Auditory steady-state rersponses to click trains from the rat temporal cortex

n order to investigate the mechanisms underlying the generation of steady-state responses (SSRs), auditory evoked potentials elicited by click trains presented at several stimulation rates (30, 40, 50, 60 Hz) were recorded in 7 awake rats by means of epidural electrodes placed over the temporal cortex. Mean amplitude-rate function calculated on the recorded responses appeared almost flat and showed the maximum value at 50 Hz, while mean phases showed a linear increase when increasing the stimulation rate. In each rat, predictions of the recorded responses at 30, 40, 50 and 60 Hz were synthesized by superimposing middle-latency auditory evoked potentials (MAEPs) at suitable time intervals at each rate. Mean amplitudes calculated on the predicted curves decreased linearly when increasing the stimulation rate and appeared higher in comparison to those obtained from the recorded SSRs. Predicted phases showed a linear increase when increasing the stimulation rate and were leading with respect to corresponding phase values calculated for recorded SSRs. Our findings indicate that the MAEP superimposition mechanism does not adequately predict the generation of temporal recorded SSRs in rats. This was explained by admitting that phenomena related to the recovery cycle and, to a lesser extent, to rate-dependent facilitating effects come into play

Reduced auditory steady state responses in autism spectrum disorder

Background Auditory steady state responses (ASSRs) are elicited by clicktrains or amplitude-modulated tones, which entrain auditory cortex at their specific modulation rate. Previous research has reported reductions in ASSRs at 40 Hz for autism spectrum disorder (ASD) participants and first-degree relatives of people diagnosed with ASD (Mol Autism. 2011;2:11, Biol Psychiatry. 2007;62:192–197). Methods Using a 1.5 s-long auditory clicktrain stimulus, designed to elicit an ASSR at 40 Hz, this study attempted to replicate and extend these findings. Magnetencephalography (MEG) data were collected from 18 adolescent ASD participants and 18 typically developing controls. Results The ASSR localised to bilateral primary auditory regions. Regions of interest were thus defined in left and right primary auditory cortex (A1). While the transient gamma-band response (tGBR) from 0-0.1 s following presentation of the clicktrain stimulus was not different between groups, for either left or right A1, the ASD group had reduced oscillatory power at 40 Hz from 0.5 to 1.5 s post-stimulus onset, for both left and right A1. Additionally, the ASD group had reduced inter-trial coherence (phase consistency over trials) at 40 Hz from 0.64-0.82 s for right A1 and 1.04-1.22 s for left A1. Limitations In this study, we did not conduct a clinical autism assessment (e.g. the ADOS), and therefore, it remains unclear whether ASSR power and/or ITC are associated with the clinical symptoms of ASD. Conclusion Overall, our results support a specific reduction in ASSR oscillatory power and inter-trial coherence in ASD, rather than a generalised deficit in gamma-band responses. We argue that this could reflect a developmentally relevant reduction in non-linear neural processing

La organizzazione funzionale del nervo ipoglosso

Il complesso nucleare del periipoglosso consiste in un raggruppamento di cellule localizzato nel bulbo rostralmente al nucleo XII. La morfologia degli elementi cellulari, le connessioni anatomiche e le caratteristiche elettrofisiologiche fanno ritenere che i tre raggruppamenti neuronali costituiscano nel loro complesso una struttura funzionalmente unitaria, di cui pu\uf2 essere considerata rappresentativa l'attivit\ue0 dei neuroni componenti il nucleo preposito. Estese ricerche di tipo neuro-anatomico ed elettrofisiologico hanno stabilito che il nucleo preposito dell'ipoglosso svolge una funzione cruciale nei movimenti che avvengono sul piano orizzontale. Infatti, numerosi dati indicano in tale nucleo la sede del "neural integrator", cio\ue8 del circuito neurale responsabile dell'integrazione del segnale di velocit\ue0 relativo ai movimenti oculari. Il risultato di tale operazione di integrazione costituisce un segnale relativo alla posizione dell'occhio nell'orbita, che, al pari del segnale di velocit\ue0 generato a livello di altre strutture nervose, viene inviato ai motoneuroni dei nuclei oculomotori nel corso della esecuzione di movimenti oculari di vario tipo

