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Most Recent Articles Published on Neuromodulation

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Multiple firing patterns in deep Dorsal Horn Neurons of the spinal cord: computational analysis of mechanisms and functional implications.

J Neurophysiol. 2010 Jul 28;

Authors: Le Franc Y, Le Masson G

Deep dorsal horn relay neurons (dDHNs) of the spinal cord are known to exhibit multiple firing patterns under the control of local metabotropic neuromodulation: tonic firing, plateau potential, and spontaneous oscillations. This work investigates the role of interactions between voltage-gated channels and the occurrence of different firing patterns and then correlates these two phenomena with their functional role in sensory information processing. We designed a conductance-based model using the NEURON software package, which successfully reproduced the classical features of plateau in dDHNs, including a wind-up of the neuronal response after repetitive stimulation. This modeling approach allowed us to systematically test the impact of conductance interactions on the firing patterns. We found that the expression of multiple firing patterns can be reproduced by changes in the balance between two currents (L-type calcium and potassium inward rectifier conductances). By investigating a possible generalization of the firing state switch, we found that the switch can also occur by varying the balance of any hyperpolarizing and depolarizing conductances. This result extends the control of the firing switch to neuromodulators or to network effects such as synaptic inhibition. The switch between the different firing patterns was observed to occur as a continuous function in the model and revealed a particular intermediate state called the accelerating mode. In order to characterize the functional effect of a firing switch on information transfer, we used correlation analysis between a model of peripheral nociceptive afference and the dDHN model. The simulations results indicate that the accelerating mode was the optimal firing state for information transfer.

PMID: 20668279 [PubMed - as supplied by publisher]

Modes and Models of Forebrain Cholinergic Neuromodulation of Cognition.

Neuropsychopharmacology. 2010 Jul 28;

Authors: Hasselmo ME, Sarter M

As indicated by the profound cognitive impairments caused by cholinergic receptor antagonists, cholinergic neurotransmission has a vital role in cognitive function, specifically attention and memory encoding. Abnormally regulated cholinergic neurotransmission has been hypothesized to contribute to the cognitive symptoms of neuropsychiatric disorders. Loss of cholinergic neurons enhances the severity of the symptoms of dementia. Cholinergic receptor agonists and acetylcholinesterase inhibitors have been investigated for the treatment of cognitive dysfunction. Evidence from experiments using new techniques for measuring rapid changes in cholinergic neurotransmission provides a novel perspective on the cholinergic regulation of cognitive processes. This evidence indicates that changes in cholinergic modulation on a timescale of seconds is triggered by sensory input cues and serves to facilitate cue detection and attentional performance. Furthermore, the evidence indicates cholinergic induction of evoked intrinsic, persistent spiking mechanisms for active maintenance of sensory input, and planned responses. Models have been developed to describe the neuronal mechanisms underlying the transient modulation of cortical target circuits by cholinergic activity. These models postulate specific locations and roles of nicotinic and muscarinic acetylcholine receptors and that cholinergic neurotransmission is controlled in part by (cortical) target circuits. The available evidence and these models point to new principles governing the development of the next generation of cholinergic treatments for cognitive disorders.Neuropsychopharmacology advance online publication, 28 July 2010; doi:10.1038/npp.2010.104.

PMID: 20668433 [PubMed - as supplied by publisher]

Phantom breast syndrome.

Indian J Palliat Care. 2009 Jul;15(2):103-7

Authors: Ramesh , Shukla NK, Bhatnagar S

Phantom breast syndrome is a type of condition in which patients have a sensation of residual breast tissue and can include both non-painful sensations as well as phantom breast pain. The incidence varies in different studies, ranging from approximately 30% to as high as 80% of patients after mastectomy. It seriously affects quality of life through the combined impact of physical disability and emotional distress. The breast cancer incidence rate in India as well as Western countries has risen in recent years while survival rates have improved; this has effectively increased the number of women for whom post-treatment quality of life is important. In this context, chronic pain following treatment for breast cancer surgery is a significantly under-recognized and under-treated problem. Various types of chronic neuropathic pain may arise following breast cancer surgery due to surgical trauma. The cause of these syndromes is damage to various nerves during surgery. There are a number of assumed factors causing or perpetuating persistent neuropathic pain after breast cancer surgery. Most well-established risk factors for developing phantom breast pain and other related neuropathic pain syndromes are severe acute postoperative pain and greater postoperative use of analgesics. Based upon current evidence, the goals of prophylactic strategies could first target optimal peri-operative pain control and minimizing damage to nerves during surgery. There is some evidence that chronic pain and sensory abnormalities do decrease over time. The main group of oral medications studied includes anti-depressants, anticonvulsants, opioids, N-methyl-D-asparate receptor antagonists, mexilitine, topical lidocaine, cannabinoids, topical capsaicin and glysine antagonists. Neuromodulation techniques such as motor cortex stimulation, spinal cord stimulation, and intrathecal drug therapies have been used to treat various neuropathic pain syndromes.

