By contrast, the MUA-LFP PPC implicitly weights each SUA that goe

By contrast, the MUA-LFP PPC implicitly weights each SUA that goes into the MUA mixture according to its firing rate: SUAs with higher firing rates will influence the MUA-PPC more than SUAs with lower firing rates. Consequently, the difference between the attentional effects on MUA and SUA PPC might be explained through one of the following scenarios or a combination of both: (1) with attention, SUAs with particularly high firing rate, and therefore particularly strong MUA contribution, might increase their gamma locking particularly strongly, and (2) with attention,

SUAs with particularly strong gamma locking might increase their firing rates particularly strongly and thereby contribute more to the MUAs. In both cases, the correlation between rates and gamma locking should increase with attention. To test this prediction, we calculated the Spearman rank correlation across SUAs, between the SUA rates and the PPC, and separately HDAC activation for the two attention conditions and show their difference between attention conditions in Figure 7A. We found that our prediction

held, selectively in the gamma-band (NS and BS, p < 0.05 and p < 0.01 respectively, bootstrap test). In fact, PPC-rate correlations were significantly greater than zero when attention was inside the neurons’ RF (NS: Spearman ρ = 0.50, p < 0.001; BS: 0.62, p < 0.001; NNS = 21, NBS = 39 for Figure 7; see Figures S1G–S1J and S6 for monkey M1 and Figures S1G–S1J and S7 for monkey M2), but not when it was outside the RF (NS: −0.07, Venetoclax purchase n.s.; BS: −0.02, n.s.). This analysis was done on the absolute SUA firing rates during sustained activation, which is a function of both baseline firing rate (defined here from fixation onset to stimulus onset), and the change in firing rate during visual stimulation relative to baseline. To investigate their relative contributions, we entered these two variables

4-Aminobutyrate aminotransferase into a multiple regression model (with every unit as one observation), predicting SUA PPC, separately for each attention condition. We show the difference in regression T-statistics between attention conditions in Figures 7B and 7C. The effect described above for the overall sustained firing rates held for both the baseline rate (BS and NS, p < 0.01 and p < 0.05 respectively, bootstrap test) and the rate change relative to baseline (BS and NS, p < 0.01 and p < 0.05 respectively, bootstrap test). The effect was again specific for the gamma-frequency band. In fact, a unit’s baseline firing rate (NS: T-stat = 2.71, p < 0.01; BS: 3.51, p < 0.001) positively predicted its gamma PPC when selective attention was directed inside its RF, but not when it was directed outside its RF (NS: −0.39; BS: −0.15, all n.s.). Similarly, a BS cell’s firing rate change relative to baseline (NS: T-stat = 1.59, n.s.; BS: 3.86, p < 0.01) positively predicted its gamma PPC when selective attention was directed inside its RF, but not when it was directed outside its RF (NS: −0.9, n.s.; BS: 0.06, n.s.).

After reaching stable performance, two more difficult mixture con

After reaching stable performance, two more difficult mixture contrasts (4% and 2% mixture contrast) were sequentially introduced ( Figure 6A, phase IV). (V)

selleck Rats were returned to a go-signal paradigm with dgo = 1.0 s at 2% mixture contrast and then trained to stable performance on 4% mixture contrast ( Figure 6A, phase V). (VI) RT performance was measured on three easier ratio pairs ( Figure 6A, phase VI). The training sequence consisted of (1) handling and habituation to the behavior box (3 sessions); (2) water-port training (1 day); (3) odor-port training, in which a single odor (usually ethyl butyrate) was rewarded at either port and the required center poke duration was increased from 0 to 300 ms (2–4 sessions); (4) introduction of test odors in 5:95 and 95:5, rewarded at left and right choice ports with assignments counterbalanced across rats (1–3 sessions); (5) introduction of increasingly difficult mixture ratio pairs rewarded at the side corresponding to the dominant component (4–7 sessions). Go-signal task training occurred between phase III and IV. For the check details purpose of experiments involving training on a new stimulus or condition, stable or asymptotic performance was defined as <5% change in performance over ≥5 sessions. All the analysis was performed in Matlab 6.5 Release 13. Behavioral accuracy