The role of the nucleus prepositus hypoglossi in the eye movement control

The nucleus prepositus hypoglossi (NPH) consists of a small cluster of neurons localized in the dorsomedial medulla rotrally to the hypoglossal nucleus. Due to its location and the results of electrical stimulation, the NPH was first believed to be involved in the control of tongue motility. However, the anatomical connections with several neural centers dealing with eye motility and the close correlation between eye movements and NPH neurons discharge point to a major role of this nucleus in the generation of eye movements. On the basis of anatomical and electrophysiological data, it is generally accepted that a common neural integrator for horizontal eye movements is located in the NPH

Ruolo della sostanza reticolare nel controllo dei riflessi vestibolari

I riflessi vestibolo-spinali e il riflesso vestibolo-oculare devono essere considerati sistemi di controllo posturale. I primi devono essere considerati di tipo \u201cA\u201d secondo la classificazione di Kuypers nel senso che la loro funzione \ue8 quella di assicurare il corretto assetto posturale in condizioni statiche e nel corso del movimento attraverso l\u2019attivazione simultanea di diversi gruppi muscolari costituiti dai muscoli assiali e dalla muscolatura prossimale degli arti. Le modalit\ue0 di controllo realizzate su alcuni distretti muscolari e i molteplici e differenziati rapporti con strutture come la sostanza reticolare e il locus coeruleus rendono ragione di alcune caratteristiche funzionali che possono essere meglio comprese nella logica del frazionamento del movimento piuttosto che quella di un mero contributo al mantenimento dell\u2019assetto posturale. Per quanto riguarda il riflesso vestibolo-oculare, varie aree della sostanza reticolare mesencefalica, pontina e midollare sono implicate nella genesi delle fasi rapide anticompensatorie come centri di integrazione deputati alla programmazione ed esecuzione di questi movimenti

Il complesso trigeminale

La funzione masticatoria \ue8 controllata dal trigemino sia per quanto riguarda l\u2019innervazione dei muscoli masticatori, sia per quel che si riferisce al ruolo delle afferenze originanti dai propriocettori muscolari e dai meccanocettori della cavit\ue0 orale nella regolazione dell\u2019attivit\ue0 motoria. In realt\ue0, contrastano con l\u2019apparente semplicit\ue0 di un controllo realizzato da un unico nervo la complessit\ue0 dell\u2019organizzazione anatomica del suddetto nervo come pure le difficolt\ue0 di chiarire i meccanismi fisiologici alla base del ritmico movimento della mandibola, soprattutto per quel che riguarda il ruolo e il peso rispettivo da attribuire all\u2019attivit\ue0 del generatore centrale e delle afferenze periferiche. Questo \ue8 il primo aspetto che viene affrontato e discusso nel presente capitolo. Il secondo aspetto \ue8 relativo al ruolo della propriocettivit\ue0 oculare, in passato ritenuto del tutto marginale e attualmente rivalutato essendone stato accertato il coinvolgimento in varie funzioni. Tra queste vengono ricordate la stabilizzazione dell\u2019occhio e il suo mantenimento in posizione primaria, il ruolo di controllo nel corso della esecuzione dei movimenti oculari e il mantenimento del loro corretto orientamento

Effects of L-NAME on Mg2+-free-induced epileptiform activity in olfactory cortical neurones, in vitro

The effects of N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, were examined on Mg2+-free-induced epileptiform activity, in guinea-pig piriform cortex slices in vitro. L-NAME (0.1-1 mM) had no effect on neuronal membrane properties or electrically-evoked postsynaptic potentials (PSPs). In contrast, during superfusion of the slices with Mg2+-free solution neurones exhibited spontaneous and stimulus-evoked epileptiform potentials that were suppressed in the presence of L-NAME (100 mu M) or the selective NMDA receptor antagonist DL-APV (100 mu M). The inhibitory effects induced by L-NAME were reversibly reduced by L-arginine (1 mM), but not D-arginine (1 mM), the latter drug not being a substrate for NO formation. It was concluded that L-NAME can suppress epileptiform activity induced by Mg2+-free exposure primarily through a decrease in presynaptic transmitter release