PMID: 20668586 [PubMed - in process]

A C-fiber-mediated neuropathic brachioradial pruritus.

J Neurosurg. 2010 Jul;113(1):118-21

Authors: De Ridder D, Hans G, Pals P, Menovsky T

A 56-year-old man presented to the outpatient clinic with a 3-year history of itch within the innervation territory of C-6 of the left arm. Sudden neck movements induced intermittent paresthesias in the same dermatome. No dermatological diseases, allergies, or trauma to the affected extremity or the spine or a history of familial pruritus were reported. Neurological physical examination and electromyography revealed normal findings. Quantitative sensory testing demonstrated selective C-fiber dysfunction at C6-8 on the left, and cervical MR imaging revealed multilevel degenerative cervical spine pathology with neuroforaminal stenoses. Brachioradial neuropathic pruritus caused by cervical neuroforaminal stenosis was the final diagnosis. Treatment consisted of 2 cervical epidural steroid applications that resulted in clinical disappearance of the itch and improvement in C-fiber function on quantitative sensory testing.

PMID: 19817537 [PubMed - indexed for MEDLINE]

The Efficacy of Web-Based Cognitive Behavioral Interventions for Chronic Pain: A Systematic Review and Meta-Analysis.

J Pain. 2010 Jul 20;

Authors: Macea DD, Gajos K, Daglia Calil YA, Fregni F

Our objective was to conduct a systematic review and meta-analysis to quantify the efficacy of web-based cognitive behavioral interventions for the treatment of patients with chronic pain. MEDLINE and other databases were searched as data sources. Reference lists were examined for other relevant articles. We included 11 studies that evaluated the effects of web-based interventions on chronic pain using specific scales of pain. The pooled effect size (standardized mean difference between intervention versus waiting-list group means) from a random effects model was .285 (95% confidence interval: .145-.424), favoring the web-based intervention compared with the waiting-list group, although the effect was small. In addition, these results were not driven by any particular study, as shown by sensitivity analysis. Results from funnel plot argue against publication bias. Finally, the average dropout rate was 26.6%. In our meta-analysis, we demonstrate a small effect of web-based interventions, when using pain scale as the main outcome. Despite the minor effects and high dropout rates, the decreased costs and minor risk of adverse effects compared with pharmacological treatments support additional studies in chronic pain patients using web-based interventions. Further studies will be important to confirm the effects and determine the best responders to this intervention. PERSPECTIVE: Our findings suggest that web-based interventions for chronic pain result in small pain reductions in the intervention group compared with waiting-list control groups. These results advance the field of web-based cognitive behavioral interventions as a potential therapeutic tool for chronic pain and can potentially help clinicians and patients with chronic pain by decreasing treatment costs and side effects.

PMID: 20650691 [PubMed - as supplied by publisher]

Deep brain stimulation in trigeminal autonomic cephalalgias.

