Biomedical subjects
Publications and source records attributed to M O'Beirne.
For the postpartum patient and her newborn, the hospitalization period continues to decrease while educational needs are unchanged. This leads to high stress and a limited ability for patients to absorb needed information for safe care after discharge. The program described below shows how one home care agency combined the skills of the in-hospital nursing staff and home care staff to develop an in-home educational program for this population.
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Electrotonic coupling was examined between hippocampal neurons in dissociated cell cultures. Injections of Lucifer yellow indicated that approximately 20% of the neurons were dye-coupled. Propionate, which causes cytoplasmic acidification, significantly decreased dye coupling. Simultaneous intracellular recordings from pairs of cultured neurons directly demonstrated electrotonic coupling. Therefore dissociated cell cultures can be used as a model system for the analysis of hippocampal electrotonic coupling.
The effects of sodium pentobarbital were studied using intracellular recordings from CA1 and CA3 pyramidal cells in slices of guinea pig hippocampus. Drugs were applied either by perfusion or by pressure ejection at concentrations of 10(-6), 10(-5), and 10(-4) M. Pentobarbital at all concentrations caused neuronal hyperpolarization, decreased spontaneous activity, and sometimes decreased input resistance. Hyperpolarization also occurred in zero calcium perfusate or with tetrodotoxin in the perfusate. The postspike train long-lasting afterhyperpolarization, which is an intrinsic calcium-mediated potassium conductance, was increased at all doses. gamma-Aminobutyric acid induced depolarizing dendritic responses were augmented only at 10(-4) M pentobarbital. It is proposed that one of the important mechanisms of pentobarbital neuronal inhibition, particularly at lower doses, is an increase in potassium conductance.
It is commonly thought that central nervous system depressant drugs exert their actions through enhancement of gamma-aminobutyrate (GABA)-mediated mechanisms. Recently, the cellular electrophysiological evidence from this laboratory and others suggests that both sedative hypnotics and general anaesthetics inhibit central neurons by increasing potassium conductance (GK). We have utilized the mammalian in vitro hippocampal and cerebellar slice preparations at 34-36 degrees C. Intracellular recordings from CA1, CA3, and cerebellar Purkinje cells were obtained. Low dose (sedative) concentrations of ethanol (less than or equal to 20 mM), two different benzodiazepines (midazolam and clonazepam in low nanomolar concentrations), and pentobarbital (10(-6) to 10(-4) M) were applied by pressure ejection or were bath perfused. All drugs caused a hyperpolarization with decreased spontaneous activity, and enhanced post spike afterhyperpolarizations (AHPs). These long-lasting AHPs are presumably due to enhanced calcium-mediated GK. Increased responsiveness to focally applied GABA was only seen at higher doses (ethanol, 100 mM; midazolam, 10(-7) M; pentobarbital, 10(-4) M). These data suggest that the above neurodepressant drugs, when applied at sedative doses to hippocampal pyramidal cells, enhance GK and not the actions of GABA.
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