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Relevant bibliographies by topics / Presynaptic inhibition

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Academic literature on the topic 'Presynaptic inhibition'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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Journal articles on the topic "Presynaptic inhibition"

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Côté, Marie-Pascale, and Jean-Pierre Gossard. "Task-Dependent Presynaptic Inhibition." Journal of Neuroscience 23, no. 5 (2003): 1886–93. http://dx.doi.org/10.1523/jneurosci.23-05-01886.2003.

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Stein, Richard B. "Presynaptic inhibition in humans." Progress in Neurobiology 47, no. 6 (1995): 533–44. http://dx.doi.org/10.1016/0301-0082(95)00036-4.

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Hayes, Heather Brant, Young-Hui Chang, and Shawn Hochman. "Stance-phase force on the opposite limb dictates swing-phase afferent presynaptic inhibition during locomotion." Journal of Neurophysiology 107, no. 11 (2012): 3168–80. http://dx.doi.org/10.1152/jn.01134.2011.

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Presynaptic inhibition is a powerful mechanism for selectively and dynamically gating sensory inputs entering the spinal cord. We investigated how hindlimb mechanics influence presynaptic inhibition during locomotion using pioneering approaches in an in vitro spinal cord–hindlimb preparation. We recorded lumbar dorsal root potentials to measure primary afferent depolarization-mediated presynaptic inhibition and compared their dependence on hindlimb endpoint forces, motor output, and joint kinematics. We found that stance-phase force on the opposite limb, particularly at toe contact, strongly influenced the magnitude and timing of afferent presynaptic inhibition in the swinging limb. Presynaptic inhibition increased in proportion to opposite limb force, as well as locomotor frequency. This form of presynaptic inhibition binds the sensorimotor states of the two limbs, adjusting sensory inflow to the swing limb based on forces generated by the stance limb. Functionally, it may serve to adjust swing-phase sensory transmission based on locomotor task, speed, and step-to-step environmental perturbations.

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AAS, P., and F. FONNUM. "Presynaptic inhibition of acetylcholine release." Acta Physiologica Scandinavica 127, no. 3 (1986): 335–42. http://dx.doi.org/10.1111/j.1748-1716.1986.tb07913.x.

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Hoffert, Marvin J. "Presynaptic inhibition of primary afferents." Journal of Pain and Symptom Management 1, no. 3 (1986): 163–64. http://dx.doi.org/10.1016/s0885-3924(86)80068-9.

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Scholz, Kenneth P. "Presynaptic inhibition in the hippocampus." Trends in Neurosciences 16, no. 10 (1993): 395–96. http://dx.doi.org/10.1016/0166-2236(93)90005-7.

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Thompson, Scott M., Marco Capogna, and Massimo Scanziani. "Presynaptic inhibition in the hippocampus." Trends in Neurosciences 16, no. 6 (1993): 222–27. http://dx.doi.org/10.1016/0166-2236(93)90160-n.

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Isaacson, Jeffry S. "GABAB Receptor-Mediated Modulation of Presynaptic Currents and Excitatory Transmission at a Fast Central Synapse." Journal of Neurophysiology 80, no. 3 (1998): 1571–76. http://dx.doi.org/10.1152/jn.1998.80.3.1571.

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Isaacson, Jeffry S. GABAB receptor-mediated modulation of presynaptic currents and excitatory transmission at a fast central synapse. J. Neurophysiol. 80: 1571–1576, 1998. Large nerve terminals (calyces of Held) in the medial nucleus of the trapezoid body (MNTB) offer a unique opportunity to explore the modulation of presynaptic channels at a mammalian central synapse. In this study I examined γ-aminobutyric acid-B (GABAB)-mediated presynaptic inhibition at the calyx of Held in slices of the rat auditory brain stem. The selective GABAB agonist baclofen caused a potent inhibition of synaptic transmission and presynaptic Ca2+ current. The inhibition of presynaptic Ca2+ channels was associated with a slowing of the activation kinetics of the underlying current, and the inhibition was relieved by strong depolarization. The inhibition of both synaptic transmission and presynaptic Ca2+ current was abolished by N-ethylmaleimide, a sulfhydryl alkylating agent that uncouples the Go/Gi class of G proteins from receptors. Baclofen does not activate a potassium conductance in the presynaptic terminal. Taken together, these results suggest that GABAB receptors inhibit synaptic transmission via G protein-mediated modulation of presynaptic Ca2+ channels at this large central synapse. Furthermore, these findings demonstrate that basic mechanisms of G protein-mediated inhibition of Ca2+ channels, proposed from recordings of neuron cell bodies, are well conserved at nerve endings in the mammalian brain.