Neurotherapeutics. 2010 Apr;7(2):220-8

Authors: Leone M, Franzini A, Proietti Cecchini A, Mea E, Broggi G, Bussone G

Cluster headache (CH), paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT syndrome) are primary headaches grouped together as trigeminal autonomic cephalalgias (TACs). All are characterized by short-lived unilateral head pain attacks associated with oculofacial autonomic phenomena. Neuroimaging studies have demonstrated that the posterior hypothalamus is activated during attacks, implicating hypothalamic hyperactivity in TAC pathophysiology and suggesting stimulation of the ipsilateral posterior hypothalamus as a means of preventing intractable CH. After almost 10 years of experience, hypothalamic stimulation has proved successful in preventing pain attacks in approximately 60% of the 58 documented chronic drug-resistant CH patients implanted at various centers. Positive results have also been reported in drug-resistant SUNCT and PH. Microrecording studies on hypothalamic neurons are increasingly being performed and promise to make it possible to more precisely identify the target site. The implantation procedure has generally proved safe, although it carries a small risk of brain hemorrhage. Long-term stimulation is proving to be safe: studies on patients under continuous hypothalamic stimulation have identified nonsymptomatic impairment of orthostatic adaptation as the only noteworthy change. Studies on pain threshold in chronically stimulated patients show increased threshold for cold pain in the distribution of the first trigeminal branch ipsilateral to stimulation. When the stimulator is switched off, changes in sensory and pain thresholds do not occur immediately, indicating that long-term hypothalamic stimulation is necessary to produce sensory and nociceptive changes, as also indicated by clinical experience that CH attacks are brought under control only after weeks of stimulation. Infection, transient loss of consciousness, and micturition syncope have been reported, but treatment interruption usually is not required.

PMID: 20430322 [PubMed - indexed for MEDLINE]

Impact to spinal cord stimulator lead integrity with direct suture loop ties: commentary on kreis et Al. (2009).

Pain Med. 2010 Jul;11(7):1136-7

Authors: Colvin M

PMID: 20642734 [PubMed - in process]

Serotonin and its metabolism in basal deuterostomes: insights from Strongylocentrotus purpuratus and Xenoturbella bocki.

J Exp Biol. 2010 Aug 1;213(Pt 15):2647-2654

Authors: Squires LN, Rubakhin SS, Wadhams AA, Talbot KN, Nakano H, Moroz LL, Sweedler JV

Serotonin (5-HT), an important molecule in metazoans, is involved in a range of biological processes including neurotransmission and neuromodulation. Both its creation and release are tightly regulated, as is its removal. Multiple neurochemical pathways are responsible for the catabolism of 5-HT and are phyla specific; therefore, by elucidating these catabolic pathways we glean greater understanding of the relationships and origins of various transmitter systems. Here, 5-HT catabolic pathways were studied in Strongylocentrotus purpuratus and Xenoturbella bocki, two organisms occupying distinct positions in deuterostomes. The 5-HT-related compounds detected in these organisms were compared with those reported in other phyla. In S. purpuratus, 5-HT-related metabolites include N-acetyl serotonin, gamma-glutamyl-serotonin and 5-hydroxyindole acetic acid; the quantity and type were found to vary based on the specific tissues analyzed. In addition to these compounds, varying levels of tryptamine were also seen. Upon addition of a 5-HT precursor and a monoamine oxidase inhibitor, 5-HT itself was detected. In similar experiments using X. bocki tissues, the 5-HT-related compounds found included 5-HT sulfate, gamma-glutamyl-serotonin and 5-hydroxyindole acetic acid, as well as 5-HT and tryptamine. The sea urchin metabolizes 5-HT in a manner similar to both gastropod mollusks, as evidenced by the detection of gamma-glutamyl-serotonin, and vertebrates, as indicated by the presence of 5-hydroxyindole acetic acid and N-acetyl serotonin. In contrast, 5-HT metabolism in X. bocki appears more similar to common protostome 5-HT catabolic pathways.

PMID: 20639426 [PubMed - as supplied by publisher]

Neuromodulation.

