Partitioning optical solitons for generating entangled light beams

It is shown that bipartition of optical solitons can be used to generate entangled light beams. The achievable amount of entanglement can be substantially larger for N-bound solitons N=2,3 than for the fundamental soliton (N=1). An analysis of the mode structure of the entangled beams shows that just N modes are essentially entangled. In particular, partitioning of the fundamental soliton effectively produces 2-mode squeezed light.Comment: 5 pages, 3 PS figure

Spatial solitary-wave optical memory

We consider some features of spatial solitary-wave switching in a unidirectional ring cavity that is partially filled with a fast and saturably self-focusing nonlinear medium. Large (part-beam switched) solitary arrays are considered. It is found that prescribed binary patterns may be encoded in the duration of a single cavity transit and subsequently remain stable over thousands of transits. Beam interrupt allows pixels to be switched off in fewer than ten cavity transits. Pixel instabilities on an unpixelated beam are shown to arise from spatial solitary attractive forces and intensity gradients

Switching dynamics of spatial solitary wave pixels

Separatrices and scaling laws in the switching dynamics of spatial solitary wave pixels are investigated. We show that the dynamics in the full model are similar to those in the plane-wave limit. Switching features may be indicated and explained by the motion of the (complex) solitary wave amplitude in the phase plane. We report generalization, into the domain of transverse effects, of the pulse area theorem for the switching process and a logarithmic law for the transient dynamics. We also consider, for what is the first time to our knowledge, phase-encoded address of solitary pixels and find that a near-square-wave temporal switching pattern is permitted without (transverse) cross switching

The Interaction of Gabapentin and N6-(2-phenylisopropyl)-adenosine R-(-)isomer (R-PIA) on Mechanical Allodynia in Rats with a Spinal Nerve Ligation

We examined the antiallodynic interaction between gabapentin and adenosine A1 receptor agonist, N6-(2-phenylisopropyl)-adenosine R-(-)isomer (R-PIA), in a rat model of nerve ligation injury. Rats were prepared with ligation of left L5-6 spinal nerves and intrathecal catheter implantation for drug administration. Mechanical allodynia was measured by applying von Frey filaments. Gabapentin and R-PIA were administered to obtain the dose-response curve and the 50% effective dose (ED50). Fractions of ED50s were administered concurrently to establish the ED50 of the drug combination. The drug interaction between gabapentin and R-PIA was analyzed using the isobolographic method. Adenosine A1 receptor antagonist was administered intrathecally to examine the reversal of the antiallodynic effect. Locomotor function changes were evaluated by rotarod testing. Intrathecal gabapentin and R-PIA and their combination produced a dose-dependent antagonism against mechanical allodynia without severe side effects. Intrathecal gabapentin synergistically enhanced the antiallodynic effect of R-PIA when coadministered. There were no significant changes in rotarod performance time, except gabapentin 300 μg. In the combination group, the maximal antiallodynic effect was reversed by A1 adenosine receptor antagonist. These results suggest that activation of adenosine A1 receptors at the spinal level is required for the synergistic interaction on the mechanical allodynia

Interaction between Intrathecal Gabapentin and Adenosine in the Formalin Test of Rats

Spinal gabapentin and adenosine have been known to display an antinociceptive effect. We evaluated the nature of the interaction between gabapentin and adenosine in formalin-induced nociception at the spinal level. Male Sprague-Dawley rats were prepared for intrathecal catheterization. Pain was evoked by injection of formalin solution (5%, 50 µL) into the hindpaw. After examination of the effects of gabapentin and adenosine, the resulting interaction was investigated with isobolographic and fractional analyses. Neither gabapentin nor adenosine affected motor function. Gabapentin or adenosine decreased the sum of the number of flinches during phase 2, but not during phase 1 in the formalin test. Isobolographic analysis, in phase 2, revealed an additive interaction between gabapentin and adenosine. Taken together, intrathecal gabapentin and adenosine attenuated the facilitated state and interacted additively with each other

Gabapentin for complex regional pain syndrome in Machado-Joseph disease: a case report

<p>Abstract</p> <p>Introduction</p> <p>Chronic pain is a common problem for patients with Machado-Joseph disease. Most of the chronic pain in Machado-Joseph disease has been reported to be of musculoskeletal origin, but now there seems to be different chronic pain in patients with Machado-Joseph disease.</p> <p>Case presentation</p> <p>A 29-year-old man (Han Chinese, Hoklo) with Machado-Joseph disease experienced severe chronic pain in both feet, cutaneous thermal change, thermal hypersensitivity, focal edema, and sweating and had a history of bone fracture. These symptoms were compatible with a diagnosis of complex regional pain syndrome. After common analgesics failed to relieve his pain, gabapentin was added and titrated to 2000 mg/day (500 mg every six hours) in less than two weeks. This relieved 40% of his pain and led to significant clinical improvement.</p> <p>Conclusions</p> <p>The pathophysiology of complex regional pain syndrome includes peripheral and central sensitizations, the latter of which might be associated with the neurodegeneration in Machado-Joseph disease. In this report, we suggest that gabapentin could inhibit central sensitization as an adjunct for complex regional pain syndrome in patients with Machado-Joseph disease.</p