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McComas, Alan J. "Hypothesis: Hughlings Jackson and presynaptic inhibition: is there a big picture?" Journal of Neurophysiology 116, no. 1 (2016): 41–50. http://dx.doi.org/10.1152/jn.00371.2015.

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Presynaptic inhibition is a very powerful inhibitory mechanism and, despite many detailed studies, its purpose is still only partially understood. One accepted function is that, by reducing afferent inflow to the spinal cord and brainstem, the tonic level of presynaptic inhibition prevents sensory systems from being overloaded. A corollary of this function is that much of the incoming sensory data from peripheral receptors must be redundant, and this conclusion is reinforced by observations on patients with sensory neuropathies or congenital obstetric palsy in whom normal sensation may be preserved despite loss of sensory fibers. The modulation of incoming signals by presynaptic inhibition has a further function in operating a “gate” in the dorsal horn, thereby determining whether peripheral stimuli are likely to be perceived as painful. On the motor side, the finding that even minimal voluntary movement of a single toe is associated with widespread inhibition in the lumbosacral cord points to another function for presynaptic inhibition: to prevent reflex perturbations from interfering with motor commands. This last function, together with the normal suppression of muscle and cutaneous reflex activity at rest, is consistent with Hughlings Jackson's concept of evolving neural hierarchies, with each level inhibiting the one below it.

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Frerking, M., and P. Ohliger-Frerking. "Functional Consequences of Presynaptic Inhibition During Behaviorally Relevant Activity." Journal of Neurophysiology 96, no. 4 (2006): 2139–43. http://dx.doi.org/10.1152/jn.00243.2006.

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Presynaptic inhibition is a widespread mechanism for regulating transmitter release in the CNS. Presynaptic inhibitors act as a high-pass filter, but the functional consequence of this filtering during the synaptic processing of behaviorally relevant activity remains unknown. Here we use analytical approaches to examine the effects of presynaptic inhibition on synaptic output in response to activity patterns from CA3 pyramidal cells during the performance of a complex behavioral task. We calculate that presynaptic inhibition enhances the contrast between background activity and responses to environmental cues and that neuronal responses to location are subject to stronger contrast enhancement than neuronal responses to olfactory information. Our analysis suggests that presynaptic inhibition also enhances the importance of integrative inputs that respond to many behavioral cues during the task at the expense of specific inputs that respond to only a few of these cues.

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Dissertations / Theses on the topic "Presynaptic inhibition"

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Guo, Da [Verfasser], and Jing [Akademischer Betreuer] Hu. "Presynaptic Gate of Pain Control : Malfunctioning Presynaptic GABAergic Inhibition in Neuropathic and Inflammatory Pain / Da Guo ; Betreuer: Jing Hu." Tübingen : Universitätsbibliothek Tübingen, 2019. http://d-nb.info/1191752461/34.

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Hale, Brendon S. "The effects of motor imagery on the Hoffmann Reflex and presynaptic inhibition." [Bloomington, Ind.] : Indiana University, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3274271.

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Thesis (Ph.D.)--Indiana University, Dept. of Kinesiology, 2007.<br>Source: Dissertation Abstracts International, Volume: 68-07, Section: B, page: 4882. Adviser: John S. Raglin. Title from dissertation home page (viewed Apr. 21, 2008).

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Robertson, Christopher Travis. "Selectivity of presynaptic inhibition supraspinal and segmental influences that shape movement parameters /." [Bloomington, Ind.] : Indiana University, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3283097.

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Thesis (Ph.D.)--Indiana University, Dept. of Kinesiology, 2007.<br>Source: Dissertation Abstracts International, Volume: 68-09, Section: B, page: 5772. Advisers: David M. Koceja; Dale R. Sengelaub. Title from dissertation home page (viewed May 12, 2008).

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Cullen, Patrick Kennedy. "NEUROBIOLOGICAL MECHANISMS OF FEAR GENERALIZATION." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1374536919.

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Rost, Benjamin [Verfasser]. "Presynaptic inhibition of transmitter release by G-Protein coupled receptors in the hippocampal formation / Benjamin Rost." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/102727529X/34.

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Hayes, Heather Brant. "Biomechanics and electrophysiology of sensory regulation during locomotion in a novel in vitro spinal cord-hindlimb preparation." Diss., Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/42797.

