Interim report on transient heat-transfer measurements of catalytic recombination in a step-function flow of atomic oxygen.

"AFOSR 3203. Contract no. AF 49(638)-782."

Simulation procedure for modeling transient water table and artesian stress and response /

Bibliography: p. 158-160.

Linear transient analysis.

Includes bibliographies.

Temperature variation, heat transfer, and void volume development in the transient atmospheric boiling of water /

"Series No. 163, Issue No. 2"--Cover.

Reactor heat transient research.

"Contract AT(11-1)-34 Project 42"

Prevalence of drug use in the Washington, DC, Metropolitan Area homeless and transient population, 1991.

Shipping list no.: 93-0546-P.

Transient and homeless persons; a bibliography ...

Appendices: 1. Periodical classification. 2. Directories. 3. Bibliographies.

Experiment data report for LOFT anticipated transient with multiple failures experiment L9-1 and small break experiment L3-3 /

"Published June 1981."

Response of bars (with internal and boundary damping) to transient and random excitation.

"Materials Laboratory, Contract no. AF 33(616)-5426, Project no. 7360."

"A survey of fruit and berry farms & farmers" and "Transient labor in the berry fields."

Cover title.

Organizational, direct support, and general support maintenance repair parts and special tools lists (including depot maintenance repair parts and special tools) for suppressor, electrical transient MX-7778A/GRC (NSN 5915-00-431-6718).

"August 1976."

The effect of linear loading capacitances upon the switching transient of colemanite.

"NAVORD report 5922, NOLC report 413."

Alternating-current and transient circuit analysis.

Mode of access: Internet.

Ca2+-activated K+(BK) channel inactivation contributes to spike broadening during repetitive firing in the rat lateral amygdala

In many neurons, trains of action potentials show frequency-dependent broadening. This broadening results from the voltage-dependent inactivation of K+ currents that contribute to action potential repolarisation. In different neuronal cell types these K+ currents have been shown to be either slowly inactivating delayed rectifier type currents or rapidly inactivating A-type voltage-gated K+ currents. Recent findings show that inactivation of a Ca2+-dependent K+ current, mediated by large conductance BK-type channels, also contributes to spike broadening. Here, using whole-cell recordings in acute slices, we examine spike broadening in lateral amygdala projection neurons. Spike broadening is frequency dependent and is reversed by brief hyperpolarisations. This broadening is reduced by blockade of voltage-gated Ca2+ channels and BK channels. In contrast, broadening is not blocked by high concentrations of 4-aminopyridine (4-AP) or alpha-dendrotoxin. We conclude that while inactivation of BK-type Ca2+-activated K+ channels contributes to spike broadening in lateral amygdala neurons, inactivation of another as yet unidentified outward current also plays a role.

Morphine-3-glucuronide's neuro-excitatory effects are mediated via indirect activation of N-methyl-D-aspartic acid receptors: Mechanistic studies in embryonic cultured hippocampal neurones

Indirect evidence indicates that morphine-3-glucuronide (M3G) may contribute significantly to the neuro-excitatory side effects (myoclonus and allodynia) of large-dose systemic morphine. To gain insight into the mechanism underlying M3G' s excitatory behaviors, We used fluo-3 fluorescence digital imaging techniques to assess the acute effects of M3G (5-500 muM) on the cytosolic calcium concentration ([Ca2+](CYT)) in cultured embryonic hippocampal neurones. Acute (3 min) exposure of neurones to M3G evoked [Ca2+](CYT) transients that were typically either (a) transient oscillatory responses characterized by a rapid increase in [Ca2+](CYT) oscillation amplitude that was sustained for at least similar to30 s or (b) a sustained increase in [Ca2+](CYT) that slowly recovered to baseline. Naloxone-pretreatment decreased the proportion of M3G-responsive neurones by 10%-25%, implicating a predominantly non-opioidergic mechanism. Although the naloxone-insensitive M3G-induced increases in [Ca2+](CYT) were completely blocked by N-methyl-D-aspartic acid (NMDA) antagonists and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (alphaamino-3-hydroxy-5-methyl-4-isoxazolepropiordc acid/ kainate antagonist), CNQX did not block the large increase in [Ca2+](CYT) evoked by NMDA (as expected), confirming that N13G indirectly activates the NMDA receptor. Additionally, tetrodotoxin (Na+ channel blocker), baclofen (gamma-aminobutyric acid, agonist), MVIIC (P/Q-type calcium channel blocker), and nifedipine (L-type calcium channel blocker) all abolished M3G-induced increases in [Ca2+](CYT), suggesting that M3G may produce its neuro-excitatory effects by modulating neurotransmitter release. However, additional characterization is required.