Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronal populations projecting to a common target may compete for neurotrophic substances. To determine if competition impairs target reinnervation, we examined the effect of capsaicin-induced sensory denervation on sympathetic nerve ingrowth to the sympathectomized rat superior tarsal smooth muscle. In tarsal muscles with intact sympathetic innervation, capsaicin injection on Day 2 reduced numbers of perimuscular CGRP-ir sensory nerves by 68% at 3-4 months; however, it did not alter dopamine-beta-hydroxylase-ir nerve density, response to nerve stimulation, or tarsal muscle adrenoceptor-mediated contraction. Tarsal muscles denervated by ipsilateral superior cervical ganglionectomy on Postnatal Day 4 were partially reinnervated by fibers from the contralateral ganglion, as noted in previous studies. Sensory denervation by capsaicin improved sympathetic reinnervation, as evidenced by a 174% increase in numbers of DBH-ir nerves and a 62% increase in neurally mediated smooth muscle contraction evoked by electrical stimulation of the contralateral pathway relative to reinnervated muscles of vehicle-injected rats; smooth muscle function was also influenced, as indicated by a decrease toward normal in adrenoceptor sensitivity. Tarsal muscles denervated at 30 days were not reinnervated in either vehicle-injected or capsaicin-treated rats, indicating that sensory denervation does not extend the developmental window during which contralateral reinnervation can occur. Both the vehicle-injected and capsaicin-treated preparations with sustained juvenile sympathectomy showed sensory hyperinnervation as adults; thus, a chronic reduction in competition from sympathetics is a sufficiently powerful stimulus to overcome the decreased nerve density induced by neonatal capsaicin treatment. We conclude that sensory nerves limit the extent of sympathetic reinnervation and functional recovery that can occur following neonatal sympathetic denervation.
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PMID:Sensory nerves impair sympathetic reinnervation and recovery of smooth muscle function. 139 80

Following axotomy, the regrowth of peripheral axons takes longer in older individuals than in young ones. The present study compares central responses of facial motor neurons to a crush injury of the facial nerve in 3-month-old and 15-month-old male rats sampled through 28 days post-crush (dpc). Neuronal somata, nuclei, and nucleoli were measured in 30 microns brain stem sections within subdivisions of the facial nucleus that contain the cell bodies responsible for the movement of the vibrissae. The temporal patterns of change in the size of the three structures were interpreted with reference to the re-establishment of functional connections, i.e., the return of voluntary vibrissae activity, which is delayed by 4 days in the older animals relative to the younger ones. There was no age-related difference in the pattern of somal swelling and recovery, nor was there an age-related difference in the response of nuclei and nucleoli to axotomy through 4 dpc. Both nuclei and nucleoli increased in size in animals of both age groups, but after 4 dpc in the older animals nuclear enlargement was prolonged and the nucleolar increases were less robust compared to the younger animals. The greatest age difference appeared with the re-establishment of functional connections. In the 3-month-old animals, the resumption of whisker activity coincided with vigorous transient increases in the sizes of nuclei and nucleoli; in the 15-month-old animals, there was little nuclear response to functional recovery and a comparatively small increase in nuclear sizes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of advancing age on the central response of rat facial neurons to axotomy: light microscope morphometry. 224 Jun 13

The potentials of postischemic functional recovery were studied in cats submitted to 1 h of complete cerebrocirculatory arrest in normothermia. Neuronal activity was estimated by recording the electroencephalogram (EEG), the pyramidal response following stimulation of the motor cortex and the somatosensorily evoked cortical potentials. During ischemia EEG was suppressed within 12-15 s, evoked potentials within 2 min, and the pyramidal response within 5 min. After recirculation following ischemia, the electrically evoked D wave of the pyramidal response began to reappear between 7 and 9 min and the synaptically evoked I wave between 25 and 60 min. The evoked cortical potentials returned in parallel with the I wave of the pyramidal response but control amplitude was not reached before 3 h. The peak latencies of the evoked potentials were consistently prolonged for at least 24 h but normalized after a few days, provided secondary postischemic circulatory disturbances could be prevented. EEG began to recover after the beginning appearance of the somatosensorily evoked cortical potentials; initially it exhibited a burst-suppression pattern but it gradually progressed to continuous activity. The frequency pattern of the EEG normalized within 24 h and the amplitude after a few days. After recovery, the behavior of the pyramidal response and of evoked potentials to repetitive stimulation was the same as under control conditions.
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PMID:Recovery of neuronal transmission after prolonged cerebral ischemia. 282 Aug 49