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The purpose of this dissertation was to gain insight into spinal sensory regulation during locomotion. To this end, I developed a novel in vitro spinal cord-hindlimb preparation (SCHP) composed of the isolated in vitro neonatal rat spinal cord oriented dorsal-up with intact hindlimbs locomoting on a custom-built treadmill or instrumented force platforms. The SCHP combines the neural and pharmacological accessibility of classic in vitro spinal cord preparations with intact sensory feedback from physiological hindlimb movements. thereby expanding our ability to study spinal sensory function. I then validated the efficacy of the SCHP for studying behaviorally-relevant, sensory-modulated locomotion by showing the impact of sensory feedback on in vitro locomotion. When locomotion was activated by serotonin and N-methyl D-aspartate, the SCHP produced kinematics and muscle activation patterns similar to the intact rat. The mechanosensory environment could significantly alter SCHP kinematics and muscle activitation patterns, showing that sensory feedback regulates in vitro spinal function. I further demonstrated that sensory feedback could reinforce or initiate SCHP locomotion. Using the SCHP custom-designed force platform system, I then investigated how presynaptic inhibition dynamically regulates sensory feedback during locomotion and how hindlimb mechanics influence this regulation. I hypothesized that contralateral limb mechanics would modulate presynaptic inhibition on the ipsilateral limb. My results indicate that contralateral limb stance-phase loading regulates ipsilateral swing-phase sensory inflow. As contralateral stance-phase force increases, contralateral afferents act via a GABAergic pathway to increase ipsilateral presynaptic inhibition, thereby inhibiting sensory feedback entering the spinal cord. Such force-sensitive contralateral presynaptic inhibition may help preserve swing, coordinate the limbs during locomotion, and adjust the sensorimotor strategy for task-specific demands. This work has important implications for sensorimotor rehabilitation. After spinal cord injury, sensory feedback is one of the few remaining inputs available for accessing spinal locomotor circuitry. Therefore, understanding how sensory feedback regulates and reinforces spinally-generated locomotion is vital for designing effective rehabilitation strategies. Further, sensory regulation is degraded by many neural insults, including spinal cord injury, Parkinson's disease, and stroke, resulting in spasticity and impaired locomotor function. This work suggests that contralateral limb loading may be an important variable for restoring appropriate sensory regulation during locomotion.

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GIUSTIZIERI, MICHELA. "Meccanismi di modulazione presinaptica nei neuroni dopaminergici della substantia nigra pars compacta." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/561.

