Foi realizado estudo experimental com ratos Wistar Albinos, com o objetivo de avaliar diferentes modelos de estudo da lesão da medula espinhal. Os controles foram formados pelos grupos Anestesia, Divulsionamento dos tecidos moles pré-vertebrais e Laminectomia. Os grupos para estudo da lesão da medula espinhal foram formados por animais nos quais o segmento vertebral localizado entre T10 e L1 foi submetido à secção total da medula espinhal, secção parcial (hemissecção), secção total precedida da aplicação local de anestésico e compressão vertebral. Os animais foram avaliados 2 e 24 horas após a realização dos procedimentos, por meio da Escala de Avaliação Locomotora, Teste do Campo Aberto, Teste de Retirada da Cauda, Teste da Placa Quente e Teste do Pinçamento da Pata (reflexos segmentares e supra-segmentares) e também por métodos histológicos, utilizando-se as colorações de Níssl, HematoxHina-Eosina e Glees. Foi observado que as escalas de avaliação locomotora utilizadas foram menos sensíveis à detecção de mudanças funcionais nos animais se comparadas com os testes de comportamento sensório-motores. O teste Exploração no Plano Vertical foi o mais sensível para detectar deficiências sensório-motoras nos diferentes grupos experimentais. Por esse método detectamos uma diminuição da capacidade de exploração do plano vertical nos animais 24 horas após os procedimentos. O teste de função reflexa mais sensível à detecção de deficiências sensório-motoras nos animais após trauma raquimedular leve, moderado e grave, foi o Teste da Placa Quente. Portanto, este estudo demonstrou que, além das Escalas de Avaliação Locomotora, o Teste do Campo Aberto e o Teste da Placa Quente são de utilização fácil, simples, barata, reprodutível e quantitativa, com sensibilidade para detectar deficiências funcionais em animais que tenham sofrido trauma raquimedular leve, moderado ou grave. A análise histológica em segmentos da medula espinhal abrangendo o sítio da lesão permitiu a avaliação da lesão e correlação entre a lesão sensitiva e motora. / An experimental study was carried out using Wistar Albine rats, aiming at an evaluation of different models for the study of spinal injury. Controls included the following groups: Anesthesia, Divulsion of the soft prevertebral tissues and Laminectomy. Groups for the study of spinal injury were composed by animals whose vertebral segment between T10 and L1 was submitted to Total Section of the Spinal cord, Partial Section (hemissection), Total Section Preceded of Application of Local Anesthetic and Vertebral Compression. Animals were evaluated, 2 and 24 hours after the experimental procedures, by means of the Locomotor Evaluation Scale, Open Field Test, Tail Flick Test, Hot Plate Test and Paw Nippering Test (segmentary and suprasegmentary reflex), as well as by means of histological methods using Níssl, Hematoxilin-Eosin and Glees Stainning. lt was observed that the Locomotor Evaluation Scales so far used were less sensitive to detection of functional changes in animals when compared with the sensorio-motor behaviour tests. The vertical Plain Exploration Test was the most sensitive for detection of sensorio-motor deficiences in different experimental groups. By means of this method we could detect a decrease in the ability to explore the Vertical Plain in the animals of 24 hours. The more sensitive reflex function test to detect sensorio-motor deficiences of animals, following light, moderate or severe spinal cord injury, was the Hot Plate Test. Therefore, this study showed that, in addition to the locomotor Evaluation scales, the Open Field Test and Hot Plate Test are of easy, simple, cheap, reproducible and quantitative utilization, showing enough sensitivity to detect functional deficiences in animals previously submitted to light, moderate or severe spinal cord injury. Histological analysis of spinal cord segments which enclosed the injured site allowed the evaluation of the injury and the relationship between sensitive and motor lesions.

No description available.

