[Preliminary experience with assessing the motor pathways and central inhibition in patients with malignant cerebral gliomas in preparation for conformal radiotherapy].

We investigated central motor pathways and central inhibition in patients with brain gliomas by transcranial magnetic stimulation (TMS). 10 glioma patients and 16 matching controls were enrolled. Central motor conduction time, MEP latencies and amplitudes and silent period were evaluated. In 90% glioma patients TMS parameters were abnormal, mostly MEP shapes and thresholds were affected. In 40% of the cases central inhibition in glioma affected hemisphere was abnormally high. We propose that TMS is safe and informative tool in glioma patients; central inhibition seems to be affected in some cases by the glioma presence in the hemisphere. One of the possible causes of that may be GABA system activation.

Sparse but specific temporal coding by spikes in an insect sensory-motor ocellar pathway.

We investigate coding in a locust brain neuron, DNI, which transforms graded synaptic input from ocellar L-neurons into axonal spikes that travel to excite particular thoracic flight neurons. Ocellar neurons are naturally stimulated by fluctuations in light collected from a wide field of view, for example when the visual horizon moves up and down. We used two types of stimuli: fluctuating light from a light-emitting diode (LED), and a visual horizon displayed on an electrostatic monitor. In response to randomly fluctuating light stimuli delivered from the LED, individual spikes in DNI occur sparsely but are timed to sub-millisecond precision, carrying substantial information: 4.5-7 bits per spike in our experiments. In response to these light stimuli, the graded potential signal in DNI carries considerably less information than in presynaptic L-neurons. DNI is excited in phase with either sinusoidal light from an LED or a visual horizon oscillating up and down at 20 Hz, and changes in mean light level or mean horizon level alter the timing of excitation for each cycle. DNI is a multimodal interneuron, but its ability to time spikes precisely in response to ocellar stimulation is not degraded by additional excitation. We suggest that DNI is part of an optical proprioceptor system, responding to the optical signal induced in the ocelli by nodding movements of the locust head during each wing-beat.

Motor cortical hyperexcitability in idiopathic scoliosis: could focal dystonia be a subclinical etiological factor?

The aetiology of idiopathic scoliosis (IS) remains unknown; however, there is a growing body of evidence suggesting that the spine deformity could be the expression of a subclinical nervous system disorder. A defective sensory input or an anomalous sensorimotor integration may lead to an abnormal postural tone and therefore the development of a spine deformity. Inhibition of the motor cortico-cortical excitability is abnormal in dystonia. Therefore, the study of cortico-cortical inhibition may shed some insight into the dystonia hypothesis regarding the pathophysiology of IS. Paired pulse transcranial magnetic stimulation was used to study cortico-cortical inhibition and facilitation in nine adolescents with IS, five teenagers with congenital scoliosis (CS) and eight healthy age-matched controls. The effect of a previous conditioning stimulus (80% intensity of resting motor threshold) on the amplitude of the motor-evoked potential induced by the test stimulus (120% of resting motor threshold) was examined at various interstimulus intervals (ISIs) in both abductor pollicis brevis muscles. The results of healthy adolescents and those with CS showed a marked inhibitory effect of the conditioning stimulus on the response to the test stimulus at interstimulus intervals shorter than 6 ms. These findings do not differ from those reported for normal adults. However, children with IS revealed an abnormally reduced cortico-cortical inhibition at the short ISIs. Cortico-cortical inhibition was practically normal on the side of the scoliotic convexity while it was significantly reduced on the side of the scoliotic concavity. In conclusion, these findings support the hypothesis that a dystonic dysfunction underlies in IS. Asymmetrical cortical hyperexcitability may play an important role in the pathogenesis of IS and represents an objective neurophysiological finding that could be used clinically.

Effect of skin thickness on sensory nerve action potential amplitude.

OBJECTIVE: It has been shown that finger circumference negatively correlates with sensory nerve action potential amplitude (SNAP-A). Also fat people have lower sensory nerve amplitudes. Factors that cause electrodes displaced further away from underlying nerves, such as increased cutaneous and subcutaneous tissue, will lower SNAP-A. This study was designed to evaluate correlation between skin thickness and SNAP amplitude. METHODS: Thirty-seven healthy 22-40-year-old subjects were selected. Nineteen (51.4%) were males and 18 (48.6%) were females, without significant difference between males and females regarding their ages. For all subjects, height and weight were measured. Anteroposterior and mediolateral diameters of the proximal phalanges of the index and little fingers and also finger circumferences were measured. Palmar digital skin thickness was measured in two ways: first with sonography machine, and second with skin fold caliper. Median and ulnar nerve sensory and motor conduction studies were performed. RESULTS: In bivariate analysis, SNAP-A correlated negatively with female sex, height, anteroposterior diameter of the fingers, finger circumference and skin thickness measured by sonography, but in multiple regression analysis only skin thickness measured by sonography could predict SNAP-A. CONCLUSIONS: This study demonstrates that among physiological factors of sex, height, BMI and also finger size measures, skin thickness is the best predictor of SNAP-A. SIGNIFICANCE: In clinical practice, this effect must be taken into account when making determination of abnormality based on sensory nerve amplitude.

