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Biomedical subjects

R Drucker-Colin

Publications and source records attributed to R Drucker-Colin.

11 recordsLinked to original sources

Normal prism adaptation but reduced after-effect in basal ganglia disorders using a throwing task.

Prism adaptation is a form of visuomotor learning in which the visual and motor systems need to be adjusted because a visual perturbation is produced by horizontally displacing prisms. Despite being known for over two centuries, the neuronal substrates of this phenomenon are not yet completely understood. In this article the possible role of the basal ganglia in this kind of learning was analysed through a study of Huntington's and Parkinson's disease patients. A throwing technique requiring the use of open loop feedback was used. The variables analysed were visuomotor performance, adaptation rate and magnitude, and the after-effect. The results clearly showed that both Huntington's and Parkinson's disease groups learned at the same rate as control subjects. In addition, despite having a disturbed visuomotor performance, both experimental groups showed the same adaptation magnitude as the control group. Finally, the after-effect, which is measured after removing the prisms, is reduced in both patients groups. This reduction leads to a disruption in the normal adaptation-after-effect correlation found in normal volunteers. These results suggest that basal ganglia are not involved in this type of open-looped visuomotor learning. The large number of patients studied as well as the similarity of the findings between both populations support this hypothesis. By contrast, there is an impairment in the after-effect on both basal ganglia patient populations. This impairment may be the result of the deterioration of the perceptual recalibration process involved in visuomotor learning.

Adaptation, Ocular↗

Cortistatin modulates memory processes in rats.

Cortistatin (CST) is a recently described neuropeptide with high structural homology with somatostatin. Its mRNA is restricted to gamma amino butyric acid (GABA)-containing cells in the cerebral cortex and hippocampus. CST modulates the electrophysiology of the hippocampus and cerebral cortex of rats; hence, it may be modulating mnemonic processes. In this study, we have evaluated the effect of CST and somatostatin (SS) on short- and long-term memory (STM and LTM, respectively), as well as on the extinction of the behavior by using the footshock passive avoidance behavioral test. In addition, we tested the ability of both neuropeptides to affect the generation of cAMP in hippocampal neurons in culture. Results showed that the administration of either CST or SS into the hippocampal CA1 deteriorates memory consolidation in a dose-response fashion and facilitates the extinction of the learned behavior. CST was more potent than SS. Likewise, CST increases cAMP while SS decreases it. These results strongly support a modulatory role for CST in memory processes.

Animals↗

Determination of dopamine-releasing protein (DARP) in cerebrospinal fluid of patients with neurological disorders.

Levels of DARP in the cerebrospinal fluid (CSF) of patients having a wide variety of neurological disorders were determined. Neurological disorders were categorized as degenerative, demyelinating, epilepsy, trauma, hydrocephalia, inflammatory, A-V malformation, CNS neoplasia, parasitic and stroke. DARP levels were determined by an enzyme-linked immunoabsorbent assay (ELISA) using monoclonal anti-DARP antibodies. A synthetic peptide corresponding to the first 36 aa of the N-terminal of DARP was used as standard. A total of 7 non-neurological patients and 73 patients with neurological disorders were tested. The relative concentrations of DARP decreased in patients with Parkinson's diseases vs. patients with non-neurological diseases and increased in other neuropathologies such as demyelinating, hydrocephalia and A-V malformations. Data obtained suggest that changes in the percentage and concentration of DARP may correlate with certain neurological disorders, showing particularly low levels in Parkinson's disease patients.

Female↗

Congenital facial palsy and crossed facial nerve grafts: age and outcome.

Crossed facial nerve grafts for treating unilateral permanent facial palsy in association with hemifacial microsomia were studied in 18 patients, ages ranging from 2 months to 10 years. Patients were divided into groups according to the age at the time of indication of surgery. It is concluded that crossed nerve grafting for facial palsy associated with hemifacial microsomia appears to be an adequate procedure especially when the surgery is indicated soon after birth.

Child↗

Recovery of congenital facial palsy in patients with hemifacial microsomia subjected to sural to facial nerve grafts is enhanced by electric field stimulation.

The effect of electric field stimulation for promoting axonal growth between sural to facial nerve grafts in cases of congenital permanent facial palsy associated with hemifacial microsomia was studied. For this purpose, a total of 17 patients with unilateral congenital permanent facial palsy associated with hemifacial microsomia were studied pre- and post-operatively. A sural to facial nerve graft was performed in all cases and long term postoperative electric field stimulation was randomly applied to half of the patients. Although improvement occurred in both groups, the results indicated that clinical and electrophysiological recovery was significantly better in patients receiving post-operative electric field stimulation. The results, therefore, suggest that electric stimulation of the grafted area induces improvements of facial palsy over and above those observed in the non-stimulated patients.

Axons↗

Early postnatal treatment of congenital facial palsy in patients with hemifacial microsomia.

Facial palsy associated with hemifacial microsomia results in a devastating deformity. To date, no attempts on early treatment of the associated facial palsy have been reported. A therapeutic approach may be to provide reinnervation to the affected muscles through a crossed facial nerve graft. The purpose of this paper is to present 8 cases of hemifacial microsomia with associated facial palsy. All these patients were treated before 1 year of age with cross-sural-to-facial nerve grafts. After a 1 year follow-up, clinical and electrodiagnostic results indicate axonal continuity through the graft and evidence of reinnervation activity in all patients. Crossed facial nerve grafting appears to be an adequate procedure in patients with hemifacial microsomia with associated facial palsy.

