Biomedical subjects

G McAuliffe

Publications and source records attributed to G McAuliffe.

6 recordsLinked to original sources

PubMed2000

Localization of brain-derived neurotrophic factor and TrkB receptors to postsynaptic densities of adult rat cerebral cortex.

Although neurotrophins are critical for neuronal survival and differentiation, recent studies suggest that they also regulate synaptic plasticity. Brain-derived neurotrophic factor (BDNF) rapidly increases synaptic transmission in hippocampal neurons, and enhances long-term potentiation (LTP), a cellular and molecular model of learning and memory. Loci and precise mechanisms of BDNF action remain to be defined: evidence supports both pre- and postsynaptic sites of action. To help elucidate the synaptic mechanisms of BDNF action, we used antisera directed against the extracellular and intracellular domains of trkB receptors, anti-trkBout and anti-trkBin, respectively, to localize the receptors in relation to synapses. Synaptic localization of BDNF was examined in parallel using anti-BDNF antisera. By light microscopy, trkBin and trkBout immunoreactivities were localized to hippocampal neurons and all layers of the overlying visual cortex. Immunoelectron microscopic analysis of the cerebral cortex revealed that trkB and BDNF localize discretely to postsynaptic densities (PSD) of axo-spinous asymmetric synaptic junctions, that are the morphological correlates of excitatory, glutamatergic synapses. TrkB immunoreactivity was also detected in the nucleoplasm by light and electron microscopy. Western blot analysis indicated that both anti-trkBout and anti-trkBin antisera react with a protein band in the PSD corresponding to the molecular weight expected for trkB; however, molecular species distinct from that for trkB were recognized in the nuclear fraction by both anti-trkBin and anti-trkBout antisera, indicating that the nuclear immunoreactivity, seen by immunocytochemistry, reflects cross-reactivity with proteins closely related to, but distinct from, trkB. The PSD localization of both BDNF and trkB supports the contention that this receptor/ligand pair participates in postsynaptic plasticity.

Animals↗

PubMed2000

Obituary

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Journal Article↗

PubMed1997

Heart rate and cardiac output after atropine in anaesthetised infants and children.

PURPOSE: Heart rate is considered to be a major determinant of cardiac output in infants and small children but the relationships between age, heart rate and cardiac output in humans have never been clearly established. This study was designed to determine the change in cardiac output following atropine iv to anaesthetised infants and small children. METHODS: Following Institutional Ethics Committee approval and written-informed consent, 20 ASA I or II unpremedicated patients aged from 1 to 36 mo were studied. Anaesthesia was induced with 5 mg.kg-1 thiopentone, 2 micrograms.kg-1 fentanyl and maintained with halothane 0.5% in nitrous oxide 66% in oxygen. Vecuronium 0.1 mg.kg-1 was used to provide muscular relaxation. Cardiac output was measured by non-invasive transthoracic blind continuous-wave Doppler echocardiography before and after the administration of 0.02 mg.kg-1 atropine iv. RESULTS: Atropine increased both heart rate and cardiac index by 31.1 +/- 12.8% and 29.4 +/- 17.3% respectively (P < 0.05). The cardiac index before atropine was 5.1 +/- 1.2 L.min-1.m-2 and the increase after atropine varied widely from 1.4 to 52.1%. Although atropine did not alter the overall stroke index the recorded changes ranged from -20.8 to +18.0%. There was no association between age and either cardiac index or % change in cardiac index after atropine. However, there was a positive but weak correlation between percentage change in heart rate and cardiac output (r2 = 0.46). CONCLUSION: Atropine causes a variable increase in cardiac output in infants and children aged between 1 and 36 mo. The change in cardiac output, considering the limits of the transthoracic echocardiography methodology, suggests that this is related to the increase in heart rate but is not dependent of age.

Anesthesia↗

PubMed1997

Subhypnotic propofol does not treat postoperative vomiting in children after adenotonsillectomy.

