Abnormalities of somatosensory evoked potentials in the quinolinic acid model of Huntington's disease: evidence that basal ganglia modulate sensory cortical input.

Intrastriatal injection of quinolinic acid (QA) in rats provides an animal model that mimics some of the neuropathological and neurochemical alterations observed in the striatum of patients with Huntington's disease (HD). One of the very early neurophysiological signs in HD is a diminution of amplitude of early somatosensory evoked potentials (SEPs) recorded over the parietal cortex. The present study investigated whether the QA model exhibits similar neurophysiological abnormalities. Two weeks after unilateral intrastriatal injection of QA (240 nmol) or of the solvent, early SEPs were recorded with chronically implanted electrodes from the somatosensory cortex or from the ventrobasal nucleus of the thalamus of lightly pentobarbital-anesthetized rats, in response to single-shock electrical stimulation of the contralateral forepaw. Whereas intrastriatal injection of solvent did not influence SEPs, the striatal QA lesion significantly reduced the amplitude of early cortical SEPs by about 40% without affecting the latency. SEPs recorded from the ventrobasal nucleus were unchanged after QA lesion. Histological examination and glial fibrillary acid protein staining after intrastriatal injection of QA revealed no evidence for damage in the somatosensory system. It is concluded that (1) the QA animal model of HD mimics some of the SEP abnormalities of patients, and (2) a striatal lesion modulates somatosensory transmission to the cortex in rats.     

Immunocytochemistry of B-50 (GAP-43) in the spinal cord and in dorsal root ganglia of the adult cat

Summary The distribution of the neural-specific growth associated protein B-50 (GAP-43), which persists in the mature spinal cord and dorsal root ganglia, has been studied by light and electron microscopic immunohistochemistry in the cat. Throughout the spinal cord, B-50 immunoreactivity was seen confined to the neuropil, whereas neuronal cell bodies were unreactive. The most conspicuous immunostaining was observed in the dorsal horn, where it gradually decreased from superficial laminae (I–II) toward more ventral laminae (III–V), and in the central portion of the intermediate gray (mainly lamina X). In these regions, the labelling was localized within unmyelinated, small diameter nerve fibres and axon terminals. In the rest of the intermediate zone (laminae VI–VIII), B-50 immunoreactivity was virtually absent. The intermediolateral nucleus in the thoracic and cranial lumbar cord showed a circumscribed intense B-50 immunoreactivity brought about by the labelling of many axon terminals on preganglionic sympathetic neurons. In motor nuclei of the ventral horn (lamina IX), low levels of B-50 immunoreactivity were present in a few axon terminals on dendritic and somal profiles of motoneurons. In dorsal root ganglia, B-50 immunoreactivity was mainly localized in the cell bodies of small and medium-sized sensory neurons. The selective distribution of persisting B-50 immunoreactivity in the mature cat throughout sensory, motor, and autonomie areas of the spinal cord and in dorsal root ganglia suggests that B-50-positive systems retain in adult life the capacity for structural and functional plasticity.     

Rapid appearance of β-amyloid precursor protein immunoreactivity in glial cells follwing excitotoxic brain injury

Clinical and experimental data have indicated an up-regulation of amyloid precursor protein (APP) after various types of CNS injury. In the present study the cellular source of lesion-induced APP has been investigated an a neurotoxic CNS model. Quinolinic acid injection into the striatum results in neuronal degeneration, while glial cells survive. APP immunoreactivity was detected in glial cells starting at postoperative day 3 and persisted until day 21, the last time point studied. Double immunocytochemistry identified the majority of APP-immunoreactive cells as glial fibrillary acidic protein-immunoreactive astrocytes. There was no evidence of amyloid fibril deposition during this time. It is concluded that following excitotoxic neuronal degneration APP is mainly produced by reactive astrocytes in the lesioned area.     

New perspectives in neurotrauma research

Traumatic brain and spinal cord injuries are severe burdens for the patients, their relatives, the health care providers and society as a whole. Recent data demonstrate the magnitude of the problem: It is mostly a disease of the young gen-eration (age 20-45 years) with mortality rates for severe traumatic brain injury (TBI) between 40-50%. In approximately 60% of cases, multiple trauma is accompanied by head injury. The outcome of TBI is determined not only by the extent and severity of the primary insult, but also by the degree of secondary brain damage. In the subgroup of severe TBI (GCS相似文献   

Long-Term Stability at ?20°C of Aspergillus Galactomannan in Serum and Bronchoalveolar Lavage Specimens

Research to develop and validate novel methods for diagnosis of aspergillosis based on detection of galactomannan requires the use of clinical specimens that have been stored frozen. Data indicating that galactomannan remains stable when frozen are scant. The objective of this study was to determine the stability of galactomannan in clinical specimens stored at −20°C that were positive in the Platelia Aspergillus enzyme immunoassay when initially tested. Prospective real-time testing of serum and bronchoalveolar lavage (BAL) fluid pools from positive and negative patient specimens showed no decline in galactomannan index (GMI) over 11 months at −20°C and no development of positive reactions in the negative-control pool. Retrospective testing of positive specimens that had been stored at −20°C for 5 years showed that 28 of 30 serum (n = 15) or BAL (n = 15) specimens remained positive. These findings support the use of frozen serum or BAL specimens stored for at least 5 years in evaluation of diagnostic tests based on detection of galactomannan.     

Disinhibition der Extensor-Motoneurone nach intercolliculärer Dezerebrierung

Zusammenfassung Trotz kontinuierlicher Anaesthesie und Unterbrechung der Gamma-Spindelschleife löst die natürliche oder elektrische Reizung homonymer Ia-Afferenzen mit konstanter Stärke nach intercolliculärer Dezerebrierung an Extensor-Motoneuronen regelmäßigere Antworten, Verkürzung der Reflexzeit, Zunahme der Entladungsfrequenz, Verstärkung der post-tetanischen Potenzierung und Rekrutierung aus. Da der Grad der recurrenten Hemmung abnimmt, schließen wir, daß die gesteigerte Erregbarkeit der Extensor-Motoneurone im Zustand der Dezerebrierung mit Disinhibition verbunden ist. Die mit einem konstanten Quantum reflexwirksamer Afferenzen erhaltenen Resultate sprechen für unsere Annahme, daß Spastizität nicht hauptsächlich auf fusimotorischer Enthemmung beruht.

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Disinhibition of extensor motoneurones after intercollicular decerebration

Summary Even with continued anesthesia and interrupted gamma-loop intercollicular decerebration leads in extensor motoneurones (excited by electrical or natural stimulation of homonymous Ia-afferents with constant strength) to the following phenomona: more regular responses, shortening of reflex time, increase of discharge frequency, enhancement of post-tetanic potentiation, and recruitment. Because the degree of recurrent inhibition is diminished we conclude that the higher excitability of extensor motoneurones in the decerebrate state is correlated with disinhibition. Furthermore the results obtained with the afferent input for motoneurones kept constant favour our assumption that spasticity is not based merely on the release of fusimotor activity.