Late Oligocene to Recent benthic foraminifers from the northeastern North Atlantic

Deep-sea benthic foraminiferal faunas were studied from Sites 608 (depth 3534 m, 42°50'N, 23°05'W) and 610 (depth 2427 m, 53°13'N, 18°53'W). The sampling interval corresponded to 0.1 to 0.5 m.y. at Site 608 and in the sections of Site 610 from which core recovery was continuous. First and last appearances of benthic foraminiferal taxa are generally not coeval at the two sites, although the faunal patterns are similar and many species occur at both sites. Major periods of changes in the benthic faunas, as indicated by the numbers of first and last appearances and changes in relative abundances, occurred in the early Miocene (19.2-17 Ma), the middle Miocene (15.5-13.5 Ma), the late Miocene (7-5.5 Ma), and the Pliocene-Pleistocene (3.5-0.7 Ma). A period of minor changes in the middle to late Miocene (10-9 Ma) was recognized at Site 608 only. These periods of faunal changes can be correlated with periods of paleoceanographic changes: there was a period of sluggish circulation in the northeastern North Atlantic from 19.2 to 17 Ma, and the deep waters of the oceans probably cooled between 15.5 and 13.5 Ma, as indicated by an increase in delta18O values in benthic foraminiferal tests. The period between 10 and 9 Ma was probably characterized by relatively vigorous bottom-water circulation in the northeastern Atlantic, as indicated by the presence of a widespread reflector. The faunal change at 7 to 5.5 Ma corresponds in time with a worldwide change in delta13C values, and with the Messinian closing of the Mediterranean. The last and largest faunal changes correspond in time with the onset and intensification of Northern Hemisphere glaciation.

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.

Differential expression of calcium channels in sympathetic and parasympathetic preganglionic inputs to neurons in paracervical ganglia of guinea-pigs

Neurons in pelvic ganglia receive nicotinic excitatory post-synaptic potentials (EPSPs) from sacral preganglionic neurons via the pelvic nerve, lumbar preganglionic neurons via the hypogastric nerve or both. We tested the effect of a range of calcium channel antagonists on EPSPs evoked in paracervical ganglia of female guinea-pigs after pelvic or hypogastric nerve stimulation. omega-Conotoxin GVIA (CTX GVIA, 100 nM) or the novel N-type calcium channel antagonist, CTX CVID (100 nM) reduced the amplitude of EPSPs evoked after pelvic nerve stimulation by 50-75% but had no effect on EPSPs evoked by hypogastric nerve stimulation. Combined addition of CTX GVIA and CTX CVID was no more effective than either antagonist alone. EPSPs evoked by stimulating either nerve trunk were not inhibited by the P/Q calcium channel antagonist, omega-agatoxin IVA (100 nM), nor the L-type calcium channel antagonist, nifedipine (30 muM). SNX 482 (300 nM), an antagonist at some R-type calcium channels, inhibited EPSPs after hypogastric nerve stimulation by 20% but had little effect on EPSPs after pelvic nerve stimulation. Amiloride (100 muM) inhibited EPSPs after stimulation of either trunk by 40%, while nickel (100 muM) was ineffective. CTX GVIA or CTX CVID (100 nM) also slowed the rate of action potential repolarization and reduced afterhyperpolarization amplitude in paracervical neurons. Thus, release of transmitter from the terminals of sacral preganglionic neurons is largely dependent on calcium influx through N-type calcium channels, although an unknown calcium channel which is resistant to selective antagonists also contributes to release. Release of transmitter from lumbar preganglionic neurons does not require calcium entry through either conventional N-type calcium channels or the variant CTX CVID-sensitive N-type calcium channel and seems to be mediated largely by a novel calcium channel. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.