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L’inibizione presinaptica è un meccanismo di modulazione sinaptica comunemente osservato nelle sinapsi del sistema nervoso centrale e periferico. Questo processo inizia in risposta all’attivazione di un’ampia varietà di recettori presinaptici e porta ad una riduzione della probabilità di fusione delle vescicole con la membrana del terminale sinaptico. Uno dei più comuni meccanismi d’azione consiste nell’inibizione dei canali del calcio voltaggio dipendenti (VDCCs) localizzati nei bottoni presinaptici. Tuttavia, esistono altre forme di inibizione presinaptica con meccanismi che coinvolgono direttamente la machinery di rilascio vescicolare. In questa tesi ho studiato il meccanismo di inibizione presinaptica mediata dal recettore metabotropico del glutammato del tipo III (mGluRs) e dal recettore GABAB nella trasmissione GABAergica dei neuroni dopaminergici della substantia nigra pars compacta (SNc) di ratto. L’AP-4 (100 μM), agonista selettivo del recettore metabotropico del glutammato del tipo III, e il baclofen (10 μM), agonista selettivo del recettore GABAB, riducono reversibilmente la frequenza delle correnti spontanee inibitorie post-sinaptiche (sIPSCs) rispettivamente del 48.5 ± 3.7 % e del 83.6 ± 2.3 % rispetto al controllo, senza avere alcun effetto sull’ampiezza della corrente. L’AP-4, non deprime la frequenza delle correnti inibitorie miniature post-sinaptiche (mIPSCs), registrate in tetrodotossina (TTX, 1 μM) e cadmio (100 μM), mentre è in grado di ridurre la frequenza delle mIPSCs del 75.3 ± 2.8 % rispetto al controllo, in presenza di TTX (1 μM) e bario (1 mM). Al contrario, il baclofen riduce la frequenza delle mIPSCs sia in cadmio (70.0 ± 6.7 % del controllo) sia in bario (52.3 ± 2.9 % del controllo). In TTX e ionomicina (2 μM), il baclofen riduce significativamente la frequenza delle mIPSCs del 71.8 ± 6.9 % del controllo, mentre l’AP-4 non ha effetto. In maniera simile, in presenza di TTX e α-latrotossina (α-LTX, 0.3 nM), la frequenza delle mIPSCs è diminuita del 64.5 ± 4.8 % del controllo dal baclofen, mentre mantiene gli stessi valori in presenza di AP-4. Infine, in continua presenza di baclofen, l’AP-4 non causa un ulteriore riduzione della frequenza delle sIPSCs. La conclusione di questi studi è che i recettori metabotropici del glutammato del tipo III deprimono il rilascio di GABA dai neuroni dopaminergici della SNc , attraverso l’inibizione dei VDCC, mentre i recettori presinaptici GABAB coinvolgono direttamente il rilascio vescicolare del neurotrasmettitore. Inoltre questi due diversi meccanismi di inibizione pre-sinaptica coesistono nello stesso terminale sinaptico. Questa caratterizzazione fornisce nuove conoscenze sul ruolo di questi recettori presinaptici nello studio della fisiologia della substantia nigra e nel loro potenziale uso come target nel trattamento farmacologico di malattie neurodegenerative come il morbo di Parkinson.<br>Presynaptic inhibition is a mechanism of synaptic modulation normally observed in the synapses of the nervous system. This process starts upon activation of a large number of presynaptic receptors and leads to the decreased probability of vesicles to fuse to the cell membrane. One of the most common mechanism consists in the inhibition of the voltage dependent calcium channels (VDCC) located on the active zone of the presynaptic neuron. However, there is evidence for another form of presynaptic inhibition with a direct impairment of the vescicular release machinery. In my thesis I have investigated the mechanisms of presynaptic inhibition by group III metabotropic glutamate receptors (mGluRs) and GABAB receptors of the GABAergic neurotransmission to dopamine (DA) neurones of the rat substantia nigra pars compacta (SNc). The group III mGluRs agonist L-(+)-2-amino-4-phosphonobutyric acid (AP4, 100 μM) and the GABAB receptor agonist baclofen (10 μM) reversibly depressed the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) to 48.5 ± 3.7 % and 83.6 ± 2.3 % of control, respectively, with no effect in their amplitude. AP4 did not affect miniature inhibitory postsynaptic currents (mIPSCs) recorded in tetrodotoxin (TTX, 1 μM) and cadmium (100 μM), while in TTX (1 μM) and barium (1 mM), mIPSCs frequency was reduced to 75.3 ± 2.8 % of control. In contrast, baclofen reduced mIPSCs frequency either in cadmium (70.0 ± 6.7 % of control) or barium (52.3 ± 2.9 % of control). In TTX and ionomycin (2 μM), baclofen significantly reduced mIPSCs frequency to 71.8 ± 6.9 % of control, while AP4 had no effect. Similarly, in TTX and α-latrotoxin (α-LTX, 0.3 nM), the frequency of mIPSCs was reduced by baclofen to 64.5 ± 4.8 % of control, but was insensitive to AP4. Finally, in the continuous presence of baclofen, AP4 failed to produce any further reduction of sIPSCs frequency. The conclusion of this study is that group III mGluRs depress GABA release to DA neurons of the SNc through inhibition of presynaptic voltage-dependent calcium channels, while presynaptic GABAB receptors also impair transmitter exocytosis, and both mechanisms coexist on the same synapses. This characterization provides new insights about the role of these presynaptic receptors in the physiology of the substantia nigra and their potential involvement in the treatment of neurodegenerative diseases such as Parkinson’s Disease.

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Martins, Emerson Fachin. "Atividade preparatória de circuitos neuronais medulares durante expectativa para contração muscular voluntária." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-27052008-104200/.

