimulação elétrica apresentaram valores de reobase, cronaxia, acomodação e coeficiente de acomodação significativamente diferentes dos animais não tratados, com valores que tendem à normalidade. Os parâmetros histológicos mostram que: 1) há uma diminuição do volume absoluto muscular e do tecido muscular nos animais lesados tanto nos animais controles como nos tratados, em relação aos não-lesados; 2) há um aumento progressivo do colágeno fibrilar ao longo do tempo tanto nos tratados como nos controles; nos animais tratados a quantidade de fibras de colágeno aos 8 dias é maior quando comparada aos controles, porém aos 30 dias a quantidade de colágeno tecidual é menor nos animais tratados se aproximando mais aos valores encontrados no grupo não-lesado; 3) para lesões severas a estimulação elétrica é capaz de prevenir parcialmente a atrofia da célula, uma vez nestes animais os valores de diâmetro do miócito foi maior nos animais tratados que nos controles. Assim sendo, os dados obtidos sugerem que a estimulação elétrica tem um efeito modulador na deposição do colágeno fibrilar e no trofismo muscular, principalmente nas lesões severas. Os resultados dos testes biomecânicos refletem os achados estruturais. Além disso, os resultados obtidos sugerem que a estimulação elétrica pode atuar positivamente na regeneração neural, pois os parâmetros do eletrodiagnóstico são próximos aqueles de músculos com inervação íntegra. / Peripheral nerve injury results in atrophy of skeletal muscles innervated by it, leading to loss of function. Electrical stimulation has been used in clinical practice as a therapeutic supplement, although there is controversy in the literature regarding its effectiveness in maintaining muscle mass and its effects on the connective tissue associated with the muscle. Therefore, this study evaluated the effects of electrical stimulation of the tibialis anterior muscle in an experimental model of mild or severe axonotmesis of the sciatic nerve of rats for 8 or 30 days. After injury, a group of animals was treated with electrical stimulation (3 times per week) and parameters being obtained by electrodiagnostic, while another group of injured animals was used as controls. We analyzed the biomechanical parameters (tension, stiffness and relative deformation), electrodiagnostic parameters and histological parameters (absolute volume of muscle, the absolute volume of muscle tissue proper, the absolute volume of the fibrillar collagen and average volume of myocytes). The results show that electrical stimulation promotes an increase in tension and stiffness in both experimental times. In relation to electrodiagnostic, animals receiving electrical stimulation showed values of rheobase, chronaxie, accommodation and accommodation coefficient significantly different from untreated animals, with values that tend to normality. The histological parameters show that: 1) there is a decrease in the absolute volume of muscle tissue and muscle proper in the injured animals both in controls and in treated animals, compared to non-injured, 2) there is a progressive increase in fibrillar collagen over time in both treated and controls, in treated animals collagen deposition at 8 days is higher compared to controls, but at 30 days the amount of collagen tissue is lower and more similar to the values found in the non-injured; 3) for severe injuries electrical stimulation is able to partially prevent the atrophy of cells, since higher values of diameter of myocytes was found in treated animals in comparison to controls. Therefore, the data suggest that electrical stimulation has a modulating effect on deposition of fibrillar collagen which can regulate the muscle mass, especially in severe injuries, as evidenced by the results of the biomechanical tests. Moreover, the results suggest that electrical stimulation can play a positive role in neural regeneration, because the electrodiagnostic parameters are similar to those of muscles with intact innervation

Malignant ventricular arrhythmias are a common cause of sudden cardiac death. Moderate therapeutic hypothermia (MTH) is routinely used in post-resuscitation care for anticipated neuroprotective effects. However, the safety of MTH in terms of the electrical stability of the heart has not been satisfactorily proved yet. Also, the increased sympathetic tone in patients with heart failure contributes to a higher incidence of malignant ventricular arrhythmias. The aim of this work was to verify the safety of MTH as regards the inducibility of ventricular fibrillation (VF) in the pig biomodel, especially in relation to spontaneous changes in the kalemia and QT interval. Furthermore, we assumed that renal denervation (RDN) could reduce the inducibility of VF. In the first part of the thesis, the extracorporeal cooling was introduced in fully anesthetized swine (n = 6) to provide MTH. Inducibility of VF was studied by programmed ventricular stimulation (8 basic stimuli with up to 4 extrastimuli) three times in each biomodel under the following conditions: during normothermia (NT), after reaching the core temperature 32 řC (HT) and after another 60 minutes of stable hypothermia (HT60). VF inducibility, effective ventricular refractory period (ERP), QTc interval, and potassium plasma level were measured. In...

To determine if greater amounts of hydroxyl radical (·OH) are formed by dopamine (DA) denervation and treatment with L-dihydroxyphenylalanine (L-DOPA), the neostriatum was DA denervated (99% reduction in DA content) by 6-hydroxydopamine treatment (134μg icv, desipramine pretreatment) of neonatal rats. At 10 weeks the peripherally restricted dopa decarboxylase inhibitor carbidopa (12.5mg/kg i.p.) was administered 30min before vehicle, L-DOPA (60mg/kg i.p.), or the known generator of reactive oxygen species, 6-hydroxydopa (6-OHDOPA) (60mg/ kg i.p.); and this was followed 30min later (and 15 min before termination) by the spin trap, salicylic acid (8 μmoles icv). By means of a high performance liquid chromatographic method with electrochemical detection, we found a 4-fold increase in the non-enzymatically formed spin trap product, 2,3-dihydroxybenzoic acid (2,3-DHBA), with neither L-DOPA nor 6-OHDOPA having an effect on 2,3-DHBA content of the neostriatum. Basal content of 2,5-DHBA, the enzymatically formed spin trap product, was 4-fold higher vs. 2,3-DHBA in the neostriatum of untreated rats, while L-DOPA and 6-OHDOPA each reduced formation of 2,5-DHBA. We conclude that DA innervation normally suppresses ·OH formation, and that the antiparkinsonian drug L-DOPA has no effect (2,3-DHBA) or slightly reduces (2,5-DHBA) ·OH formation in the neostriatum, probably by virtue of its bathing the system of newly formed ·OH.