was defined as the percentage of correct choices over the total number of correct and incorrect choices. Odor sampling duration (OSD) was calculated as the difference between odor valve actuation until odor port exit, with 100 ms subtracted to account for the delay from valve opening to odor reaching the nose (Feierstein et al., 2006; Figure 1C). Movement time (MT) was defined as the time between odor port exit and choice port entry. We excluded from calculation of performance accuracy and OSD trials in which odor port withdrawal occurred less than 100 ms after odor

onset (<10% of trials) or before the go signal in go-signal paradigms (<25% of trials) and trials in which no choice was made or choice port entry occurred after the response deadline (<1% of trials) (Figure S1E). Performance accuracy as a function of mixture difficulty was fitted with a Weibull function using a maximum likelihood method and OSDs using a linear regression, except in Figure 2Cii where a logistic Farnesyltransferase regression using binomial distribution was used. Logistic regression was also used to fit the psychometric function in Figure 2Ci. Error bars are mean ± SEM (n across rats) or mean ± SD (n across sessions). The effect of difficulty on accuracy or OSD was tested using one-way ANOVA with pairwise comparisons between different mixture contrast ratios (MULTCOMPARE function in Matlab) at a significance level of p < 0.0125 (i.e., adjusted for multiple comparisons). In order to estimate the ability of the subject to anticipate the occurrence of a go signal, we calculated the subjective anticipation function, as described in Janssen and Shadlen (2005).

01 were considered for the analysis Right-tailed Fisher’s exact

01 were considered for the analysis. Right-tailed Fisher’s exact test was used to calculate a p value determining the probability that each biological function

and/or disease assigned to that data set is due to chance alone. Two milliliters of shaved synaptosomes collected from sucrose gradients were diluted in 5 ml PBS and centrifuged for 30 min at 5,500 × gmax, 4°C, in a swing out rotor. The synaptosomal pellet was then resuspended in 2.4 ml PBS. One hundred microliters of this suspension were carefully aliquoted onto each poly-L-lysine precoated coverslip placed in a 12-well plate and incubated for 45 min at room temperature. Afterward, 1 ml PBS was selleck compound added to each well and synaptosomes pelleted on the coverslip by centrifugation for 30 min at 5,580 × gmax (5,500 rpm) at 4°C in a HIGHplate rotor Epacadostat supplier 75006444 (Sorvall Heraeus). Synaptosomes were then fixed with 4% paraformaldehyde (PFA), permeabilized with 0.1% Triton X-100 and stained with primary and secondary antibodies. Synaptosomal images were acquired using an AOBS SP2 confocal microscope (Leica Microsystems) with a 63× oil-immersion objective, standard filter sets (Leica Microsystems), and Leica LCS software. Line scan analyses

were performed using the LAS AF Lite software (Leica). The extent of colocalization between different protein pairs in glutamaterigic versus GABAergic synaptosomes were determined using a custom written Matlab algorithm (The Mathworks Inc.) kindly provided by Prof. Silvio Rizzoli. Colocalization with either enough VGLUT1 or VGAT was considered when the center of intensity in

the two channels was within a distance of 200 nm. At least 500 synaptosomes were analyzed for each given protein pair in three independent biological replicates. We thank Prof. Silvio Rizzoli for providing the MatLab program and Maria Druminski for excellent technical assistance. The research leading to these results has received funding from the European Union Seventh Framework Programme under grant agreement no. HEALTH-F2-2009-241498 (“EUROSPIN”) to R.J. and of the Deutsche Forschungsgemeinschaft (SFB 889, TP4) to R.J. and H.U. “
“The formation of long-lasting memory requires de novo synthesis of mRNA and proteins and is blocked by inhibitors of transcription or translation, whereas short-term memory relies on the modification of pre-existing proteins and is not affected by such inhibitors. Similarly, long-term potentiation (LTP), a cellular model for learning and memory, is dependent on transcription and translation for its late phase (late LTP; L-LTP), which lasts for many hours, while its early phase (early LTP; E-LTP) lasts 1–2 hr and is translation independent (Kandel, 2001; Silva, 2003). Neuronal mRNA translation is tightly regulated by synaptic activity (Banerjee et al., 2009; Kelleher et al., 2004a; Richter and Klann, 2009; Sutton and Schuman, 2006).