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Antecedendo movimentos voluntariamente gerados, existe atividade neuronal encefálica que se inicia alguns segundos antes da execução deste movimento. Esta atividade preparatória é responsável pela elaboração de um plano de execução que alcança a via final comum para realização de um ato motor voluntário, os motoneurônios. Entretanto, na última década, evidências apontam para a participação de circuitos neuronais na medula espinhal apresentando padrão de atividade similar aos padrões observados em áreas encefálicas e que, possivelmente, estaria relacionado a uma atividade preparatória para o movimento voluntariamente gerado. Por este motivo, o presente trabalho teve por objetivo verificar a atividade de circuitos neuronais na medula espinhal durante diferentes instantes de proximidade da ação voluntariamente gerada em paradigma de tarefa motora com período de instrução. Para isso, inicialmente, 15 sujeitos saudáveis, sem histórico de doença neuromuscular foram submetidos ao protocolo experimental. O protocolo experimental constituiu-se do processo de recrutamento dos sujeitos, sua preparação para o ensaio dentro do ambiente experimental, bem como as orientações necessárias para execução dos procedimentos e paradigmas. Os procedimentos referem-se às etapas realizadas para captação do reflexo H, bem como desta captação sob a influência de técnica de condicionamento por inibição pré-sináptica. Essa captação ocorreu em janelas de aquisição em que o sujeito encontrava-se em repouso e em três instantes de expectativa para a execução de ação voluntária, estando o músculo sóleo atuando como agonista (flexão plantar) ou antagonista (dorsiflexão), em paradigma de tarefa motora voluntária com período de instrução. Após os registros, por meio de processamento dos sinais coletados, foi possível se calcular a amplitude pico-a-pico do reflexo H nas diferentes condições experimentais de proximidade da execução (1000, 600 e 200 milissegundos) e de atuação do músculo sóleo (agonista e antagonista) que foi usado para: (1) análise da variação da excitabilidade reflexa, em porcentagem da onda M máxima, (2) análise da ocorrência de inibição pré-sináptica e (3) análise da variação da inibição pré-sináptica, em porcentagem de inibição. Os resultados mostram que a porcentagem da onda M máxima aumentou significativamente nos três instantes de proximidade com os sujeitos estando em expectativa da execução da tarefa motora quando o músculo sóleo atuaria como agonista da contração, quando comparados com os registros obtidos nas mesmas condições em repouso. Contudo, somente a 200 ms da execução é que foi observado aumento da porcentagem da onda M máxima quando o músculo sóleo atuaria como antagonista. Inibição pré-sináptica ocorreu em todas as condições experimentais, contudo aumento significativo da porcentagem de inibição pré-sináptica foi somente observado a 200 ms da execução da tarefa motora em que o músculo sóleo atuaria como antagonista. Diferenças entre agonista e antagonista com relação ao padrão de excitabilidade reflexa foi somente observado a 600 ms de proximidade da execução da tarefa e essas diferenças com relação à porcentagem de inibição pré-sináptica foi somente detectada a 200 ms. Nossos resultados nos permitem concluir que circuitos neuronais na medula espinhal apresentam atividade no período preparatório para a execução de tarefa motora voluntária que podem estar relacionadas ao comportamento de expectativa da realização de uma ação motora eminente, bem como relacionada ao planejamento motor para a ação a longa proximidade da execução de movimentos.<br>There is brain activity preceding voluntary movements a few seconds before the execution of the movement. This preparatory activity is responsible for the execution plan that reaches the final common pathway, i.e., the motoneurons. In the last decade, there have been reports indicating the involvement of spinal cord circuits in the preparatory activity for movement. The present work has the objective of verifying the activity of spinal cord neuronal circuits at different times preceding a voluntary action, under an instructed delay period paradigm. Fifteen healthy subjects participated in the study. The protocol included an explanation of the experimental tasks. Electrophysiological recordings of the H reflex with and without presynaptic inhibition conditioning were employed. The epochs of H reflex recording were associated either with a resting period or with one of three pre-action periods. The subject received a cue at an appropriate time about the type of contraction: plantarflexion or dorsiflexion. Peak to peak H reflex values were computed in the control resting period and at 1000 ms, 600 ms and 200 ms before the action. Percent values of H amplitude with respect to maximum M values were computed as well as the level of presynaptic inhibition. The results have shown that the relative H reflex value increased significantly at the three premovement times for the soleus under an agonist contraction (i.e., plantarflexion) when compared to control. However, when the soleus was an antagonist to the contraction (i.e., dorsiflexion) there was a statistical difference in the H amplitude only at 200 ms before movement. Presynaptic inhibition occurred in all experimental conditions, however only at 200 ms before contraction there was a significant increase. Differences in reflex excitability between agonist and antagonist activity were only observed at 600 ms before action. On the other hand, differences in presynaptic inhibition were only found at 200 ms before contraction. The results indicated that spinal cord neuronal circuits are activated during the preparatory period preceding a voluntary action. These may be correlated with an expectancy behavior for the execution of an imminent motor action and also with the planning of a motor action at larger times preceding movement execution.

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Mattos, Eugênia Casella Tavares de. "Adaptações neurais na medula espinhal de humanos para diferentes tipos de treinamento físico." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-26082009-150531/.