Action Potentials↗

Effects of biperiden on sleep at baseline and after 72 h of REM sleep deprivation in the cat.

We examined the effects of the muscarinic M1 antagonist biperiden in cats. In the first experiment a dose-response analysis was performed with intraventricular injection (IV ventricle) of biperiden. In the second experiment after REM sleep deprivation cats were injected with either biperiden (0.1 mg/kg) or saline. Biperiden produced a reduction in REM sleep percentage and an increase in REM sleep latency with these high doses. The 0.1 mg/kg biperiden dose, which did not suppress REM sleep at baseline, did reduce the REM sleep rebound. The present study suggests a modulatory role of biperiden on REM sleep regulatory processes. The fact that an effect of biperiden is noted only at the high doses suggests that at these doses the drug is influencing non-M1 receptors. Changes in the sensitivity of these receptors as a result of REM sleep deprivation might explain why a dose of biperiden will reduce REM sleep rebound, while being ineffective in suppressing REM sleep at baseline.

Animals↗

Effects of auditory stimulation during rapid eye movement sleep in healthy volunteers and depressed patients.

Auditory and somesthesic forms of stimulation have substantially increased rapid eye movement (REM) sleep in cats. We investigated whether auditory stimulation, applied during REM sleep or outside REM sleep, would have similar effects in normal volunteers. We also administered auditory stimulation to depressed patients during REM sleep. Subjects were studied during 1 acclimatization night, 2 baseline nights, 4 consecutive nights with auditory stimulation, and 1 followup night without auditory stimulation. Normal volunteers were randomly divided into Group R, which received auditory stimulation during each REM sleep episode, and Group NR, which received auditory stimulation at the end of each REM sleep episode. Depressed patients (Group D) received auditory stimulation during each REM sleep period. Only Group R showed increased REM sleep time during the nights of auditory stimulation and throughout the followup night. This group also increased their sleep efficiency. Group NR showed reduced sleep efficiency due to an increase in both the duration and frequency of awakenings. Group D did not show increased REM sleep time, but did show shortened REM sleep episodes, increased REM sleep frequency, and increased duration of awakenings. Group D did not show clinical changes.

Acoustic Stimulation↗

Vasoactive intestinal polypeptide (VIP) and cerebrospinal fluid (CSF) of sleep-deprived cats restores REM sleep in insomniac recipients.

In the past few years a steadily increasing number of substances have been suggested to qualify as sleep-inducing factors. Most 'sleep factors' appear to exert their effects on slow-wave sleep. Recently, however, it has been shown that the cerebrospinal fluid (CSF) of sleep-deprived cats may contain a rapid eye movement (REM) sleep factor, and that vasoactive intestinal peptide (VIP) may be a specific REM sleep inducer. The purpose of this study is to determine whether the CSF of sleep-deprived cats and VIP can reverse insomnia produced by parachlorophenylalanine (PCPA). Donor cats were sleep-deprived for 24 h and their CSF extracted. Some donor cats were additionally pre-treated with chloramphenicol, and some extracted CSF was heated. Recipient cats were injected with 400 mg/kg i.p. of PCPA on two consecutive days. Twenty-four h after the second injection, the recipient cats were intraventricularly injected with a 100-microliters of the various CSF types or 200 ng of VIP. The results showed that only CSF from sleep-deprived cats and VIP were capable of restoring REM sleep in the otherwise PCPA insomniac cats. Since the return of REM sleep was through an increase in its frequency, it is suggested that the CSF of sleep-deprived cats contains a VIP-like sleep factor possibly involved in triggering REM sleep.

Animals↗

Reversal of rapid eye movement sleep without atonia by chloramphenicol.

Bilateral pontine tegmental lesions produce in cats the phenomenon known as rapid eye movement (REM) sleep without atonia. During episodes of REM sleep without atonia cats are capable of exhibiting such complex behaviors as head-raising, body-righting, standing, and in some cases, walking and attacking. Since release of such behaviors implies disinhibition of specific motor systems, the purpose of this study was to determine whether the administration of chloramphenicol (CAP), which is known to attenuate the firing frequencies of cells that become activated during REM and motor activity, could reverse this phenomenon. Cats with dorsolateral tegmental pontine (DLTP) lesions producing REM without atonia were thoroughly studied in terms of the muscular and behavioral activity they displayed during REM before and after systemic CAP administration. Thiamphenicol (TAP), a CAP analogue that does not reduce neuronal firing frequency during REM sleep, was used as a control drug. The results of these experiments showed that CAP but not TAP induced a return of the atonia during REM sleep. It is suggested that the return of atonia induced by CAP in DLPT lesioned cats is caused by attenuation in the activity of medial reticular neurons which have somatotopical representation. Such cells, which have high levels of activity during REM sleep and motor activation is wakefulness, are normally overwhelmed by the inhibitory mechanism of the atonia of REM. The return of atonia and consequent reduction in complex behavior following CAP administration may be due to withdrawal of the excitatory influence of these neurons.

Animals↗