Enhancement of short-term learning and plasticity by long-term

Enhancement of short-term learning and plasticity by long-term

training is an intriguing possibility that has great potential as an enhancing factor for applications of training protocols. These findings bear some conceptual resemblance to findings of increased plasticity on the cellular level due to pretreatment or previous learning or excitation history of the neurons involved, an effect termed metaplasticity to indicate that the rate of plasticity is altered on a higher-order level (Abraham, 2008; Abraham and Bear, 1996). While the concept of metaplasticity stems from cellular and molecular phenomena such as long-term potentiation (e.g., Huang et al., 1992), it has also been applied to explain features of experience-dependent plasticity in visual cortex (Bienenstock et al., 1982), and it can DAPT supplier also explain enhanced short-term plastic effects due to modulation of the involved networks by previous sensory experience or learning (Hofer et al., 2006; Zelcer et al., 2006). The framework of musical training offers an excellent CP-690550 datasheet possibility

to explore the potential for metaplastic effects at higher levels of organization in the human brain. However, while the results so far clearly indicate that long- and short-term effects of musical training and other types of short-term plasticity interact and may enhance 3-mercaptopyruvate sulfurtransferase one another, more research is needed to reveal if the enhancement is due to top-down influences such as attention to relevant input, or if the properties of the sensory systems are also altered on lower levels of processing. Although musical training can sometimes be very tedious and frustrating, as every professional musician can certainly confirm, the reward value and positive feedback associated with producing music

might contribute to the observed efficacy of the approach in comparison to other, less rewarding training paradigms. Listening to certain musical passages has been shown to engage the dopaminergic component of the reward system (Blood and Zatorre, 2001; Salimpoor et al., 2011). Therefore, another interesting aspect of musical training is the possible modulation of neuronal plasticity via the reward circuitry, in particular through aminergic systems, whose modulatory effects on cortical plasticity have been shown in animal models and to some extent also in humans (Gu, 2002; Thiel, 2007). For example, Bao et al. (2001) showed in rats that pairing a tone with stimulation of the ventral tegmental area, resulting in dopamine release to projections in the auditory cortex, enhanced responses to this tone and sharpened the neuronal tuning curve in A1 and secondary auditory cortex.

, 2008) Another possibility is that K+ channels may be modulated

, 2008). Another possibility is that K+ channels may be modulated, since many conditions associated with altered neuronal excitability involve changes in K+ channel expression (Lüscher and Slesinger,

2010). To test this possibility, we examined VTA from mice that received sham or morphine pellets and analyzed by PCR the expression of K+ channels whose regulation has been implicated in other systems. We observed a significant decrease in expression levels of two K+ channel subunits, KCNAB2 and GIRK3, with a trend seen for several others ( Figure 3A). To examine whether decreased K+ channel expression is regulated at the transcriptional level, we performed chromatin immunoprecipitation (ChIP) on VTA dissected from sham- and morphine-treated rats. Overall,

we observed epigenetic changes consistent with K+ channel downregulation learn more (Figures 3B and 3C). Modifications consistent with increased transcription—acetylation of histones H3 and H4, trimethylation of Lys-4 of H3, and binding of RNA polymerase II (POL2)—were significantly decreased at the KCNAB2 and KCNF1 promoters ( Figure 3B) and decreased trimethylation of Lys-4 of H3 and binding of RNA polymerase II (POL2) was observed at the GIRK3 promoter. These changes suggest that, in addition to morphine potentially reducing GABAA responses in VTA DA neurons, expression of specific K+ channel subunits is reduced via transcriptional mechanisms to further mediate enhanced excitability of these neurons. see more Since both chronic morphine and decreased AKT signaling increase VTA DA neuron firing rate, we next examined whether decreasing AKT activity also Thymidine kinase decreases K+ channel

expression similarly to chronic morphine. To test this possibility, we analyzed VTA from mice that had received intra-VTA injections of either HSV-GFP or HSV-IRS2dn. We overexpressed IRS2dn because this is the most direct way of reducing AKT activity without affecting total levels of the enzyme, as seen with chronic morphine. We observed a significant decrease in levels of expression of three K+ channel subunits, KCNF1, KCNJ2, and GIRK3 ( Figure 4A). These data suggest that, in addition to altering DA neuronal activity via GABAA channel regulation, altering AKT signaling can also modulate K+ channel expression. Finally, since both chronic morphine and decreased IRS2/AKT signaling control VTA DA neuronal morphology and excitability, we determined whether decreased AKT signaling also affects DA output to NAc. As found with chronic morphine, HSV-IRS2dn in VTA decreased electrically evoked DA output in rat NAc (Figure 4B). Based on our prior research in rats showing that IRS2 downregulation mediates the chronic morphine-induced decrease in VTA DA soma size (Russo et al., 2007), we assumed that this morphological change was likewise dependent on AKT downregulation.

