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PubMed1995

Axonal growth and fasciculation linked to differential expression of BDNF and NT3 receptors in developing cerebellar granule cells.

In the developing cerebellum, young granule neurons in the external germinal layer respond preferentially to BDNF, while mature neurons within the inner portion of the cerebellum respond preferentially to NT3. Here we show that this anatomic distinction reflects a developmentally regulated switch at the level of neurotrophin receptor gene expression. The salient feature of the developmental switch is a change in the ration of mRNA transcripts encoding functional BDNF and NT3 receptor tyrosine kinases. The ratio of the BDNF receptor trkB to the NT3 receptor trkC reverses from 5:1 in neonatal cerebellum to 1:3 in adult cerebellum. TrkB and TrkC are closely related transmembrane tyrosine protein kinases. However, activation of BDNF and NT3 receptors in cerebellar granule neurons do not give equivalent biological responses. In aggregate cell culture and single cell assays, BDNF enhances axonal outgrowth of early granule cells by influencing neurite elongation. In contrast, NT3 alters the morphology of outgrowth. Collectively, these findings suggest that regulation of neurotrophin receptors during cerebellar development is important for the timing and morphology of axonal growth.

Animals↗
PubMed1979

Bedside evaluation of large motor units in childhood spinal muscular atrophy.

One hundred patients with motor unit disease were examined to determine the diagnostc reliability of several clinical signs of large motor units. These signs were high-intensity, low-pitched rumbling on skeletal muscle auscultation, voluntary contraction fasciculations, contraction fasciculation trembling, and palpable contraction fasciculations. Among 22 cases of spinal muscular atrophy, contration fasciculation trembling was noted in 86 percent, abnormal muscle auscultation in 68 percent, palpable contraction fasciculations in 64 percent, and voluntary contraction fasciculations in 50 percent.

Adolescent↗
PubMed2005

Physostigmine does not effect arousal but produces toxicity in an animal model of severe gamma-hydroxybutyrate intoxication.

OBJECTIVES: Physostigmine is an acetylcholinesterase inhibitor and can produce fasciculations, seizures, bradycardia, and asystole. gamma-hydroxybutyrate (GHB) increases acetylcholine levels in the central nervous system and can decrease heart rate. Despite this, physostigmine has been proposed as an arousal agent to treat coma from overdoses of GHB. The authors hypothesized that in the setting of severe GHB intoxication, physostigmine would reverse sedation without producing adverse effects such as a decrease in heart rate, seizures, and fasciculations. METHODS: GHB intoxication was induced in 20 rats by intraperitoneal injection of 700 mg/kg of the GHB precursor gamma-butyrolactone. One hour later, rats were randomly assigned to receive either physostigmine (0.06 mg/kg) intraperitoneally or an equivalent volume of saline. After administration of physostigmine, rats were continuously monitored by a blinded observer for arousal (return of righting reflex), fasciculations, and seizures. Heart rate and respiratory rate were recorded at 0, 5, 15, and 60 minutes after administration of physostigmine. Data were analyzed using repeated-measures analysis of variance and chi-square test. A pretest sample size calculation determined that 10 rats per group would detect a change in arousal from 0% to 50% and a 10% change in heart rate. RESULTS: No rats in either group had arousal within one hour (p = 1.0); however, ten of ten physostigmine-treated rats developed signs of physostigmine toxicity (fasciculations, 7; seizures, 3), while no controls developed signs of physostigmine toxicity (p = 0.00). The authors were unable to detect a decrease in heart rate. CONCLUSIONS: Physostigmine did not produce a 50% change in arousal as measured by a return of righting reflex but did produce physostigmine toxicity (fasciculations and seizures) in this rat model of severe GHB intoxication.

Animals↗
PubMed1998

Defasciculation of neurites is mediated by tenascin-R and its neuronal receptor F3/11.

Fasciculation and defasciculation of axons are major morphogenetic events in the formation of neuronal pathways during development. We have identified the extracellular matrix glycoprotein tenascin-R (TN-R) and its neuronal receptor, the immunoglobulin superfamily recognition molecule F3, as promoters of neurite defasciculation in cerebellar explant cultures. Perturbation of the interaction between these two molecules using both antibodies and an antisense oligonucleotide resulted in increased neurite fasciculation. The domains involved in defasciculation were identified as the N-terminal region of TN-R containing the cysteine-rich stretch and the 4.5 epidermal growth factor-like repeats and the immunoglobulin-like domains of F3. Fasciculation induced by antibodies and the antisense oligonucleotide could be reverted by a phorbol ester activator of protein kinase C, whereas the protein kinase inhibitor staurosporine increased fasciculation. Our observations indicate that defasciculated neurite outgrowth does not only depend on the reduction of the expression of fasciculation enhancing adhesion molecules, such as L1 and the neural cell adhesion molecule (NCAM), but also on recognition molecules that actively induce defasciculation by triggering second messenger systems.

Animals↗
PubMed2001

Succinylcholine pretreatment using gallamine or mivacurium during rapid sequence induction in children: a randomized, controlled study.

STUDY OBJECTIVE: To determine if pretreatment with either gallamine or mivacurium before succinylcholine in children is associated with reduction in fasciculations; postoperative myalgias; or serum levels of potassium, creatinine phosphokinase (CPK), and myoglobin. DESIGN: Prospective, randomized, double-blinded study. SETTING: Operating room at a children's hospital. PATIENTS: 45 ASA physical status IE children, aged 3 to 15 years, scheduled for emergency surgery. INTERVENTIONS: The children received either normal saline 0.5 mL, mivacurium chloride 0.03 mg. kg(-1), or gallamine triethiodide 0.04 mg. kg(-1)2 minutes prior to rapid sequence induction (RSI) using thiopental sodium 5 mg. kg(-1), fentanyl 2 microg. kg(-1), and succinylcholine 2 mg. kg(-1). MEASUREMENTS: Serum potassium concentration (0, 3, 5, 7.5, and 15 min), myoglobin concentration (5 and 15 min), and CPK concentration (0 min and 24 hr). Fasciculation and myalgia were rated on a 0 to 3 score. MAIN RESULTS: There was no difference between groups for fasciculation (p = 0.87) or myalgia score (p = 0.52). The mivacurium group had significantly less increase in potassium at 5 minutes (0.45 vs. 0.0, p = 0.01), myoglobin at 5 minutes (56 vs. 2, p < 0.001), myoglobin at 15 minutes (128 vs. 2.5, p < 0.001), and CPK at 24 hours (399 vs. 138, p < 0.001) following succinylcholine when compared with normal saline. Additionally, we found a significant level of association (p < 0.001) between fasciculation and myoglobin levels and fasciculation and CPK levels (p < 0.001). Gallamine was not effective in reducing the increase of potassium, myoglobin, or CPK. However, the dose of gallamine used for pretreatment was 13 times less than the dose of mivacurium. CONCLUSIONS: Administration of mivacurium 0.03 mg. kg(-1) intravenously 2 minutes before administration of succinylcholine 2 mg. kg(-1) in children is effective in reducing the increase in serum potassium at 5 minutes, the increase in myoglobin at 5 minutes and 15 minutes, and the increase in CPK at 24 hours.

Adolescent↗