The purpose of this study was to explore the differences in the aerobic response to wheeling between wheelchair dependent individuals and able-bodied individuals of similar genders and ages. Five wheelchair dependent men (WC) and five able-bodied men (AB) performed a 13 minute wheeling test (5 min. at rest, 8 min. wheeling) at 4.0 km∙hr-1. Heart rate (HR) and VO2 were recorded using a Vmax ST system during the constant speed test. There was no significant difference in HR or VO2 between the two groups during rest. Both HR and VO2 were higher for WC during exercise. The mean METS during exercise for WC and AB were 3.589 ± 0.516 and 2.726 ± 0.164, respectively. The results indicate that at a given workload a spinal cord injured wheelchair user will have a greater aerobic response than an able-bodied person in a wheelchair completing the same task.

The exceptional abilities of top-tier athletes – from Simone Biles’ dizzying gymnastics to LeBron James’ gravity-defying bounds – can easily lead one to forget to marvel at the exceptional breadth of everyday movements. Whether holding a cup of coffee, reaching out to grab a falling object, or cycling at a quick clip, every motor action requires activating multiple muscles with the appropriate intensity and timing to move each limb or counteract the weight of an object. These actions are planned and executed by the motor cortex, which transmits its intentions to motoneurons in the spinal cord, which ultimately drive muscle contractions. A central problem in neuroscience is precisely how neural activity in cortex and the spinal cord gives rise to this diverse range of behaviors. At the level of spinal cord, this problem is considered to be well understood. A foundational tenet in motor control asserts that motoneurons are controlled by a single input to which they respond in a reliable and predictable manner to drive muscle activity, akin to the way that depressing a gas pedal by the same degree accelerates a car to a predictable speed. Theories of how motor cortex flexibly generates different behaviors are less firmly developed, but the available evidence indicates that cortical neurons are coordinated in a similarly simplistic, well-preserved manner. Yet a potential complication for both these old and new theories are the relative paucity of diverse behaviors during which motor cortex and spinal motoneurons have been studied. In this dissertation, I present results from studying these two neuronal populations during a broader range of behaviors than previously considered. These results indicate, in essence, that diverse behaviors involve greater complexity and flexibility in cortical and spinal neural activity than indicated by current theories.

No description available.

Antibody microprobes were used to study release of immunoreactive neurokinins in the dorsal horn of the anaesthetized spinal cat following sustained isometric contraction of ipsilateral hindlimb muscles. Microprobes had immobilized antibodies to neurokinin A (NKA) on their outer surfaces and bound a proportion of released molecules when inserted in the central nervous system. Bound molecules were detected in autoradiographs as zones of reduced binding of 125I-NKA in which microprobes were incubated after withdrawal from the spinal cord. The left hindlimb was immobilized using an epoxy bandage splint and isometric contraction of muscles induced by intermittent tetanic stimulation of a ventral root. A basal presence of immunoreactive neurokinins was detected and this was increased by sustained isometric muscle contraction. It is probable that ergoreceptors contain and release neurokinins.

1. Whole-cell patch recordings were made from substantia gelatinosa (SG) neurons in transverse lumbar spinal cord slices of 15- to 30-day-old rats. 2. Endomorphin 1 (EM-1) or EM-2 (≤ 10 μM) hyperpolarized or induced an outward current in 26 of the 66 SG neurons. The I-V relationship showed that the peptide activates an inwardly rectifying K + current. 3. EM-1 or EM-2 (0.3-10 μM) suppressed short-latency excitatory postsynaptic currents (EPSCs) and long-latency inhibitory postsynaptic currents (IPSCs) in nearly all SG neurons tested or short-latency IPSCs in six of the 10 SG neurons. [Met 5] enkephalin or [D-Ala 2, N-Me-Phe 4, Gly 5-ol]-enkephalin (DAMGO) (1-10 μM) depressed EPSCs and IPSCs. EM-1 or EM-2 depressed synaptic responses without causing a significant change in holding currents or inward currents induced by glutamate. 4. Glutamate also evoked a short-latency outward current in five SG neurons or a biphasic current in two neurons; the outward current was blocked by tetrodotoxin (TTX, 0.3 μM) or bicuculline (10 μM). EM-1 or DAMGO (1 or 5 μM) attenuated the glutamate-evoked outward or biphasic currents in four of the seven SG neurons. 5. EM-1 (1 μM) reduced the frequency, but not the amplitude of miniature EPSCs or miniature IPSCs. 6. Naloxone (1 μM) or the selective μ-opioid receptor antagonist β-funaltrexamine (β-FNA, 25 μM) antagonized the action of EM; EM-induced hyperpolarizations persisted in the presence of the κ-opioid receptor antagonist (nor-binaltorphimine dihydrochloride, 1 μM) and/or σ-opioid receptor antagonist (naltrindole hydrochloride, 1 μM). 7. It may be concluded that EM acting on μ-opioid receptors hyperpolarizes a population of SG neurons by activating an inwardly rectifying K + current, and attenuates excitatory and inhibitory synaptic currents evoked in a population of SG neurons, probably by a presynaptic site of action.

