Biomedical subjects
Publications and source records attributed to Adam Wasserman.
A method is given that extracts accurate Rydberg excitations from density functional calculations in the local density approximation, despite the short-ranged potential. For the case of He and Ne, the asymptotic quantum defects predicted by the calculations are in less than 5% error, yielding transition frequency errors of less than 0.1 eV.
Linear response time-dependent density functional theory is used to study low-lying electronic continuum states of targets that can bind an extra electron. Exact formulas to extract scattering amplitudes from the susceptibility are derived in one dimension. A single-pole approximation for scattering phase shifts in three dimensions is shown to be more accurate than static exchange for singlet electron-He(+) scattering.
Despite the incorrect asymptotic behavior of its potential, the time-dependent local density approximation can yield accurate optical spectra. The oscillator strengths of Rydberg excitations appear in the calculated spectrum as continuum contributions with excellent optical intensity. We explain why, illustrate this for the neon and helium atoms, and also discuss when such calculations of the optical response will be inaccurate.
To determine the predominant nicotinic ACh receptor (nAChR) located on neurones in the dorsal motor nucleus of the vagus (DMV) that project to the gastrointestinal tract, we used the rat brainstem slice preparation and whole-cell recordings of DMV neurones identified by retrograde DiI tracing to pharmacologically characterize nAChRs. Pressure ejection of acetylcholine (ACh, 250 microM for 200 ms) from a patch pipette placed approximately 10-20 microm from the surface of the recorded cell produced an inward current in most DMV neurones sampled. The average currents for neurones projecting to the fundus, antrum and caecum were 149 +/- 38 (n = 25), 115 +/- 18 (n = 29) and 117 +/- 23 pA (n = 6), respectively. Blockade of the alpha7 subtype of nAChR with either alpha-bungarotoxin (alpha-BGT) or methyllycaconitine (MLA) counteracted 60-75 % of the ACh-evoked current in DMV neurones projecting to the fundus, antrum and caecum. In neurones projecting to the fundus and the antrum, currents resistant to alpha-BGT were significantly blocked by dihydro-beta-erythroidine (10-20 nM), an antagonist of the alpha4beta2 subtype of nAChR. In neurones projecting to the caecum, currents resistant to alpha-BGT were significantly depressed by a low concentration of mecamylamine (1 microM). Cytisine (100 microM), an agonist of nAChRs that contain the alpha7 or the beta4 subunit, evoked significant currents in caecum-projecting neurones that were previously exposed to alpha-BGT. In contrast, cytisine had no effect on DMV neurones previously exposed to alpha-BGT that project to the fundus or antrum. Our data indicate that the prevailing nAChR subtype in DMV neurones projecting to the GI tract is the alpha7 subtype. In addition, we obtained evidence for the co-expression of the alpha4beta2 nAChR subtype on DMV neurones projecting to the fundus and antrum, and the alpha3beta4 nAChR subtype on DMV neurones projecting to the caecum.
The purposes of our study were to determine (1) the effects of intravenous (i.v.) nicotine on gastric mechanical function of anesthetized rats, (2) the CNS site of action of nicotine to produce these effects, (3) the CNS nicotinic acetylcholine receptor (nAChR) subtype(s) responsible for mediating the i.v. effects of nicotine, and (4) the brainstem neurocircuitry engaged by i.v. nicotine for eliciting its gastric effects. This was accomplished by monitoring intragastric pressure (gastric tone) and contractility of the fundus and antrum while administering five doses of i.v. nicotine and microinjecting nicotine into specific brainstem nuclei. Additionally, c-Fos expression in the brainstem after i.v. nicotine and pharmacological agents were used as tools to identify the CNS site and circuitry and reveal the nAChR subtype(s) mediating the gastric effects of nicotine. Using these experimental approaches, we found the following. (1) When given intravenously in doses of 56.5, 113, 226, 452, and 904 nmol/kg, nicotine elicited only inhibitory effects on gastric mechanical function. The most sensitive area of the stomach to nicotine was the fundus, and this effect was mediated by the vagus nerve at doses of 56.5, 113, and 226 nmol/kg. (2) The CNS site of action and nAChR subtype responsible were glutamatergic vagal afferent nerve terminals in the medial subnucleus of the tractus solitarious (mNTS) and alpha4beta2, respectively. (3) The brainstem neurocircuitry that was involved appeared to consist of a mNTS noradrenergic pathway projecting to the dorsal motor nucleus of the vagus (DMV). This pathway seems to be activated via nitriergic interneurons engaged by vagally released glutamate in the mNTS and results in alpha2 adrenergic receptor-mediated inhibition of DMV neurons projecting to the fundus and controlling gastric tone.