Improved cardiovascular function with aminoguanidine in DOCA-salt hypertensive rats

1 The ability of aminoguanidine (AG), an inhibitor of collagen crosslinking, to prevent changes in cardiac and vascular structure and function has been determined in the deoxycorticosterone acetate (DOCA)-salt hypertensive rat as a model of the cardiovascular remodelling observed in chronic human hypertension. 2 Uninephrectomized rats (UNX) administered DOCA (25 mg every fourth day s.c.) and 1% NaCl in drinking water for 28 days developed cardiovascular remodelling shown as systolic hypertension, left ventricular hypertrophy, increased thoracic aortic and left ventricular wall thickness, increased left ventricular inflammatory cell infiltration together with increased interstitial collagen and increased passive diastolic stiffness, impaired contractility, prolongation of the action potential duration and vascular dysfunction. 3 Treatment with AG (0.05-0.1% in drinking water; average 182 +/- 17 mg kg(-1) day(-1) in DOCA-salt rats) decreased blood pressure (DOCA-salt 176 +/- 4; + AG 144 +/- 5 mmHg; *P < 0.05 vs DOCA-salt), decreased left ventricular wet weights (DOCA-salt 3.17 +/- 0.07; + AG 2.66 +/- 0.08 mg g(-1) body wt*), reduced diastolic stiffness constant (DOCA-salt 30.1 +/- 1.2; + AG 24.3 +/- 1.2* (dimensionless)), improved cardiac contractility (DOCA-salt 1610 +/- 130; + AG 2370 +/- 100 mmHg s(-1)*) and vascular reactivity (3.4-fold increase in maximal contractile response to noradrenaline, 3.2-fold increase in maximal relaxation response to acetylcholine, twofold increase in maximal relaxation response to sodium nitroprusside) and prolonged the action potential duration at 50% repolarization without altering collagen content or inflammatory cell infiltration. 4 Thus, cardiovascular function in DOCA-salt hypertensive rats can be improved by AG independent of changes in collagen content. This suggests that collagen crosslinking is an important cause of cardiovascular dysfunction during cardiovascular remodelling in hypertension.

Benthic foraminifera groups of ODP Site 162-982

The pulsed decline and eventual extinction of 51 species of elongate, cylindrical deep-sea benthic foraminifera (Stilostomellidae, Pleurostomellidae, and some Nodosariidae) occurred at intermediate water depths (1145-2168 m, Sites 980 and 982) in the northern North Atlantic during the mid-Pleistocene transition (MPT, 1.2-0.6 Ma). In the early Pleistocene, prior to their disappearance, these species comprised up to 20% of the total abundance of the benthic foraminiferal assemblage at 2168 m, but up to only 2% at 1145 m. The MPT extinction of 51 species represents ?20% of the total benthic foraminiferal diversity at bathyal depths in the North Atlantic (excluding the myriad of small unilocular forms). The extinction rate during the MPT was approximately 10 species per 0.1 myr, being one or two orders of magnitude greater than normal background turnover rates of deep-sea benthic foraminifera. Comparison of the precise timings of declines and disappearances (= highest occurrences) of each species shows that they were often diachronous between the two depths. The last of these species to disappear in the North Atlantic was Pleurostomella alternans at ~0.679 and ~0.694 Ma in Sites 980 and 982, respectively, which is in good agreement with the previously documented global "Stilostomella extinction" datum within the period 0.7-0.58 Ma. Comparison with similar studies in intermediate depth waters in the Southwest Pacific Gateway indicates that ~61% of the extinct species were common to both regions, and that although the pattern of pulsed decline was similar, the precise order and timing of the extinction of individual species were mostly different on opposite sides of the world. Previous studies have indicated that this extinct group of elongate, cylindrical foraminifera lived infaunally and had their greatest abundances in poorly ventilated, lower oxygen environments. This is supported by our study where there is a strong positive correlation (r = ~+ 0.8) between the flux of the extinction group and low-oxygen/high organic input species (such as Uvigerina, Bulimina and Bolivina) during the MPT, suggesting a close relationship with lower oxygen levels and high food supply to the sea floor. The absolute abundance, flux, and number of the extinction group of species show a progressive withdrawal pattern with major decreases occurring in cold periods with high d13C values. This might be related to increasing chemical ventilation of glacial intermediate water.