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E Reilly

Publications and source records attributed to E Reilly.

11 recordsLinked to original sources
PubMed1989

Genetic and molecular analysis of a Caenorhabditis elegans beta-tubulin that conveys benzimidazole sensitivity.

Benzimidazole anti-microtubule drugs, such as benomyl, induce paralysis and slow the growth of the nematode Caenorhabditis elegans. We have identified 28 mutations in C. elegans that confer resistance to benzimidazoles. All resistant mutations map to a single locus, ben-1. Virtually all these mutations are genetically dominant. Molecular cloning and DNA sequence analysis established that ben-1 encodes a beta-tubulin. Some resistant mutants are completely deleted for the ben-1 gene. Since the deletion strains appear to be fully resistant to the drugs, the ben-1 product appears to be the only benzimidazole-sensitive beta-tubulin in C. elegans. Furthermore, since animals lacking ben-1 are viable and coordinated, the ben-1 beta-tubulin appears to be nonessential for growth and movement. The ben-1 function is likely to be redundant in the nematode genome.

Alleles↗
PubMed1986

Reduced sensitivity of red blood cell (Na+,K+)-ATPase to ethanol in vitro in male alcoholic patients: relationship to clinical characteristics.

We examined red blood cell (Na+,K+)-ATPase, its sensitivity to inhibition by ethanol in vitro, and its relationship to clinical characteristics and history in 41 newly admitted alcoholic patients and 14 age-matched healthy controls. Sensitivity to ethanol was significantly lower in the alcoholic patients and correlated negatively with ethanol intake. In addition, sensitivity of enzyme to ethanol was lower in patients with high agitation-anxiety ratings and correlated negatively with agitation and anxiety scores on the Brief Psychiatric Rating Scale. There were no relationships between (Na+,K+)-ATPase measures and depressive symptoms, history of treatment for depression, or family history of depression. These data suggest that tolerance to the effects of ethanol on (Na+,K+)-ATPase occurs in man and may be related to the severity of ethanol dependence or withdrawal.

Adult↗
PubMed1986

Mutations affecting microtubule structure in Caenorhabditis elegans.

Three types of microtubules are seen in the neuronal processes of the nematode Caenorhabditis elegans. Single cytoplasmic microtubules of most neurones have 11 protofilaments whereas those of six touch receptor cells have 15 protofilaments. The axonemes of sensory cilia have nine outer doublets with a variable number (up to seven) of singlet microtubules. Mutations in 11 genes affect the appearance of these microtubules.

Animals↗
PubMed1975

The freezing lesion. III. The effects of diphenylhydantoin on potassium transport within nerve terminals from the primary foci.

Possible mechanisms by which dephenylhydantoin (DPH) controls seizures were examined. The effects of intraperitoneal DPH on seizure discharges within epileptogenic freeze lesions were correlated with DPH action on in vitro potassium uptake within synaptosomes isolated from the same freeze foci. When in vivo DPH suppressed seizure discharges, it stimulated in vitro potassium uptake within synaptosomes incubated in a high-Kplus (10 mM) media. With 2-5 mM Naplus and 10mM Kplus, DPH stimulation of synaptosome potassium uptake was reversed by ouabain. With 50 mM Naplus and 10 mM Kplus, DPH stimulation of potassium uptake was not reversed by ouabain. In low-Kplus (0.2-5 mM) media, DPH did not affect potassium uptake even when sodium concentrations were varied at 10-100 mM. In sham-operated controls and in non-epileptogenic lesions, the effects of DPH on synaptosome potassium uptake were identical to those previously reported in normal brains. These results strongly suggest that DPH controls the epileptogenic state by stimulating potassium uptake within synaptic terminals. DPH controls the epileptogenic state by stimulating potassium uptake within synaptic terminals. DPH enhances synaptic potassium uptake by stimulating the (Naplus-Kplus) pump and a second potassium uptake process which is insensitive to ouabain.

Animals↗
PubMedDate not supplied

Urethane modification of EEG-like activity and acoustically evoked field potentials recorded from deep nuclei.

Average acoustic-evoked responses (AAER) and EEGs were recorded from the lateral hypothalamus (LH), ventromedial hypothalamus (VMH), medial forebrain bundle (MFB) and reticular formation (RF) of freely behaving rats before and after various doses (0.2, 0.4, 0.8, 1.2 g/5g) of the anesthetic drug, urethane. The effect of a surgical level of urethane (1.2 g/5g) over time (8--14 h) was also studied. Urethane produced a dose-dependent slowing in the EEG frequency. The effect of 1.2 g/kg over time was a bimodal depression of the EEG frequency. Three components of the AAER were recorded consistently and evaluated in terms of amplitude. With increasing doses, the early component (P2) was depressed in the LH2, VMH and MFB, but not in the RF which remained at control values or higher. The later components (N2 and P2) were depressed in all four structures. This suggests that urethane may be blocking the integrative function of the RF, as well as in the thalamus, resulting in lower sensory input to higher CNS structures.

Acoustic Stimulation↗