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Introdução:As adaptações neurais ao treinamento físico vêm sendo amplamente estudadas e a medula espinhal é um dos locais de possível adaptação. No entanto nenhuma avaliação longitudinal havia sido feita diretamente sobre as circuitarias inibitórias medulares. Até o presente momento as alterações eram somente suposições. O presente trabalho verificou as circuitarias medulares responsáveis pela inibição recíproca (IR) e inibição pré-sináptica (IPS) em sujeitos submetidos a diferentes treinamentos. Materiais e Métodos: Para o treino aeróbico (resistência) foram avaliados 25 soldados submetidos ao treinamento militar do Exército Militar Brasileiro. Foram feitas 3 avaliações uma pré-treino e outras duas com 3 e 9 meses após o inicio das atividades no ano de 2006. Outros 29 sujeitos foram divididos em 3 grupos: controle (permaneceram 8 semanas sem atividades de reinamento), grupo de treino de força máxima e treino de potência. Eles foram submetidos a 8 semanas de treino, realizado com séries de agachamento livre com peso. Para avaliação das circuitarias medulares foi utilizado o reflexo H do sóleus condicionado com estímulos no nervo fibular comum (NFC) - que inerva o músculo tibial anterior (TA). O intervalo entre o estímulo condicionante e o estímulo teste determinou a avaliação da IR, da inibição D1 e da inibição D2 (IPS). Outras variáveis também foram calculadas como: contração voluntária máxima isométrica (CVM) do sóleus e TA e seus respectivos eletromiogramas (EMG), relação elétrica e mecânica entre Hmax/Mmax e condicionamento do EMG do sóleus por estímulos no NFC. Foram feitas análises pareadas com teste t-student para o grupo militar e ANOVA two-way para comparação dos grupos de força máxima e potência com o grupo controle. Principais Resultados: O grupo do exército apresentou aumento na força do sóleus e do TA, juntamente com aumento no RMS do EMG do sóleus e do torque gerado pela onda Mmax, sem alterações nos relações Hmax/Mmax. O treinamento militar reduziu significativamente a inibição D1 e mostrou tendências a aumento da IPS. O grupo de força máxima não mostrou aumento de força isométrica, no entanto apresentou aumento na relação elétrica Hmax/Mmax, com concomitante redução da IR e aumento da IPS. O grupo de potência mostrou ganho na força máxima isométrica somente do sóleus. A capacidade de gerar torque reflexamente também aumentou neste grupo, com aumento significativo na relação mecânica Hmax/Mmax. Esta melhora na utilização do arco reflexo também foi verificada com redução da IPS e aumento da IR neste grupo.Conclusões: Estes resultados mostraram que a medula espinal sofre plasticidade nas vias inibitórias IR, inibição D1 e D2, e que esta plasticidade é dependente do tipo de tarefa realizada.<br>Introduction: Neural adaptations with physical training have been widely studied. The spinal cord is a possible locus of adaptation. However, longitudinal studies that evaluate directly the spinal cord pathways have not been found in the literature. Therefore, all reports from the literature justify changes found in measured responses to exercise by hypotheses on spinal cord mechanisms. This study had the objective of measuring features of specific spinal cord pathways to check if they change according to the type of physical training. The pathways related to reciprocal inhibition (RI) and pre-synaptic inhibition (PSI) were investigated in subjects undergoing different trainings. Materials and Methods: For endurance training 25 soldiers were subjected to military training of the Brazilian Army. Evaluations were made three times, one previous to the beginning of the activity and twice post-training (within 3 and 9 months). Other 29 subjects were divided into: control group (with no training), maximal strength group and power group. They were subjected to 8 weeks of training with series of squat movements. The soleus H reflex conditioning with stimuli in the common peroneal nerve (CPN) was used to evaluate the spinal cord pathways. The interval between the conditioning and the test stimulus determine the assessment of RI, D1 inhibition and D2 inhibition (PSI). Other variables were also calculated: maximum voluntary isometric contraction from soleus and tibialis anterior and their electromyograms (EMG), electrical and mechanical Hmax/Mmax ratio and 3 inhibitions over the soleus EMG conditioned by stimuli to the CPN. The results were analyzed with paired t-student test for the military group and with two-way ANOVA to compare the maximal strength and power groups with the control group. Main Results: The military group had increased strength of the soleus and the TA muscles, with an increase in the RMS of the soleus EMG. This group also increased the torque generated by the Mmax-wave, without changes in Hmax/Mmax ratio. The military training significantly reduced D1 inhibition and showed tendencies to increase the PSI. The maximal strength group showed no differences in isometric strength, but had increased Hmax/Mmax ratio with concomitant reduction of RI and increased PSI. The power group increased isometric strength only for the soleus muscle. This group also improved the ability to generate torque by reflex pathways, with significant increase in the mechanical Hmax/Mmax ratio, with a reduction of PSI and increase of RI. Conclusions: These results show that spinal cord plasticity occurs in the inhibitory pathways of reciprocal inhibition, D1 inhibition and D2 inhibition (pre-synaptic inhibition), and that plasticity is dependent on the type of trained movement.