We analyzed levels of p-STAT3 in the proximal nerve stump 1 day a

We analyzed levels of p-STAT3 in the proximal nerve stump 1 day after sciatic nerve lesion. In WT, p-STAT3 is barely detectable in the unlesioned contralateral learn more nerve but is dramatically upregulated by injury (Figure 3C). p-STAT3 is localized in neuronal axons, as shown by immunostaining (Figure 3D). In the absence of DLK, STAT3 is still phosphorylated in the injured axons, and the levels

are similar to WT (Figures 3C and 3D; n = 3). These data show that the local activation of STAT3 does not require DLK. Instead, these findings suggest that DLK may be necessary for translocation of the injury signal to the cell body. We next examined whether DLK is indeed required for the transport of p-STAT3 to the cell body. To track the movement of the phosphorylated protein upon injury, we performed a double nerve ligation in which the sciatic nerve is sutured at two locations

(Figure 3E). The nerve ligation injures axons and blocks axonal transport, so that transported cargoes accumulate near the knots. Retrograde cargoes accumulate in the proximal segment of the nerve, while anterograde cargoes concentrate in the distal segment, so the ratio of protein present in the proximal/distal segment is a measure selleck inhibitor of retrograde transport (Cavalli et al., 2005). Upon double ligation of WT sciatic nerves for 6 hr, p-STAT3 levels are 1.5-fold higher in the proximal segment, consistent with the retrograde transport of p-STAT3 after injury. However, this accumulation is blocked in DLK KOs (p < 0.05) (Figures 3E and 3F). We also analyzed transport of JIP3, a scaffolding protein that links DLK and JNK to the axon transport machinery (Cavalli et al., 2005; Ghosh et al., 2011). Injury facilitates the association of

JIP3 with the retrograde transport machinery and increases the retrograde transport of both JIP3 and phosphorylated JNK (Cavalli et al., Astemizole 2005). In the double ligation assay, injury-induced accumulation of JIP3 in the proximal stump is abolished in the absence of DLK (p < 0.05) (Figures 3E and 3F). Therefore, DLK is necessary for the retrograde transport of both p-STAT3 and JIP3 upon axon injury. Collectively, these results demonstrate that DLK plays an essential role for the axonal transport of injury signaling components to the cell body. Taken together, these data demonstrate that DLK is required for robust axon regeneration in the vertebrate PNS in vivo, DLK promotes retrograde transport of injury signals that enhance axonal regenerative capacity, and injury-induced potentiation of axonal regeneration requires DLK. Trauma, neurotoxins, and neurological disease can all trigger axonal damage and the loss of neuronal connections. The capacity of a neuron to regenerate an injured axon is crucial for the recovery of neural function.

This approach presumes that what we now call “depression” or “sch

This approach presumes that what we now call “depression” or “schizophrenia” are, in fact, many different disorders with distinct underlying biological causes that require different treatments. While this approach is not ready for clinical use,

Y-27632 datasheet it demonstrates the extent to which mental disorders are now addressed as brain disorders, or, more specifically, as brain circuit disorders. Across brain disorders, whether primarily neurologic or psychiatric, there is an increasing recognition that behavioral symptoms are late manifestations of disease. This insight for Alzheimer’s, Parkinson’s, schizophrenia, and autism represents a fundamental shift in emphasis, similar to the shift in the treatment of atherosclerosis and hypertension before they cause ischemic heart disease or stroke. This preemptive approach focuses on early detection of brain changes and the development of early interventions that can prevent or forestall neurodegenerative or neurodevelopmental disorders.

