RESUMO
High doses of salicylate induce reversible tinnitus in experimental animals and humans, and is a common tinnitus model. Salicylate probably acts centrally and induces hyperactivity in specific auditory brainstem areas like the dorsal cochlear nucleus (DCN). However, little is known about the effect of high doses of salicylate in synapses and neurons of the DCN. Here we investigated the effects of salicylate on the excitability and evoked and spontaneous neurotransmission in the main neurons (fusiform, cartwheel and tuberculoventral) and synapses of the DCN using whole cell recordings in slices containing the DCN. For this, we incubate the slices for at least 1 h in solution with 1.4 mM salicylate, and recorded action potentials and evoked and spontaneous synaptic currents in fusiform, cartwheel (CW) and putative tuberculoventral (TBV) neurons. We found that incubation with salicylate did not affect the firing of fusiform and TBV neurons, but decreased the spontaneous firing of cartwheel neurons, without affecting AP threshold or complex spikes. Evoked and spontaneous glutamatergic neurotransmission on the fusiform and CW neurons cells was unaffected by salicylate and evoked glycinergic neurotransmission on fusiform neurons was also unchanged by salicylate. On the other hand spontaneous glycinergic transmission on fusiform neurons was reduced in the presence of salicylate. We conclude that high doses of salicylate produces a decreased inhibitor drive on DCN fusiform neurons by reducing the spontaneous firing of cartwheel neurons, but this effect is not able to increase the excitability of fusiform neurons. So, the mechanisms of salicylate-induced tinnitus are probably more complex than simple changes in the neuronal firing and basal synaptic transmission in the DCN.
Assuntos
Núcleo Coclear/efeitos dos fármacos , Glicina/metabolismo , Inibição Neural/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Salicilato de Sódio/toxicidade , Transmissão Sináptica/efeitos dos fármacos , Zumbido/induzido quimicamente , Animais , Núcleo Coclear/metabolismo , Núcleo Coclear/fisiopatologia , Potenciais Evocados Auditivos , Técnicas In Vitro , Masculino , Neurônios/metabolismo , Ratos Wistar , Zumbido/metabolismo , Zumbido/fisiopatologiaRESUMO
UNLABELLED: To investigate the transient evoked otoacoustic emissions (TEOAE) contralateral suppression in neonates at risk for hearing loss, 55 neonates at risk for hearing loss (risk group) and 72 full-term neonates not at such risk (control group) were bilaterally tested. In all neonates, the TEOAE were recorded in two stimulation modes (linear and nonlinear clicks), with and without contralateral acoustic stimulation. Findings revealed significant contralateral suppression of otoacoustic emissions in both groups, but the amount of TEOAE contralateral suppression was reduced for at risk group (p=0.001), supporting the hypothesis that medial olivocochlear bundle function is reduced in neonates at risk for hearing loss. The combination of contralateral acoustic stimulation and TEOAE enables easy and noninvasive study of auditory efferent function. However it should be emphasized that the reduction in TEOAE contralateral suppression in the risk group, statistically identified as a group effect, might not be detectable in individual cases. Further studies are needed in order to determine whether the lower amount of TEOAE contralateral suppression in neonates at risk for hearing loss represents a risk for developing auditory processing disorders. LEARNING OUTCOMES: The reader will be introduced to the study using auditory efferent pathway activation by contralateral acoustic stimulation (CAS), resulting in the TEOAE suppression effect. The characteristics of TEOAE suppression in the neonatal population, in which it provides evidence of the reduced medial olivocochlear system function in those at risk for hearing loss, will also be addressed.
Assuntos
Audiometria de Resposta Evocada/métodos , Dominância Cerebral/fisiologia , Transtornos da Audição/congênito , Doenças do Prematuro/diagnóstico , Emissões Otoacústicas Espontâneas/fisiologia , Processamento de Sinais Assistido por Computador , Estimulação Acústica , Núcleo Coclear/fisiopatologia , Vias Eferentes/fisiopatologia , Feminino , Transtornos da Audição/diagnóstico , Transtornos da Audição/fisiopatologia , Humanos , Recém-Nascido , Doenças do Prematuro/fisiopatologia , Masculino , Núcleo Olivar/fisiopatologia , Valores de Referência , Fatores de RiscoRESUMO
To assess to what extent auditory sensory deprivation affects biological rhythmicity, sleep/wakefulness cycle and 24 h rhythm in locomotor activity were examined in golden hamsters after bilateral cochlear lesion. An increase in total sleep time as well as a decrease in wakefulness (W) were associated to an augmented number of W episodes, as well as of slow wave sleep (SWS) and paradoxical sleep (PS) episodes in deaf hamsters. The number of episodes of the three behavioural states and the percent duration of W and SWS increased significantly during the light phase of daily photoperiod only. Lower amplitudes of locomotor activity rhythm and a different phase angle as far as light off were found in deaf hamsters kept either under light-dark photoperiod or in constant darkness. Period of locomotor activity remained unchanged after cochlear lesions. The results indicate that auditory deprivation disturbs photic synchronization of rhythms with little effect on the clock timing mechanism itself.