Ann N Y Acad Sci. 2010 Jun;1199:204-11

Authors: Andrews RJ

Neuromodulation (deep brain stimulation; DBS) has become an established treatment for movement disorders (e.g., Parkinson's disease), and is in trials for refractory epilepsy, headache, and certain mood disorders. Two main themes will advance DBS significantly in the next five years: closed-loop DBS, that is, feedback from brain electrical activity to direct the stimulation; and computational analysis (CA)-electrophysiological modeling to enhance DBS. Closed-loop DBS is currently in clinical trials for refractory epilepsy. New imaging techniques offer preoperative modeling for DBS surgery, including nerve fiber tracts (diffusion tensor imaging), and imaging of volume of tissue activated by a specific electrode. CA techniques for DBS include mathematical models of the abnormally synchronized electrical activity which underlies epilepsy, movement disorders, and likely many mood disorders as well. By incorporating feedback loops and multiple recording and/or stimulating sites, the abnormally synchronized brain electrical activity can be desynchronized, then "unlearned" ("unkindling" in epilepsy). Characteristics of DBS utilizing CA include low frequency rather than high frequency stimulation; multiple stimulation and/or recording sites; likely 10-fold or more reduction in electrical current needs (much smaller "pulse generators"); more focused and less disruptive stimulation-fewer unwanted side effects; and potential to "cure" certain disorders by resetting abnormal firing patterns back to normal. These advantages of more sophisticated DBS techniques bring the following challenges, which may require a decade of research before reaching clinical practice because many brain disorders involve neurotransmitter abnormalities (e.g., dopamine in Parkinson's disease and certain mood disorders). Namely, how do we monitor and modulate neurotransmitters in addition to electrical activity? How do we get multiple microelectrodes into the brain in a minimally invasive manner? In the accompanying article, I address these two issues and offer some potential solutions.

PMID: 20633126 [PubMed - in process]

Neuromodulation.

Ann N Y Acad Sci. 2010 Jun;1199:212-20

Authors: Andrews RJ

Many nervous system disorders (e.g., Parkinson's disease, mood disorders) involve neurotransmitters as well as electrical activity. Pharmacologic treatment does not target the precise location(s) where neurotransmitter imbalances occur. Additionally, non-neuronal cells in the brain-notably astrocytes-influence neuronal activity through both electrical and neurochemical modulation of nearby neurons. Precise monitoring/recording and modulating/stimulating (both electrical and neurochemical) can optimize therapy in specific disorders and specific patients. Carbon-fiber microelectrodes (5 mum diameter) in freely moving rodents have shown that dopamine release is heterogeneous within various regions in the nucleus accumbens, a region involved in many mood disorders. Because neurons are only several microns in diameter (axons, dendrites, and synaptic clefts smaller still), ultramicroelectrodes will be essential to selectively monitor/modulate the cell body, the axon, or at the intracellular level. Nanoelectrode arrays can monitor both electrical activity and dopamine in real time with submicron resolution, and stimulate neurons with equal precision. Computational models indicate that precise monitoring/modulating (electrically and neurochemically) at the subnucleus or neuron level will be necessary to restore normal firing patterns and neurotransmitter levels in many brain disorders. Endovascular techniques can introduce ultramicroelectrodes (0.5 micron or smaller) into the brain via capillaries; such electrodes can stimulate/record neuronal tissue with a response virtually identical to extra-vascular microelectrodes. Within the next decade, hundreds if not thousands of submicron-sized monitoring/modulating electrodes can be placed wherever needed to restore brain function to normal. The term "neuromodulation" will likely replace deep brain stimulation (DBS) as both neurochemistry and electrical activity are included in the therapeutic modalities.

PMID: 20633127 [PubMed - in process]

From the Editor-in-Chief's desk.

Brain Stimul. 2009 Jul;2(3):121-2

Authors: George MS

PMID: 20633410 [PubMed - in process]

Neuromodulation in hypoxic-ischemic injury.

Brain Stimul. 2009 Jul;2(3):179-81

Authors: Boggio PS, Coutinho de Macedo E, Pascual-Leone A, Tormos Muñoz JM, Schwartzman JS, Fregni F

PMID: 20633417 [PubMed - in process]

Sacral Nerve Modulation in Overactive Bladder.

Curr Urol Rep. 2010 Jul 16;

Authors: Occhino JA, Siegel SW

This article represents a general overview of therapies for urinary urgency, frequency, and overactive bladder, with specific emphasis on sacral neuromodulation. The history of sacral neuromodulation is discussed along with an update of the current literature. Future directions for neuromodulation of the pelvic floor also are discussed.

PMID: 20635172 [PubMed - as supplied by publisher]

Peripheral neuromodulation via posterior tibial nerve stimulation - a potential treatment for faecal incontinence?

