Thermo-Electrical Conduction of the 2,7-Di([1,1'-Biphenyl]-4-yl)-9H-Fluorene Molecular System: Coupling between Benzene Rings and Stereoelectronic Effects.

Theoretical and analytical thermal and electrical properties are studied through the 2,7-Di([1,1'-biphenyl]-4-yl)-9H-fluorene aromatic system as a prototype of a molecular switch. Variations of the dihedral angles between the two Benzene rings at each end of the molecule have been considered, thus determining the dependence on the structural variation of the molecule when the aromatic system is connected between metal contacts. The molecule is modeled through a Tight-Binding Hamiltonian where-from the analytical process of decimation and using Green's functions-the probability of transmission (T) is calculated by using the Fisher-Lee relationship. Consequently, the thermal and electrical transport properties such as I - V curves, quantum noise (S), Fano factor (F), electrical conductance (G), thermal conductance ( κ ), Seebeck coefficient (Q), and merit number ( Z T ) are calculated. The available results offer the possibility of designing molecular devices, where the change in conductance or current induced by a stereoelectronic effect on the molecular junctions (within the aromatic system) can produce changes on the insulating-conductive states.

Diabetes mellitus alters electrophysiological properties in neurons of superior cervical ganglion of rats.

Diabetic neuropathy is the most prevalent complication associated with diabetes mellitus (DM). The superior cervical ganglion (SCG) is an important sympathetic component of the autonomic nervous system. We investigated the changes in cellular electrophysiological properties and on Na+K+-ATPase activity of SCG neurons of rats with DM induced by streptozotocin (STZ). Three types of action potentials (AP) firing pattern were observed in response to a long (1 s) depolarizing pulse. Whilst some neurons fired a single AP (single firing phasic, SFP), others fired few APs (multiple firing phasic, MFP). A third type fired APs during more than 80% of the stimulus duration (tonic-like, TL). The occurrence of SFP, MFP and TL was 84.5, 13.8, and 1.7%, respectively. SFP and MFP differed significantly in their membrane input resistance (Rin). At the end of the 4th week of its time course, DM differently affected most types of neurons: DM induced depolarization of resting membrane potential (RMP), decreased AP amplitude in SFP, and decreased Rin in MFP. DM decreased spike after-hyperpolarization amplitude in MFP and the duration in SFP. Based on the RMP depolarization, we investigated the Na+K+-ATPase action and observed that DM caused a significant decrease in Na+K+-ATPase activity of SCG. In conclusion, we have demonstrated that DM affects several parameters of SCG physiology in a manner likely to have pathophysiological relevance.

Melatonin Reduces Excitability in Dorsal Root Ganglia Neurons with Inflection on the Repolarization Phase of the Action Potential.

Melatonin is a neurohormone produced and secreted at night by pineal gland. Many effects of melatonin have already been described, for example: Activation of potassium channels in the suprachiasmatic nucleus and inhibition of excitability of a sub-population of neurons of the dorsal root ganglia (DRG). The DRG is described as a structure with several neuronal populations. One classification, based on the repolarizing phase of the action potential (AP), divides DRG neurons into two types: Without (N0) and with (Ninf) inflection on the repolarization phase of the action potential. We have previously demonstrated that melatonin inhibits excitability in N0 neurons, and in the present work, we aimed to investigate the melatonin effects on the other neurons (Ninf) of the DRG neuronal population. This investigation was done using sharp microelectrode technique in the current clamp mode. Melatonin (0.01-1000.0 nM) showed inhibitory activity on neuronal excitability, which can be observed by the blockade of the AP and by the increase in rheobase. However, we observed that, while some neurons were sensitive to melatonin effect on excitability (excitability melatonin sensitive-EMS), other neurons were not sensitive to melatonin effect on excitability (excitability melatonin not sensitive-EMNS). Concerning the passive electrophysiological properties of the neurons, melatonin caused a hyperpolarization of the resting membrane potential in both cell types. Regarding the input resistance (Rin), melatonin did not change this parameter in the EMS cells, but increased its values in the EMNS cells. Melatonin also altered several AP parameters in EMS cells, the most conspicuously changed was the (dV/dt)max of AP depolarization, which is in coherence with melatonin effects on excitability. Otherwise, in EMNS cells, melatonin (0.1-1000.0 nM) induced no alteration of (dV/dt)max of AP depolarization. Thus, taking these data together, and the data of previous publication on melatonin effect on N0 neurons shows that this substance has a greater pharmacological potency on Ninf neurons. We suggest that melatonin has important physiological function related to Ninf neurons and this is likely to bear a potential relevant therapeutic use, since Ninf neurons are related to nociception.