Noradrenergic blockade and memory in patients with major depression and healthy participants

Objective: Patients with major depressive disorder (MDD) often suffer from impaired declarative, episodic and working memory. Further, MDD is associated with alterations in the noradrenergic system. There is evidence that presynaptic alpha 2 receptors that inhibit release of noradrenaline are upregulated in MDD. Results from our recent study demonstrated that increasing noradrenergic activity by blocking the alpha 2 receptor with yohimbine leads to stronger memory consolidation in MDD patients. In the current study, we further examined the role of noradrenaline on memory in MDD by administering clonidine that activates presynaptic alpha 2 receptors and thereby globally suppresses the noradrenergic output. Methods: In a placebo-controlled, within-subject crossover design, 20 patients with MDD and 20 healthy controls received either 0.15 mg of clonidine or placebo orally before memory testing. A word list paradigm (memory consolidation), an autobiographical memory test (retrieval) and a working memory test were applied. Salivary alpha-amylase and blood pressure were measured. Results: Across groups, clonidine decreased blood pressure and alpha-amylase. Clonidine impaired memory consolidation (word list learning) in depressed patients and controls. Memory retrieval and working memory were not affected by clonidine. Conclusions: Reducing noradrenergic activity had a specific effect on memory consolidation in patients with MDD and healthy controls. The underlying mechanisms need further scrutiny

Changes in motor unit behavior following isometric fatigue of the first dorsal interosseous muscle

The neuromuscular strategies employed to compensate for fatigue-induced muscle force deficits are not clearly understood. This study utilizes surface electromyography (sEMG) together with recordings of a population of individual motor unit action potentials (MUAPs) to investigate potential compensatory alterations in motor unit (MU) behavior immediately following a sustained fatiguing contraction and after a recovery period. EMG activity was recorded during abduction of the first dorsal interosseous in 12 subjects at 20% maximum voluntary contraction (MVC), before and directly after a 30% MVC fatiguing contraction to task failure, with additional 20% MVC contractions following a 10-min rest. The amplitude, duration and mean firing rate (MFR) of MUAPs extracted with a sEMG decomposition system were analyzed, together with sEMG root-mean-square (RMS) amplitude and median frequency (MPF). MUAP duration and amplitude increased immediately postfatigue and were correlated with changes to sEMG MPF and RMS, respectively. After 10 min, MUAP duration and sEMG MPF recovered to prefatigue values but MUAP amplitude and sEMG RMS remained elevated. MU MFR and recruitment thresholds decreased postfatigue and recovered following rest. The increase in MUAP and sEMG amplitude likely reflects recruitment of larger MUs, while recruitment compression is an additional compensatory strategy directly postfatigue. Recovery of MU MFR in parallel with MUAP duration suggests a possible role for metabolically sensitive afferents in MFR depression postfatigue. This study provides insight into fatigue-induced neuromuscular changes by examining the properties of a large population of concurrently recorded single MUs and outlines possible compensatory strategies involving alterations in MU recruitment and MFR.Irish Research Counci

Miniature-Laser-Endoscope (MikroEndo) Final report

Available from TIB Hannover: F99B1095+a / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEBundesministerium fuer Bildung und Forschung (BMBF), Bonn (Germany)DEGerman