Phylogenetically "lower" species in some cases use different biological strategies for recovery after injury to the CNS than do "higher" species. One approach that we have taken in our laboratory has been to study the mechanisms of functional recovery of the CNS after injury in those vertebrate species where recovery does occur. The present report reviews recent studies on a model system, the spinal electromotor system of the gymnotiform teleost Sternarchus albifrons, which exhibits regeneration and neurogenesis after injury. Regeneration in this system leads to a recapitulation of relatively normal morphologic structure by the damaged or extirpated spinal cord. In Sternarchus, new spinal cord is generated from ependymal cells; some ependymal cells in the adult remain pluripotent and retain the capability to generate new neurons. The Sternarchus spinal cord thus represents an especially useful model for the study of neurogenesis after injury to the CNS. Recent studies in our laboratory indicate that neurogenesis in adult Sternarchus spinal cord tissue occurs both in vivo and in vitro. Neurogenesis has been demonstrated by incorporation of tritiated thymidine into explant cultures from the spinal cord of adult Sternarchus. Autoradiography reveals the presence of thymidine-labeled neurons. Neuronal identity of 3H-labeled cells has been confirmed by positive staining with neuron-specific monoclonal antibodies. Thymidine labeling occurs in cultured neurons derived from both normal (histologically and functionally mature) and regenerating spinal cord of adult Sternarchus albifrons. These results provide evidence that some cells in spinal cord of adult Sternarchus retain the ability to incorporate thymidine and undergo neuronal differentiation in vitro. This system provides a new model in which neurogenesis from adult tissue can be studied in vivo and in vitro.
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PMID:Neurogenesis in adult vertebrate spinal cord in situ and in vitro: a new model system. 391 65

After partial deafferentation of one of the hindlimbs changes of the cord dorsal potential and mass discharge from the anterior-lateral filament of the exposed spinal cord were studied after maximal recovery of function of the deafferented limb in adult cats. Neuronal activity in response to electrical stimulation of the dorsal roots was considerably higher on the deafferented side than on the intact one. This seems to be due to plastic properties of the c. n. s. responsible for the recovery of functions.
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PMID:[Plastic changes in the sensory elements of the spinal cord after decreasing the afferent inflow]. 718 55

Mid-thoracic spinal cord transection produces dramatically different behavioral results depending upon a rat's age at the time of surgery. The present study was initiated to determine whether the synaptic development in the gray matter of the normal, developing spinal cord differs before and after the period when maximal behavioral recovery occurs. The L6 segments from 10 groups of animals, 0--30 days of age, taken at 3 day intervals (4 animals/group) were studied by light microscopy. Areal measurements of the gray matter were made using an integrating x-y tablet interfaced to a computer. Cell size, cell density and area of neuropil were evaluated in the lateral portions of the intermediate gray matter, laminae VI and VII. Electron microscopic analyses of synaptogenesis were performed on material from the same region in animals 3, 12, 15, 21 and 30 days old using similar morphometric methods while taking note of vesicle, junctional, and mitochondrial morphology. A 60% increase in area of neuropil paralleled a linear increase, of comparable magnitude, in area of the gray matter until 15 days of age when both curves reached plateau. Neuronal perikaryal size remained constant (congruent to 200 sq. microns in plane of nucleolus) throughout development and so could not have contributed to the increase in area of gray matter. Areal measurements of the size and counts of the number of vesicle containing profiles demonstrated a 50% increase in density of axon terminals between 3 and 12 days of age and a steady decline thereafter. The size of vesicle-containing profiles in laminae VI and VII remained constant at a small value (congruent to 0.35 sq microns) until 12 days of age, showed rapid growth to 0.54 sq. microns between 12 and 15 days of age, followed by a more moderate increase in sectional area after 15 days. These results suggest that during the period when recovery of function follows spinal injury, synaptogenesis in the intermediate gray region of the lumbar spinal cord proceeds rapidly, while at stages when little recovery of function follows spinal transection, synaptogenesis is essentially complete.
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PMID:Synaptogenesis in the intermediate gray region of the lumbar spinal cord in the postnatal rat. 735 75

