In the present study, the potential involvement of nitric oxide (NO) system in attenuating effects of low-intensity laser therapy (LILT) on naloxone-induced morphine withdrawal signs was evaluated. A hundred mice were rendered morphine-dependent using three escalating doses of morphine sulfate during three consecutive days. After the last dose on day 4, animals were given naloxone HCl (2 mg/kg s.c) to induce withdrawal signs. The effects of LILT (12.5 J/cm(2)) and L-NG-nitroarginine methyl ester (L-NAME) (10, 20, 50, and 100 mg/kg) and their coadministration on escape jump count and stool weight as typical withdrawal signs were assessed. LILT and L-NAME (20, 50, and 100 mg/kg) per se significantly decreased escape jump count and stool weight in morphine-dependent naloxone-treated mice (p < 0.01). Coadministration of LILT and L-NAME (20, 50, and 100 mg/kg) also reduced escape jump and stool weight (p < 0.05) but with no synergetic or additive response. Here, LILT at this fluence may show its maximal effects on NO and therefore no noticeable effects appeared during coadministration use. Moreover, LILT and L-NAME follow the same track of changes in escape jump and stool weight. Conceivably, it seems that LILT acts partly via NO system, but the exact path is still obscure and rather intricate. The precise mechanisms need to be clarified.

Alzheimer's disease (AD) is a multifactorial and debilitating condition without precise etiology and definite cure burdened with high monetary and human resources to the society around the globe. Given that Iranian traditional medicine has a valuable treasure of medicinal plants with multi-dimensional effects, we designed this study to examine one week daily low single-dose treatment protocol of 3 mg/kg Teucrium polium (TP) hydro-alcoholic extract effects on rat's spatial memory performance and CA1 hippocampal neuronal count in rat Aβ25-35 as an AD model. Animals were bilaterally microinjected with single 10 µg/2 µg intrahippocampal Aβ25-35 fragment for the AD induction. After a two-week recovery period, daily intraperitoneal injection of TP for a week was initiated in Aβ-received TP-treated (treated) and TP-received animals (control). Spatial memory performance and CA1 neuronal count were evaluated. TP significantly reduced time latency and distance swum during the first three days of the training protocol compared with Aβ-received rats (sham). Probe reference test findings, however, were not statistically different in treated, sham, and control groups. Intact CA1 hippocampal neuronal count showed a significant increase in Aβ-received TP-treated (case) rats in comparison with Aβ-received (sham) animals. It seems that the least reported low dose TP has the active chemical components capable of memory enhancing effects in Morris water maze (MWM) setting and potential neuronal survival property in hippocampal tissue. In spite of myriad claims against TP use, we should reconsider the matter and do more research to find the exact active ingredients of various species of the plant plus possible underlying mechanisms for ensuring potential use for human clinical trials in AD and other central nervous system-related diseases.

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