Microinfusion of N-nitro-L-arginine methyl ester (L-NAME) into the inferior colliculus depresses auditory middle latency responses in the rat

Nitric oxide (NO) is a short-lived radical species endowed with intercellular signalling functions in the mammalian brain. In the present study we have investigated the effects of focal injection into one inferior colliculus of N-omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, on the acoustic middle latency responses (MLRs) evoked by click stimuli and recorded from the auditory cortex in anaesthetized rats. Microinfusion of L-NAME (1.0 mM) did not alter the latency of MLRs nor did it affect the evoked brain stem responses (ABRs), By contrast, L-NAME reduced P-1a-N-1 amplitude of MLRs by 51.7 +/- 6.6% (mean +/- SEM; n = 5) and almost complete recovery to background amplitude was obtained 15-25 min after treatment. The less active isomer, D-NAME (1.0 mM; n = 5), failed to produce consistent effects on the evoked MLRs. A higher concentration of L-NAME (5.0 mM; n = 5) yielded a 69.0 +/- 13.3% inhibition whereas maximum inhibition produced by 0.5 mM (n = 3) L-NAME was congruent to 10% of control value. The inhibitory effect typically evoked by 1.0 mM L-NAME was prevented by treating rats with L-arginine (5.0 mM; n = 5), the endogenous precursor of NO synthesis. Reduction of MLR amplitude was also obtained in rats receiving intracollicular injection of dizocilpine (MK801; 1.0 mu M) and LY274614 (1.0 mM), two selective N-methyl-D-aspartate (NMDA) receptor antagonists. In conclusion, the present data support a role for intracollicular NO in the processing and transmission of the acoustic input to the auditory cortex in the rat

Generation of human auditory steady-state responses

The linear summation of the responses elicited by individual stimuli can be considered the main mechanism underlying SSR generation. Moreover other phenomena become involved so that individual responses elicited at fast repetition rates (LCRs) are different from those recorded at stimulus rates preventing their overlapping (MLRs). First, phenomena related to the recovery cycle can determine parameters of individual responses within the SSR causing a reduction in amplitude and an increase in latency with increasing repetition rates. Second, other mechanisms related to the resonant frequency of the auditory system come into play enhancing the contribution of individual responses during 40 Hz steady state stimulation. Assuming linearity and admitting that the system behaves as a damped harmonic oscillator having resonant frequency of 40 Hz and damping ratio between 0 and 1, one can speculate that, for a given damping value, the output modulus depends on the frequency components of the input as well as on the system resonant frequency. The increase in the input of the frequency components close to the system resonant frequency causes the output modulus to increase and this make more likely the appearance of further oscillations in the system output. In conclusion it seems that the surface recorded SSR results from the linear summation of the responses to individual stimuli and these responses are different from MLRs since they can be enhanced or depressed by resonant and adaptation phenomena. The interplay between these effects is strictly dependent on the stimulus repetition rate

Inhibition of nitric oxide synthase prevents magnesium-free-induced epileptiform activity in guinea-pig olfactory cortex neurones in vitro.

The effects of N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, were examined on Mg2+-free-induced epileptiform activity, in guinea-pig piriform cortex slices in vitro. L-NAME (0.1-1 mM) had no effect on neuronal membrane properties or electrically-evoked postsynaptic potentials (PSPs). In contrast, during superfusion of the slices with Mg2+-free solution neurones exhibited spontaneous and stimulus-evoked epileptiform potentials that were suppressed in the presence of L-NAME (100 mu M) or the selective NMDA receptor antagonist DL-APV (100 mu M). The inhibitory effects induced by L-NAME were reversibly reduced by L-arginine (1 mM), but not D-arginine (1 mM), the latter drug not being a substrate for NO formation. It was concluded that L-NAME can suppress epileptiform activity induced by Mg2+-free exposure primarily through a decrease in presynaptic transmitter release, although additional actions on the NMDA-receptor complex were also considered