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PubMedDate not supplied

Unit responses of the first and second somatosensory areas to stimulation of the ventroposterior thalamic nucleus.

Single unit responses of the first (SI) and second (SII) somatosensory areas to stimulation of the ventroposterior thalamic nucleus (VP) were investigated in cats immobilized with D-tubocurarine. In response to VP stimulation 12.0% of reacting SI neurons and 9.5% of SII neurons generated an antidromic spike. In most antidromic responses of both SI and SII neurons the latent period did not exceed 1.0 msec. The minimal latent period of spike potentials during orthodromic excitation was 1.5 msec in SI and 1.7 msec in SII. Neurons with an orthodromic spike latency of not more than 3.0 msec were more numerous in SI than those with a latency of 3.1--4.5 msec. The ratio between the numbers of neurons of these two groups in SII was the opposite. In SII there were many more neurons with a latency of 5.6--8.0 msec than in SI. EPSPs appeared after a latent period of 1.1--9.0 msec in SI and of 1.4--6.6 msec in SII. The latent period of IPSPs was 1.5--6.8 msec in SI and 2.2--9.4 msec in SII. The relative importance of different pathways for excitatory and inhibitory influences of VP on SI and SII neurons is discussed.

Animals↗
PubMedDate not supplied

Electrophysiological analysis of efferent neurons of cat associative parietal cortex.

We have studied in acute experiments the neurons of the associative parietal cortex in the cat, using the microelectrode take-off technique. We identified the efferent neurons sending axons to the sensomotor cortex, the red nucleus, and the pontine nuclei by antidromic stimulation. We investigated the collateral branching of axons of neurons projected simultaneously into two of the formations mentioned, using the impulse collision technique. We studied the characteristics of the spatial distribution of efferent neurons in the parietal cortex.

Animals↗
PubMed1993

Abnormal response from the sternocleidomastoid muscle in patients with spasmodic torticollis: observations during microvascular decompression operations.

Electromyographic (EMG) recordings from patients undergoing microvascular decompression (MVD) operations to relieve spasmodic torticollis were studied. When EMG potentials were recorded from the sternocleidomastoid muscle in response to electrical stimulation of the spinal accessory nerve (SAN) at the neck, an abnormal (delayed) response was seen in 9 of 12 patients who had unilateral symptoms. In 5 patients with bilateral symptoms, no such delayed response was seen. We assume that this abnormal muscle response depends on an abnormal cross-transmission. Neural conduction time measurements, using electrical stimulation of the intracranial portion of the SAN, indicated that the location of this cross-transmission was more central than the vascular compression of the SAN. We hypothesize that this location might be in the motonucleus of the SAN. Similarities between these abnormal EMG findings in patients with spasmodic torticollis and those reported earlier in patients with hemifacial spasm (HFS) are presented.

Accessory Nerve↗
PubMed1994

Facial nerve demyelination and vascular compression are both needed to induce facial hyperactivity: a study in rats.

It is generally assumed that hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at the root exit zone (REZ), but the mechanism for the development of HFS is not known. Evidence has been previously presented that the signs of HFS are caused by hyperactivity of the facial motonucleus that is caused by the irritation to the facial nerve from the vascular contact. This assumption has been supported by the finding that daily electrical stimulation of the facial nerve in the rat facilitates the development of an abnormal muscle response that is a characteristic sign of HFS in man and is an indication of an abnormal cross-transmission that makes it possible to elicit a contraction of muscles innervated by one branch of the facial nerve by electrically stimulating another branch of the facial nerve. In the present study we show that close contact between a peripheral branch of the facial nerve and an artery also facilitates the development of an abnormal muscle response, but only if the facial nerve has previously been slightly injured (by a chromic suture) at the location of the arterial contact. We also show that blocking neural conduction in the facial nerve proximal to the artificial vascular compression abolishes the abnormal muscle contraction, which supports the assumption that the anatomical location of cross-transmission that is causing the abnormal muscle response is central to the vascular compression, most likely in the facial motonucleus. These findings may explain why the facial nerve is only susceptible to vascular compression near its REZ, where an injury to its myelin is more likely to occur than where the nerve is covered with schwann cell myelin.

Animals↗
PubMed1979

The Ornstein-Uhlenbeck process as a model for neuronal activity. I. Mean and variance of the firing time.

Mean and variance of the first passage time through a constant boundary for the Ornstein-Uhlenbeck process are determined by a straight-forward differentiation of the Laplace transform of the first passage time probability density function. The results of some numerical computations are discussed to shed some light on the input-output behavior of a formal neuron whose dynamics is modeled by a diffusion process of Ornstein-Uhlenbeck type.

Dendrites↗
PubMed1979

Nonlinear dynamics of paleocortex manifested in the olfactory EEG.

The olfactory bulb is the first central component in a highly sensitive yet markedly stable sensory system. It receives a surge of receptor activity with each inspiration and transmits output as a brief burst of oscillatory activity that is most clearly seen in the EEG. These properties together with the known anatomy and physiology of the bulb are used as design criteria to synthesize, evaluate and solve a set of nonlinear differential equations that represent lumped bulbar dynamics. According to the model bulbar processing is in two stages. In the outer layers the interneurons perform the operations of input range compression, integration, clipping, holding, and bias control. In the inner layers the input surge is converted to a burst, which is transmitted by the mitral cells as a pulse density wave. The phase, frequency duration and amplitude of the wave convey information centrally about both the input and the state of the system. The model suffices to replicate the forms of the EEG burst; the pulse probability distributions conditional on the EEG; the waveforms of averaged evoked potentials (AEPs) and post stimulus time (PST) histograms from the bulb and cortex; and the changes in waveform induced by behavioral control of attentiveness and habituation. It is inferred that with selective attention there is a permanent change in the strength of mutually excitatory connections among excitatory neurons, and that with habituation there is a reversible change in the effectiveness of excitatory synapses. The limitations and deficiencies of the model and the need for centrifugal controls of bulbocortical function are discussed.

Action Potentials↗