Role of subaerial volcanic rocks and mantle plumes in creation of South Atlantic margins: implications for salt tectonics and source rocks

Seaward-dipping re¯ectors (SDRs) represent ¯ood basalts rapidly extruded during either rifting or initially subaerial sea-¯oor spreading. Evaporites can form on this basaltic proto-oceanic crust, as in the Afar Triangle today. Evidence for SDRs in South Atlantic deep-water regions comes from proximity to the uniquely large Paranaà ±Etendeka volcanic province onshore, the Tristan and Gough hot spots, drilled volcanic rocks, and seismic pro®les showing SDR provinces more than 100 km wide, as much as 7 km thick, and thousands of kilometers long. SDRs are clearest adjoining the Aptian salt basins. However, we speculate that SDRs are also present but seismically obscured below the salt basins. We argue that the conjugate Aptian salt basins are post-breakup, not pre-breakup; they were separated from the start by a mid-oceanic ridge; distal salt accumulated on proto-oceanic crust, not rift basins. This hypothesis is supported by: seismic stratigraphy and structure; magnetic anomalies; plate reconstructions; and hydrothermal potash evaporites. An important implication for exploration is that thick basalts, rather than rift-age source rocks, may underlie distal parts of the salt basins

α4* Nicotinic Receptors in preBotzinger Complex Mediate Cholinergic/Nicotinic Modulation of Respiratory Rhythm

Acetylcholine and nicotine can modulate respiratory patterns by acting on nicotinic acetylcholine receptors (nAChRs) in the preBötzinger complex (preBötC). To further explore the molecular composition of these nAChRs, we studied a knock-in mouse strain with a leucine-to-alanine mutation in the M2 pore-lining region (L9′A) of the nAChR α4 subunit; this mutation renders α4-containing receptors hypersensitive to agonists. We recorded respiratory-related rhythmic motor activity from hypoglossal nerve (XIIn) and patch-clamped preBötC inspiratory neurons in an in vitro medullary slice preparation from neonatal mice. Nicotine affected respiratory rhythm at concentrations ∼100-fold lower in the homozygous L9′A knock-in mice compared with wild-type mice. Bath application of 5 nm nicotine increased the excitability of preBötC inspiratory neurons, increased respiratory frequency, and induced tonic/seizure-like activities in XIIn in L9′A mice, effects similar to those induced by 1 μm nicotine in wild-type mice. In L9′A mice, microinjection of low nanomolar concentrations of nicotine into the preBötC increased respiratory frequency, whereas injection into the ipsilateral hypoglossal (XII) nucleus induced tonic/seizure-like activity. The α4*-selective nAChR antagonist dihydro-β-erythroidine produced opposite effects and blocked the nicotinic responses. These data, showing that nAChRs in the preBötC and XII nucleus in L9'A mice are hypersensitive to nicotine and endogenous ACh, suggest that functional α4* nAChRs are present in the preBötC. They mediate cholinergic/nicotinic modulation of the excitability of preBötC inspiratory neurons and of respiratory rhythm. Furthermore, functional α4* nAChRs are present in XII nucleus and mediate cholinergic/nicotinic modulation of tonic activity in XIIn

Genetic Approaches Identify Differential Roles for α₄β₂* Nicotinic Receptors in Acute Models of Antinociception in Mice

The effects of nicotine on the tail-flick and hot-plate tests were determined to identify nicotinic receptor subtypes responsible for spinally and supraspinally mediated nicotine analgesia in knockin mice expressing hypersensitive α4 nicotinic receptors (L9′S), in seven inbred mouse strains (C57BL/6, DBA/2, A/2, CBA/2, BALB/cByJ, C3H/HeJ, and 129/SvEv), and in two F1 hybrids (B6CBAF1 and B6D2F1). L9′S heterozygotes were ∼6-fold more sensitive to the antinociceptive effects of nicotine than the wild-type controls in the hot-plate test but not in the tail-flick assay. Large differences in the effects of nicotine were also observed with both tests for the seven mouse strains. A/J and 129 mice were 6- to 8-fold more sensitive than CBA and BALB mice. In addition, B6CBAF1 hybrid mice were even less sensitive than CBA mice. Nicotinic binding sites were measured in three spinal cord regions and the hindbrain of the inbred strains. Significant differences in cytisine-sensitive, high affinity [¹²⁵I]epibatidine binding site levels (α₂β₂* subtypes), but not in ¹²⁵I-α-bungarotoxin binding (α7* subtypes), were observed. Significant negative correlations between cytisine-sensitive [¹²⁵I]epibatidine binding and nicotine ED50 for both tests were noted. Our results indicate that α₄β₂* acetylcholine nicotinic receptors (nAChR) are important in mediating nicotine analgesia in supraspinal responses, while also showing that α₄β₂*-nAChR and at least one other nAChR subtype appear to modulate spinal actions