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Zimmerman, Amanda L. "Neuromodulation of spinal autonomic regulation." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/42777.

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The central nervous system is largely responsible for receiving sensory information from the environment and determining motor output. Yet, centrally-derived behavior and sensation depends on the optimal maintenance of the cells, tissues, and organs that feed and support these functions. Most of visceral regulation occurs without conscious oversight, making the spinal cord a key site for integration and control. How the spinal cord modulates output to our organs, or sensory information from them, is poorly understood. The overall aim of this dissertation was to better understand spinal processing of both visceral sensory information to and sympathetic output from the spinal cord. I first established and validated a HB9-GFP transgenic mouse model that unambiguously identified sympathetic preganglionic neurons (SPNs), the spinal output neurons for the sympathetic nervous system. Using this model, I investigated the electrophysiological similarities and diversity of SPNs, and compared their active and passive membrane properties to those in other animal models. My results indicate that while many of the same characteristics are shared, SPNs are a heterogeneous group that can be differentiated based on their electrophysiological properties. Since descending monoaminergic pathways have particularly dense projections to sympathetic regions of the spinal cord, I next examined the modulatory role that the monoamines have on spinal sympathetic output. While each neuromodulator tested had a unique signature of action, serotonin and norepinephrine appeared to increase the excitability of individual SPNs, while dopamine had more mixed actions. Since many autonomic reflexes are integrated by the spinal cord, I also questioned whether these reflexes would be similarly modulated. I therefore developed a novel in vitro spinal cord and sympathetic chain preparation, which allowed for the investigation of visceral afferent-mediated reflexes and their neuromodulation by monoamines. This preparation exposed a dichotomy of action, where sympathetic and somatic motor output is generally enhanced by the monoamines, but reflexes mediated by visceral input are depressed. Utilizing the spinal cord and sympathetic chain preparation, I also investigated how the spinal cord modulates visceral sensory information. One of the most powerful means of selectively inhibiting afferent information from reaching the spinal cord is presynaptic inhibition. I hypothesized that both spinal visceral afferents and descending monoaminergic systems would depress transmission of visceral afferents to the spinal cord. My results demonstrated that activity in spinal visceral afferents can lead to spinally generated presynaptic inhibition, and that in addition to depressing synaptic transmission to the spinal cord, the monoamines also depress the intrinsic circuitry that generates this activity-dependent presynaptic inhibition. Taken together, my results indicate that descending monoaminergic pathways act to limit the amount of visceral sensory information reaching the central nervous system and increase sympathetic output, resulting in an uncoupling of output from visceral sensory input and transitioning to a feed-forward, sympathetically dominant control strategy. This combination offers complex modulatory strategies for descending systems.

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Books on the topic "Presynaptic inhibition"

1

Pablo, Rudomin, Romo Ranulfo, and Mendell Lorne M, eds. Presynaptic inhibition and neural control. Oxford University Press, 1998.

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Tse, Frederick Wan-Yip. Presynaptic inhibition of crustacean neuromuscular synapses. 1987.

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Stafstrom, Carl E., and Thomas P. Sutula. 2-Deoxyglucose. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0036.

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Metabolic regulation of excitability is increasingly appreciated as a strategy to control seizures and reduce pathogenesis. Inhibiting or bypassing glycolysis may be one way in which the ketogenic diet suppresses seizures. 2-deoxy-D-glucose (2DG) is a glucose analog that partially inhibits glycolysis and has antiseizure effects in several acute and chronic seizure models. The mechanisms underlying the acute and chronic effects of 2DG are being investigated. Preliminary studies provide evidence that the acute anticonvulsant actions of 2DG involve activity-dependent presynaptic suppression of excitatory synaptic transmission during network synchronization. The chronic effects of 2DG entail reduction of the expression of brain-derived neurotrophic factor and its receptor, tyrosine kinase B. Preclinical toxicology studies demonstrate that 2DG has a favorable toxicity profile at doses effective for seizure protection. Currently available preclinical studies support 2DG as a novel first-in-class metabolic treatment for epilepsy with an antiglycolytic mechanism distinct from all other anticonvulsants.