Short peptide sequences of ACTH 1-39 (the ACTH 4-9 analog Org 2766, ACTH 4-10 and its analog BIM 22015, and ACTH 1-13 [alpha-MSH]), which do not stimulate the adrenal cortex, have profound effects on the developing and regenerating neuromuscular system, in neonatal and in adult rats. Both development and regeneration are accelerated, as indicated by improved morphological, electrophysiological, behavioral and biochemical parameters. Regeneration in the central nervous system is problematic but the ACTH peptides may provide protection for CNS neurons, enhance denervation sensitivity or permit compensatory processes which facilitate functional recovery. Neuronal cells in culture respond to ACTH peptides by greater neurite outgrowth, and in some cell types, by increased B-50 expression. In all cases, susceptibility to ACTH peptide treatment varies with cell type, age, the specific peptide administered, its dosage and pattern of administration. External stress and the gender of the animal are additional factors that interact with the neurotrophic actions of the melanocortins.
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PMID:Non-corticotropic ACTH peptides modulate nerve development and regeneration. 827 76

Neuronal connections and cortical maps are continuously remodeled by our experience. Knowledge of the potential capabilityof the brain to compensate for lesions is a prerequisite for optimal stroke rehabilitation strategies. Experimental focal cortical lesions induce changes in adjacent cortex and in the contralateral hemisphere. Neuroimaging studies in stroke patients indicate altered poststroke activation patterns, which suggest some functional reorganization. To what extent functional imaging data correspond to outcome data needs to be evaluated. Reorganization may be the principle process responsible for recovery of function after stroke, but what are the limits, and to what extent can postischemic intervention facilitate such changes? Postoperative housing of animals in an enriched environment can significantly enhance functional outcome and can also interact with other interventions, including neocortical grafting. What role will neuronal progenitor cells play in future rehabilitation-stimulated in situ or as neural replacement? And what is the future for blocking neural growth inhibitory factors? Better knowledge of postischemic molecular and neurophysiological events, and close interaction between basic and applied research, will hopefully enable us to design rehabilitation strategies based on neurobiological principles in a not-too-distant future.
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PMID:Brain plasticity and stroke rehabilitation. The Willis lecture. 1062 41

Injury to the central nervous system is the leading cause of disability in the United States. Neuronal death is one of the causes of disability. Among patients who survive this type of injury, various degrees of recovery in brain function are observed. The molecular basis of functional recovery is poorly understood. Clinical observations and research using experimental injury models have implicated several metabolites in the cascade of events that lead to neuronal degeneration. The levels of intracellular ATP (energy source) and pH are decreased, whereas levels of extracellular glutamate, intracellular calcium ions, and oxidative damage to RNA/DNA, protein, and lipid are increased. These initiating events can be associated with energy failure and mitochondrial dysfunction, resulting in functional or structural brain damage. The injured brain is known to express immediate early genes. Recent studies show that reactive oxygen species (ROS) cause lesions in genes from which mRNA is transcribed as part of the endogenous neuroprotective response. Although degenerating proteins and lipids may contribute to necrosis significantly after severe injury, abnormalities in genetic material, if not repaired, disturb cellular function at every level by affecting replication, transcription, and translation. These lesions include abnormal nucleic acids, known as oxidative lesions of DNA (ODLs) or of RNA (ORLs). In this review, we focus on our current understanding of the various effects of neuronal nitric oxide synthase on the formation of modified bases in DNA and RNA that are induced in the brain after injury, and how ODLs and ORLs affect cell function.
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PMID:The association between neuronal nitric oxide synthase and neuronal sensitivity in the brain after brain injury. 1207 78

Gap junctions are intercellular channels which directly connect the cytoplasm between neighboring cells. In the central nervous system (CNS) various kinds of cells are coupled by gap junctions, which play an important role in maintaining normal function. Neuronal gap junctions are involved in electrical coupling and may also contribute to the recovery of function after cell injury. Astrocytes are involved in the pathology of most neuronal disorders, including brain ischemia, Alzheimer's disease and epilepsy. In the pathology of brain tumors, gap junctions may be related to the degree of malignancy and metastasis. However, the role of connexins, gap junctions and hemichannels in the pathology of the diseases in the CNS is still ambiguous. Of increasing importance is the unraveling of the function of gap junctions in the neural cell network, involving neurons, astrocytes, microglia and oligodendrocytes. A better understanding of the role of gap junctions may contribute to the development of new therapeutic approaches to treating diseases of the CNS.
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PMID:Gap junctions and neurological disorders of the central nervous system. 1503 85


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