Neurally augmented sexual function.

Neurally Augmented Sexual Function (NASF) is a technique utilizing epidural electrodes to restore and improve sexual function. Orgasmic dysfunction is common in adult women, affecting roughly one quarter of populations studied. Many male patients suffering from erectile dysfunction are not candidates for phosphdiesterase therapy due to concomitant nitrate therapy. Positioning the electrodes at roughly the level of the cauda equina allows for stimulation of somatic efferents and afferents as well as modifying sympathetic and parasympathetic activity. Our series of women treated by NASF is described. Our experience shows that the evaluation of potential candidates for both correctable causes and psychological screening are important considerations.

Stress reverses plasticity in the pathway projecting from the ventromedial prefrontal cortex to the basolateral amygdala.

We have previously shown that high-frequency stimulation to the basolateral amygdala (BLA) induces long-term potentiation (LTP) in the ventromedial prefrontal cortex (vmPFC) and that prior exposure to inescapable stress inhibits the induction of LTP in this pathway [Maroun & Richter-Levin (2003)J. Neurosci., 23, 4406-4409]. Here, we show that the reciprocal pathway projecting from the vmPFC to the BLA is resistant to the induction of LTP. Conversely, long-term depression (LTD) is robustly induced in the BLA in response to low-frequency stimulation to the vmPFC. Furthermore, prior exposure to inescapable stress reverses plasticity in this pathway, resulting in the promotion of LTP and the inhibition of LTD. Our findings suggest that, under normal and safe conditions, the vmPFC is unable to exert excitatory synaptic plasticity over the BLA; rather, LTD, which encodes memory of safety in the BLA, is favoured. Following stressful experiences, LTP in the BLA is promoted to encode memory of fear.

The cortically evoked secondary depolarization affects the integrative properties of thalamic reticular neurons.

Corticothalamic terminals on thalamic reticular (RE) neurons account for most synapses from afferent pathways onto this nucleus and these inputs are more powerful than those from axon collaterals of thalamocortical neurons. Given the supremacy of cortical inputs, we analysed here the characteristics and possible mechanisms underlying a secondary component of the cortically elicited depolarization in RE neurons, recorded in cats under barbiturate anesthesia. Electrical stimulation of corticothalamic axons in the internal capsule evoked fixed and short-latency excitatory postsynaptic potentials (EPSPs) that, by increasing stimulation intensity and at hyperpolarized levels (< -70 mV), developed into low-threshold spikes and spindle oscillations. The threshold for spindle oscillations was 60% higher than that required for evoking minimal EPSPs. The evoked EPSPs included a secondary depolarizing component, which appeared approximately 5 ms after the peak of the initial component and was voltage dependent, i.e. most prominent between -70 mV and -85 mV, while being greatly reduced or absent at more hyperpolarized levels. The secondary depolarizing component was sensitive to QX-314 in the recording micropipette. We suggest that the secondary component of cortically evoked EPSPs in RE neurons is due to the dendritic activation of T-currents, with a probable contribution of the persistent Na+ current. This late component affected the integrative properties of RE neurons, including their spiking output and temporal summation of incoming cortical inputs.

Descending modulation of pain.

Although interest in descending modulation of spinal cord function dates back to the time of Sherrington, the modern era began in the late 1960s when it was shown that focal electrical stimulation in the midbrain of the rat produced analgesia sufficient to permit surgery. From this report evolved the concept of endogenous systems of pain modulation. Initial interest focused on descending inhibition of spinal nociceptive processing, but we now know that descending modulation of spinal nociceptive processing can be either inhibitory or facilitatory. As our understanding of descending facilitatory, or pro-nociceptive influences grows, so too has our appreciation of its potential importance. Accumulating evidence suggests that descending facilitatory influences may contribute to the development and maintenance of hyperalgesia and thus contribute to chronic pain states.

Repetitive transcranial magnetic stimulation improves open field locomotor recovery after low but not high thoracic spinal cord compression-injury in adult rats.