Ann R Coll Surg Engl. 2010 Jul;92(5):385-90

Authors: Findlay JM, Yeung JM, Robinson R, Greaves H, Maxwell-Armstrong C

INTRODUCTION: Faecal incontinence is a prevalent and important condition, with a range of treatment options. Neuromodulation via sacral nerve stimulators is efficacious, but expensive and associated with complications due to device implantation. Peripheral neuromodulation via posterior tibial nerve stimulation (PTNS) has been assessed in urinary incontinence, but there is minimal evidence for its use in faecal incontinence and no literature from the UK. This retrospective review aimed to assess the efficacy of PTNS in faecal incontinence. PATIENTS AND METHODS: Thirteen consecutive female patients with faecal incontinence of various causes (9 idiopathic, 3 obstetric, 1 surgery) underwent PTNS at a UK hospital. All were investigated with colonic imaging, anorectal physiology and endo-anal ultrasound. Prior treatments included physiotherapy (13), sphincteroplasty (3) biofeedback (3) and PTQ implants (1). PTNS was performed for 30 min, weekly for 12 weeks. RESULTS: Median monthly episodes of incontinence of wind, liquid and solid reduced from 6, 10 and 18 respectively to 0 with 12 weeks' treatment (P < 0.05). Significant improvements in quality of life indices were also seen. At 1-month follow up, a sustained reduction in incontinence of wind was seen (0 episodes), with non-significant reductions of liquid and solid stool. CONCLUSIONS: PTNS is a potentially efficacious, technically simple and minimally invasive alternative treatment modality for faecal incontinence. These early results are encouraging, but we await medium- and long-term follow-up, and a larger randomised trial comparing PTNS with alternative treatments and placebo.

PMID: 20626970 [PubMed - in process]

Modafinil Blocks Reinstatement of Extinguished Opiate-Seeking in Rats: Mediation by a Glutamate Mechanism.

Neuropsychopharmacology. 2010 Jul 14;

Authors: Tahsili-Fahadan P, Carr GV, Harris GC, Aston-Jones G

Opiate addiction is characterized by high rates of relapse even after long periods of abstinence, requiring new relapse-prevention treatments that do not have abuse potential. Recently, clinical studies suggested that the wake-promoting drug modafinil might decrease relapse in cocaine addicts. In addition, group II metabotropic glutamate receptors (mGlu2/3R) have been suggested as a new therapeutic target for drug addiction. Here, we investigated the ability of modafinil to prevent the acute morphine to promote reinstatement of extinguished preference for morphine, and the involvement of mGlu2/3Rs in this effect. Conditioned place preference (CPP) for morphine was induced in Sprague-Dawley rats, followed by extinction training. Preference for the morphine-paired side was reinstated following extinction by a morphine-priming injection. The results of our study showed that modafinil (300 mg/kg, i.p., but not 100 mg/kg) 30 min before the morphine-priming injection blocked reinstatement of extinguished CPP. The anti-reinstatement effect of modafinil was completely prevented by pretreatment with the selective mGlu2/3 antagonist LY341495. Additional experiments indicated that modafinil alone did not produce a preference, and that modafinil did not alter the expression of morphine CPP or the cueing properties of morphine either 1 or 14 days after morphine CPP conditioning. These data reveal a novel mechanism for modafinil actions, a role for mGlu2/3 receptors in reinstatement of opiate-seeking, and a new therapeutic option to treat relapse in opiate addiction.Neuropsychopharmacology advance online publication, 14 July 2010; doi:10.1038/npp.2010.94.

PMID: 20631691 [PubMed - as supplied by publisher]

Posterior tibial nerve stimulation for faecal incontinence.

Br J Nurs. 2010 Jun 24-Jul 7;19(12):750-4

Authors: Findlay J, Maxwell-Armstrong C

Faecal incontinence is a common multifactorial condition with a range of invasive treatment options, all of which may be associated with significant complications. Posterior tibial stimulation by continence nurses is an established treatment for urinary incontinence; however, its use in faecal incontinence, while rapidly evolving, is limited to eight small and differing studies. In this article, the background of current management options for faecal incontinence is discussed, as are the physiology and evidence underlying neuromodulation. The evidence base for posterior tibial nerve stimulation in faecal incontinence is reviewed, as well as the implications for practice and further research. While this early evidence base is encouraging, it has yet to be established whether this novel approach may be the minimally invasive, effective and cheap treatment hoped for, for this common and debilitating condition.

PMID: 20622793 [PubMed - in process]

Sacral nerve stimulation for treatment of intractable pain associated with cauda equina syndrome.