Beta-arrestins have been suggested to regulate μ-, δ-, and κ-opioid receptor-mediated responses. In the present study, we examined the effects of pretreatment with β-arrestin-2 antibody on tail-flick inhibition induced by opioid receptor agonists in the mouse spinal cord. Intrathecal (i.t.) pretreatment with β-arrestin-2 antibody potentiated the antinociception induced by i.t.-administered μ-opioid receptor agonists [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAMGO) and endomorphin-1, but not endomorphin-2, the δ-opioid receptor agonist [D-Ala2]deltorphin II or the κ-opioid receptor agonist U50,488H. The present result suggests that β-arrestin-2 may tonically down-regulate a selected population of μ-opioid receptors activated by endomorphin-1 or DAMGO in the mouse spinal cord.

A 6 year old boy developed a fatal, rapidly progressive encephalopathy 5 months after a matched unrelated cord blood transplant. Autopsy findings revealed spongiform changes in his brain. The clinical course of this child's illness had many findings consistent with that of a transmissible spongiform encephalopathy (TSE). Pre-mortem and post-mortem studies failed to definitively determine an etiology. Spongiform encephalopathies include the TSEs and mitochondrial encephalopathies. Both should be considered in a post-hematopoietic stem cell transplant patient who develops a progressive encephalopathy when more common etiologies are not found.

Electrical excitation of the dorsal aspect of the rostral thoracic spinal cord imparts long-term therapeutic benefits to patients with angina pectoris. Such spinal cord stimulation also induces short-term suppressor effects on the intrinsic cardiac nervous system. The purpose of this study was to determine whether spinal cord stimulation (SCS) induces long-term effects on the intrinsic nervous system, particularly in the presence of myocardial ischaemia. The activity generated by right atrial neurons was recorded in 10 anesthetized dogs during basal states, during prolonged (15 min) occlusion of the left anterior descending coronary artery, and during the subsequent reperfusion phase. Neuronal activity and cardiovascular indices were also monitored when the dorsal T1-T4 segments of the spinal cord were stimulated electrically (50 Hz; 0.2 ms) at an intensity 90% of motor threshold (mean 0.32 mA) for 17 min. SCS was performed before, during and after 15-min periods of regional ventricular ischaemia. Occlusion of a major coronary artery, one that did not perfuse investigated neurons, resulted in their excitation. Ischaemia-induced neuronal excitatory effects were suppressed (-76% from baseline) by SCS. SCS suppression of intrinsic cardiac neuronal activity persisted during the subsequent reperfusion period; after terminating 17 min of SCS, at least 20 min elapsed before intrinsic cardiac neuronal activity returned to baseline values. It is concluded that populations of intrinsic cardiac neurons are activated by inputs arising from the ischaemic myocardium. Ischaemia-induced activation of these neurons is nullified by SCS. The neuronal suppressor effects that SCS induces persist not only during reperfusion, but also for an extended period of time thereafter. These long-term effects may account, in part, for the fact that SCS imparts clinical benefit to patients with angina of cardiac origin not only during its application, but also for a time thereafter.