Electromagnetic fields are able to promote axonal regeneration in vitro and in vivo. Repetitive transcranial magnetic stimulation (rTMS) is used routinely in neuropsychiatric conditions and as an atraumatic method to activate descending motor pathways. After spinal cord injury, these pathways are disconnected from the spinal locomotor generator, resulting in most of the functional deficit. We have applied daily 10 Hz rTMS for 8 weeks immediately after an incomplete high (T4-5; n = 5) or low (T10-11; n = 6) thoracic closed spinal cord compression-injury in adult rats, using 6 high- and 6 low-lesioned non-stimulated animals as controls. Functional recovery of hindlimbs was assessed using the BBB locomotor rating scale. In the control group, the BBB score was significantly better from the 7th week post-injury in animals lesioned at T4-5 compared to those lesioned at T10-11. rTMS significantly improved locomotor recovery in T10-11-injured rats, but not in rats with a high thoracic injury. In rTMS-treated rats, there was significant positive correlation between final BBB score and grey matter density of serotonergic fibres in the spinal segment just caudal to the lesion. We propose that low thoracic lesions produce a greater functional deficit because they interfere with the locomotor centre and that rTMS is beneficial in such lesions because it activates this central pattern generator, presumably via descending serotonin pathways. The benefits of rTMS shown here suggest strongly that this non-invasive intervention strategy merits consideration for clinical trials in human paraplegics with low spinal cord lesions.

Both dorsal and ventral spinal cord pathways contribute to overground locomotion in the adult rat.

Identification of long tracts responsible for spontaneous locomotion is critical for spinal cord injury (SCI) repair strategies. We recently demonstrated that extensive demyelination of adult rat thoracic ventral columns, ventromedial, and ventrolateral white matter produces persistent, significant open-field hindlimb locomotor deficits. Locomotor movements resulting from stimulation of the pontomedullary locomotor region are inhibited by dorsolateral funiculus (DLF) lesions suggesting that important pathways for locomotion may also exist in the dorsal white matter. However, dorsal hemisections that interrupt dorsal columns/dorsal corticospinal tract (DC/CST) and DLF pathways do not produce persistent, severe locomotor deficits in the adult rat. We studied the contributions of myelinated tracts in the DLF and DC/CST to overground locomotion following complete conduction blockade of axons in the ventrolateral funiculus (VLF), a region important for locomotor movements and for transcranial magnetic motor-evoked potentials (tcMMEP). Animals received ethidium bromide plus photon irradiation to produce discrete demyelinating lesions sufficient to stop axonal conduction in the VLF, combined VLF + DLF, or combined VLF + DC/CST. Open-field BBB scores and tcMMEPs were studied at 1, 2, 3, and 4 weeks postlesion. VLF lesions resulted in mean BBB scores of 17 at 4 weeks. VLF + DC/CST and VLF + DLF lesions resulted in mean BBB scores of 15.9 and 11.1, respectively. TcMMEPs were absent in all lesion types confirming VLF conduction blockade throughout the study. Our data indicate that significant contributions to locomotion from myelinated pathways within the rat DLF can be revealed when combined with simultaneous compromise of the VLF.

Serotonin sets the day state in the neurons that control coupling between the optic lobe circadian pacemakers in the cricket Gryllus bimaculatus.

The bilaterally paired optic lobe circadian pacemakers of the cricket Gryllus bimaculatus mutually exchange photic and circadian information to keep their activity synchronized. The information is mediated by a neural pathway, consisting of the so-called medulla bilateral neurons, connecting the medulla areas of the two optic lobes. We investigated the effects of serotonin on the neural activity in this coupling pathway. Spontaneous and light-induced electrical activity of the neurons in the coupling pathway showed daily variations, being more intense during the night than the day. Microinjection of serotonin or a serotonin-receptor agonist, quipazine, into the optic lobe caused a dose- and time-dependent inhibition of spontaneous and light-induced responses, mimicking the day state. The amount of suppression was greater and the recovery from the suppression occurred faster during the night. Application of metergoline, a non-selective serotonin-receptor antagonist, increased spontaneous activity and light-evoked responses during both the day and the night, with higher effect during the day. In addition, metergoline effectively attenuated the effects of serotonin. These facts suggest that in the cricket's optic lobe, serotonin is released during the daytime and sets the day state in the neurons regulating coupling between the bilaterally paired optic lobe circadian pacemakers.

[Biological action of electromagnetic fields of 4 MHz decametric waves]. / Biologicheskoe deistvie élektromagnitnogo polia dekametrovykh voln chastotoi 4MHz.

Exposure to the amplitude-modulated electromagnetic field, 4 MHZ, 400, 200, and 100 V/m over two months for 16 hours a day was found out to bring low the adaptation potential of a number of bodily physiological systems in animals (non-linebred rats). Changes in the brain functional activity, cell-bound, and humoral immunity were ascertained to be the structural-and-functional basis of reorganization of physiological prosesses.