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Book chapters on the topic "Presynaptic inhibition"

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Williams, Stephen H., and Daniel Johnston. "Muscarinic Cholinergic Inhibition of Glutamatergic Transmission." In Presynaptic Receptors in the Mammalian Brain. Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6825-0_3.

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Moreno-Díaz, Roberto, and Olga Bolívar Toledo. "An invariant representation mechanism after presynaptic inhibition." In New Trends in Neural Computation. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/3-540-56798-4_120.

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Volterra, Andrea, Steven A. Siegelbaum, J. David Sweatt, and Eric R. Kandel. "Presynaptic Inhibition, Presynaptic Facilitation, and the Molecular Logic of Second-Messenger Systems." In Molecular and Cellular Aspects of the Drug Addictions. Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8817-3_6.

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Belardetti, Francesco, Eric R. Kandel, and Steven A. Siegelbaum. "The Molecular Logic of Presynaptic Facilitation and Inhibition." In Receptor-Receptor Interactions. Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_37.

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Belardetti, Francesco, Eric R. Kandel, and Steven A. Siegelbaum. "The Molecular Logic of Presynaptic Facilitation and Inhibition." In Receptor-Receptor Interactions. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5415-4_37.

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Colmers, William F., A. Rory McQuiston, Samuel B. Kombian, and Gloria J. Klapstein. "Presynaptic Inhibition Mediated by Neuropeptide Y in the Mammalian CNS: Possible Physiological Implications." In Presynaptic Receptors in the Mammalian Brain. Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6825-0_6.

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Kirk, Mark D., and C. K. Govind. "Presynaptic Inhibition of Primary Afferent Synapses in the Crayfish." In Frontiers in Crustacean Neurobiology. Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-5689-8_15.

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Person, R., and G. Kozhina. "Presynaptic Inhibition and Disinhibition of Monosynaptic Reflex in Man." In Motor Control. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-7508-5_10.

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Dutar, Patrick, and Roger A. Nicoll. "GABAB Receptor-Mediated Inhibition of Synaptic Transmission in the Hippocampus: Pharmacology and Intracellular Mechanisms." In Presynaptic Receptors in the Mammalian Brain. Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6825-0_2.

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Schmied, Annie, Jean-Marc Aimonetti, and Jean-Pierre Vedel. "Presynaptic and Disynaptic Inhibition Induced by Group I Muscle Afferents." In Advances in Experimental Medicine and Biology. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0713-0_21.

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Conference papers on the topic "Presynaptic inhibition"

1

Gladchenko, D. A., S. M. Bogdanov, L. V. Roshchina та A. A. Chelnokov. "Effect of percutaneous electrical stimulation of the spinal cord on the manifestation of reciprocal and presynaptic inhibition α-motor neurons of the lower leg muscles against the background of a weak isometric contraction in magnitude". У VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-65-67.

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The article presents the results of a study of the reflex mechanisms of reciprocal and presynaptic inhibition at rest and when performing an isometric reduction of 5% of MPS against the background of twenty-minute non-invasive electrical stimulation of the spinal cord. It was found that at rest against the background of electrical stimulation, reciprocal and presynaptic inhibition was inverted to their relief, and when performing plantar flexion of the foot, on the contrary, reciprocal and presynaptic inhibition increased, but the severity of presynaptic inhibition was greater. Key words: percutaneous electrical stimulation of the spinal cord, reciprocal inhibition, presynaptic inhibition, isometric contraction.

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Ohta, Hiroyuki, Daisuke Uragami, Yasuhiro Nishida, and James C. Houk. "Presynaptic inhibition balances the trade-off between differential sensitivity and reproducibility." In 2012 Joint 6th Intl. Conference on Soft Computing and Intelligent Systems (SCIS) and 13th Intl. Symposium on Advanced Intelligent Systems (ISIS). IEEE, 2012. http://dx.doi.org/10.1109/scis-isis.2012.6505222.

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Moreno-Diaz, Jr., Roberto, Alexis Quesada Arengbia, and Miguel Aleman-Flores. "Bases of a pre-attentional mechanism by means of presynaptic inhibition in the lateral geniculate nucleus." In Medical Imaging 2000, edited by Elizabeth A. Krupinski. SPIE, 2000. http://dx.doi.org/10.1117/12.383122.

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