PURPOSE: To investigate the efficacy of a subhypnotic dose of propofol to treat vomiting in children after adenotonsillectomy. METHODS: Two hundred and fifty-two children, aged 2-12 yr, underwent a standardized anaesthetic opioid administration, and postoperative care after adenotonsillectomy, adenoidectomy or tonsillectomy. A prospective, double-blinded, placebo-controlled study was performed in 70 of the patients who retched or vomited after surgery and who had intravenous access. Patients were assigned randomly to receive either 0.2 mg.kg-1) propofol (n = 35), or placebo (intralipid 10%, n = 35). RESULTS: The overall incidence of vomiting during the first 18-24 hr was 50%. Of those who had received propofol after the first episode of vomiting, 63% relapsed requiring a rescue antiemetic compared with 57% of those who had received intralipid (P = NS). Of the children who received propofol, 54% experienced pain on injection and 46% were mildly sedated compared with 3% and 11%, respectively, in the placebo group (P < 0.003). CONCLUSION: We conclude that an intravenous bolus of 0.2 mg.kg-1 propofolis not effective in the treatment of postoperative vomiting in children after adenotonsillectomy when a standardized anaesthetic with thiopentone, halothane, nitrous oxide, and 1.5 mg.kg-1 codeine phosphate is used, but it does cause sedation and pain on injection.

Adenoidectomy↗

PubMed1995

Should the routine use of atropine before succinylcholine in children be reconsidered?

It is common practice to administer atropine before a first dose of succinylcholine in infants and children. However, the administration of succinylcholine without atropine has not been investigated in children. This study was designed to compare cardiovascular changes after the administration of either atropine with succinylcholine or succinylcholine alone. In 41 ASA I or II patients aged from 1 to 12 yr anaesthesia was induced with thiopentone 5 mg.kg-1. Patients were randomly allocated to receive either atropine 20 micrograms.kg-1 and succinylcholine 1.5 mg.kg-1 (n = 20) or succinylcholine 1.5 mg.kg-1 alone (n = 21). Heart rate and rhythm were recorded continuously from two minutes before induction until two minutes after tracheal intubation. Blood pressure was measured non-invasively before and after induction of anaesthesia and both immediately and two minutes after laryngoscopy. One self-limiting episode of bradycardia was recorded during laryngoscopy in a child who received atropine. Heart rate increased in both groups compared with baseline values (108 +/- 25), with a greater increase in patients who had received atropine (150 +/- 13) than in those who had not (128 +/- 18) (P < 0.05). There was no difference in mean arterial pressure or incidence of arrythmias between the two groups. No recorded arrythmias were judged to be clinically important by a cardiologist. The incidence of bradycardia after succinylcholine in the absence of atropine in children aged from 1 to 12 yr appears to be lower than previously estimated. The use of atropine before a single dose of succinylcholine in children deserves to be reconsidered.

Adjuvants, Anesthesia↗

PubMed1995

Selective localization of amyloid precursor-like protein 1 in the cerebral cortex postsynaptic density.

Senile plaques, a hallmark of Alzheimer's disease (AD), contain amyloid beta-peptide (A beta), which is generated from the larger amyloid beta protein precursor (APP). In addition to APP, several APP-related proteins have been recently identified in different organisms, including Drosophila amyloid precursor protein-like protein (APPL). Deficiency of APPL causes behavioral deficits in Drosophila, implicating a role in brain function. Moreover, mouse and human cDNA clones encoding amyloid precursor-like proteins (APLP1 and APLP2) have been identified and exhibit extensive sequence similarity to the APPL and APP genes. To define the potential role of APLP in the mammalian brain, we sought to directly localize APLP1 within the complex cortical synaptic structure. We focused on the postsynaptic density (PSD), which appears to be central to synaptic function. We now report that the 90 kDa APLP1, the first known APLP, is localized to the PSD from rat and human cerebral cortex. APLP1 increased during cortical synaptic development, suggesting a role in synaptogenesis or synaptic maturation. In contrast, APP was predominantly expressed in the synaptic membrane fraction, but was barely detectable in the PSD, including different subcellular distributions of APP and APLP1. Our observations raise the possibility that APLP1, a homologue of APPL, which appears to be necessary for normal behavior in Drosophila, participates in brain synaptic function in mammals.

Amyloid beta-Protein Precursor↗