J Korean Neurosurg Soc. 2010 Jun;47(6):473-6

Authors: Kim JH, Hong JC, Kim MS, Kim SH

Sacral nerve stimulation (SNS) is an effective treatment for bladder and bowel dysfunction, and also has a role in the treatment of chronic pelvic pain. We report two cases of intractable pain associated with cauda equina syndrome (CES) that were treated successfully by SNS. The first patient suffered from intractable pelvic pain with urinary incontinence and fecal incontinence after surgery for a herniated lumbar disc. The second patient underwent surgery for treatment of a burst fracture and developed intractable pelvic area pain, right leg pain, excessive urinary frequency, urinary incontinence, voiding difficulty and constipation one year after surgery. A SNS trial was performed on both patients. Both patients' pain was significantly improved and urinary symptoms were much relieved. Neuromodulation of the sacral nerves is an effective treatment for idiopathic urinary frequency, urgency, and urge incontinence. Sacral neuromodulation has also been used to control various forms of pelvic pain. Although the mechanism of action of neuromodulation remains unexplained, numerous clinical success reports suggest that it is a therapy with efficacy and durability. From the results of our research, we believe that SNS can be a safe and effective option for the treatment of intractable pelvic pain with incomplete CES.

PMID: 20617098 [PubMed - in process]

Highlights in basic autonomic neurosciences: Glia and neuromodulation.

Auton Neurosci. 2010 Jul 6;

Authors: Machado BH, Moraes DJ, Costa KM, Gilbey MP

PMID: 20609632 [PubMed - as supplied by publisher]

Sustained cortical and subcortical neuromodulation induced by electrical tongue stimulation.

Brain Imaging Behav. 2010 Jul 8;

Authors: Wildenberg JC, Tyler ME, Danilov YP, Kaczmarek KA, Meyerand ME

This pilot study aimed to show that information-free stimulation of the tongue can improve behavioral measures and induce sustained neuromodulation of the balance-processing network in individuals with balance dysfunction. Twelve balance-impaired subjects received one week of cranial nerve non-invasive neuromodulation (CN-NINM). Before and after the week of stimulation, postural sway and fMRI activation were measured to monitor susceptibility to optic flow. Nine normal controls also underwent the postural sway and fMRI tests but did not receive CN-NINM. Results showed that before CN-NINM balance-impaired subjects swayed more than normal controls as expected (p </= 0.05), and that overall sway and susceptibility to optic flow decreased after CN-NINM (p </= 0.005 & p </= 0.05). fMRI showed upregulation of visual sensitivity to optic flow in balance-impaired subjects that decreased after CN-NINM. A region of interest analysis indicated that CN-NINM may induce neuromodulation by increasing activity within the dorsal pons (p </= 0.01).

PMID: 20614202 [PubMed - as supplied by publisher]

Interleukin-6-type cytokines in Neuroprotection and Neuromodulation: Oncostatin M, but not Leukemia inhibitory factor, requires neuronal Adenosine A(1) Receptor function.

J Neurochem. 2010 Jun 28;

Authors: Moidunny S, Dias R, Wesseling E, Sekino Y, Boddeke HW, Sebastião A, Biber K

ABSTRACT Neuroprotection is one of the prominent functions of the interleukin (IL)-6-type cytokine family, for which the underlying mechanism(s) are not fully understood. We have previously shown that neuroprotection and neuromodulation mediated by IL-6 require neuronal adenosine A(1) receptor (A(1)R) function. We now have investigated whether two other IL-6-type cytokines (Oncostatin M (OSM) and Leukemia inhibitory factor (LIF)) use a similar mechanism. It is presented here that OSM but not LIF, enhanced the expression of A(1)Rs (both mRNA and protein levels) in cultured neurons. Whereas the neuroprotective effect of LIF was unchanged in A(1)R deficient neurons, OSM failed to protect neurons in the absence of A(1)R. In addition, OSM pretreatment for 4 hours potentiated the A(1)R-mediated inhibition of electrically-evoked excitatory post-synaptic currents (EPSCs) recorded from hippocampal slices either under normal or hypoxic conditions. No such effect was observed after LIF pretreatment. Our findings thus strongly suggest that, despite known structural and functional similarities, OSM and LIF use different mechanisms to achieve neuroprotection and neuromodulation.

PMID: 20598020 [PubMed - as supplied by publisher]

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