Protective Effects of Gabapentin on Allodynia and α2δ1-Subunit of Voltage-dependent Calcium Channel in Spinal Nerve-Ligated Rats

This study was designed to determine whether early gabapentin treatment has a protective analgesic effect on neuropathic pain and compared its effect to the late treatment in a rat neuropathic model, and as the potential mechanism of protective action, the α2δ1-subunit of the voltage-dependent calcium channel (α2δ1-subunit) was evaluated in both sides of the L5 dorsal root ganglia (DRG). Neuropathic pain was induced in male Sprague-Dawley rats by a surgical ligation of left L5 nerve. For the early treatment group, rats were injected with gabapentin (100 mg/kg) intraperitoneally 15 min prior to surgery and then every 24 hr during postoperative day (POD) 1-4. For the late treatment group, the same dose of gabapentin was injected every 24 hr during POD 8-12. For the control group, L5 nerve was ligated but no gabapentin was administered. In the early treatment group, the development of allodynia was delayed up to POD 10, whereas allodynia was developed on POD 2 in the control and the late treatment group (p<0.05). The α2δ1-subunit was up-regulated in all groups, however, there was no difference in the level of the α2δ1-subunit among the three groups. These results suggest that early treatment with gabapentin offers some protection against neuropathic pain but it is unlikely that this action is mediated through modulation of the α2δ1-subunit in DRG

GABA ergic transmission in rat pontine reticular formation regulates the induction phase of anesthesia and modulates hyperalgesia caused by sleep deprivation

The oral part of the pontine reticular formation (PnO) contributes to the regulation of sleep, anesthesia and pain. The role of PnO γ‐aminobutyric acid ( GABA ) in modulating these states remains incompletely understood. The present study used time to loss and time to resumption of righting response (Lo RR and Ro RR ) as surrogate measures of loss and resumption of consciousness. This study tested three hypotheses: (i) pharmacologically manipulating GABA levels in rat PnO alters Lo RR , Ro RR and nociception; (ii) propofol decreases GABA levels in the PnO; and (iii) inhibiting GABA synthesis in the PnO blocks hyperalgesia caused by sleep deprivation. Administering a GABA synthesis inhibitor [3‐mercaptopropionic acid (3‐ MPA )] or a GABA uptake inhibitor [nipecotic acid ( NPA )] into rat PnO significantly altered Lo RR caused by propofol. 3‐ MPA significantly decreased Lo RR for propofol (−18%). NPA significantly increased Lo RR during administration of propofol (36%). Neither 3‐ MPA nor NPA altered Ro RR following cessation of propofol or isoflurane delivery. The finding that Lo RR was decreased by 3‐ MPA and increased by NPA is consistent with measures showing that extracellular GABA levels in the PnO were decreased (41%) by propofol. Thermal nociception was significantly decreased by 3‐ MPA and increased by NPA , and 3‐ MPA blocked the hyperalgesia caused by sleep deprivation. The results demonstrate that GABA levels in the PnO regulate the time for loss of consciousness caused by propofol, extend the concept that anesthetic induction and emergence are not inverse processes, and suggest that GABA ergic transmission in the PnO mediates hyperalgesia caused by sleep loss. The intravenous anesthetic propofol significantly decreases extracellular GABA levels in rat PnO. Pharmacologically increasing or decreasing extracellular GABA levels increases or decreases, respectively, the time to loss of consciousness caused by propofol. GABAergic transmission in the PnO does not modulate the resumption of consciousness after isoflurane‐ and propofol‐anesthesia. Administration of a GABA synthesis inhibitor into the PnO blocks the hyperalgesia caused by sleep deprivation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108018/1/ejn12571.pd

Cannabinoids and Dementia: A Review of Clinical and Preclinical Data

The endocannabinoid system has been shown to be associated with neurodegenerative diseases and dementia. We review the preclinical and clinical data on cannabinoids and four neurodegenerative diseases: Alzheimer’s disease (AD), Huntington’s disease (HD), Parkinson’s disease (PD) and vascular dementia (VD). Numerous studies have demonstrated an involvement of the cannabinoid system in neurotransmission, neuropathology and neurobiology of dementias. In addition, several candidate compounds have demonstrated efficacy in vitro. However, some of the substances produced inconclusive results in vivo. Therefore, only few trials have aimed to replicate the effects seen in animal studies in patients. Indeed, the literature on cannabinoid administration in patients is scarce. While preclinical findings suggest causal treatment strategies involving cannabinoids, clinical trials have only assessed the suitability of cannabinoid receptor agonists, antagonists and cannabidiol for the symptomatic treatment of dementia. Further research is needed, including in vivo models of dementia and human studies