What about new treatments? Basic science has yielded several new molecular targets that have become the basis of new therapies. For neurological disorders, the past two decades have brought breakthroughs in the treatment of migraine (triptans; Lipton, 2011), multiple sclerosis (beta interferon, copolymer, fingolimide, and difumarate; Stankiewicz et al., 2013), acute stroke (tissue plasminogen activator), and a number of new agents for epilepsy, including rapamycin for epilepsy in tuberous sclerosis (Krueger et al., 2013). For mental disorders, we have seen the development of second-generation antipsychotics and antidepressants, with different side effect profiles but little improvement in efficacy over the medications of 1988. There have been few

novel targets in this space, in part because of the limited understanding of the pathophysiology of neurodevelopmental disorders, relative to the progress on neurodegenerative Urease diseases (Hyman, 2012). One hopeful discovery is the relatively recent insight that antidepressant effects can be achieved within hours rather than weeks (Martinowich et al., 2013). The observation that ketamine resolves even treatment-refractory depression in less than 24 hr has changed our expectations for the development of new antidepressants. Basic science has also yielded insights about circuitry that have been translated into new, effective therapies. Modulation of circuits through deep brain stimulation (DBS) has proven to be effective for movement disorders including Parkinson’s disease, essential tremor, and dystonia (Miocinovic et al., 2013). Development of DBS surgery for Parkinson’s disease resulted from decades of basic science studies of basal ganglia circuitry in nonhuman primates (DeLong and Wichmann, 2007). More recently, DBS in the subcallosal cingulate region, identified as metabolically hyperactive in patients with severe drug-resistant depression, showed dramatic antidepressant effects (Holtzheimer et al.

—with external sensory cues—such as food or mate availability, li

—with external sensory cues—such as food or mate availability, light and temperature, suitability for egg deposition, etc.—in the choice of what behaviors to perform at any given moment in time. This requires the development and use of richer, more sophisticated

naturalistic behavioral paradigms that will permit this behavioral choice function of neuropeptide modulation to be directly experimentally addressed. Work in the laboratory of M.N.N. is supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH) (R01NS055035, R01NS058443, SCH772984 molecular weight R21NS058330) and the National Institute of General Medical Sciences (NIGMS), NIH (R01GM098931). Work in the laboratory of P.H.T. is supported in part by NINDS, NIH (R01NS021749), NIGMS, selleck chemicals llc NIH (R01GM085788), and the National Institute of Mental Health, NIH (R01MH067122). “
“Just as there are multiple perceptions for the proverbial blind men as to what an elephant is, there are numerous perspectives one can adopt to view neuropeptide modulation in the CNS. Here, I take the view that neuropeptide modulation in the CNS is inextricably linked with fast amino acid GABA and glutamate signaling. Many other viable perspectives exist and are not mutually exclusive. I have used a few examples of peptide

secretion and actions which may be representative of many brain regions not discussed herein; many of the examples used here are from the hypothalamus, the part of the brain where neuropeptides have Thymidine kinase been most thoroughly studied. Many important neuropeptides are not included in the review. Although the focus here is on neuropeptides, some of the mechanisms of release and many of the mechanisms of response to neuropeptides may generalize to other neuromodulators in the brain, including the catecholamines, serotonin, adenosine, endocannabinoids, and neurotrophic factors. Neuropeptides can exert direct effects on neuronal physiology within seconds to minutes, and can also modulate gene expression over the course of hours to days; the focus here is

on the direct neurophysiological actions. The nomenclature of neuropeptides can initially be confusing. Names of CNS neuropeptides often give a historical perspective indicating what the peptide-pioneers initially discovered as the putative function. Since many neuropeptides were discovered in the context of regulation of hormone release, neuropeptide names may bear that functional link. True to its name, somatostatin released into the portal blood supply of the median eminence from nearby hypothalamic neurons can decrease growth hormone secretion from the pituitary gland; on the other hand, the somatostatin-synthesizing neurons in the cortex and hippocampus have no functional relation to hormone regulation.

GluA, TARP and CNIH cDNAs were cotransfected with a GFP-expressin

GluA, TARP and CNIH cDNAs were cotransfected with a GFP-expressing reporter plasmid for identification in electrophysiology experiments. One hundred percent CNIH-2 transfection indicates equal amounts of CNIH-2 and GluA subunit cDNAs and 50% CNIH-2 reduces this ratio by one

half. The cells were trypsinized 1 day after transfection and plated on glass coverslips at low density (∼5000/cm2). Experiments were performed 48–72 hr posttransfection. Stargazer mice were obtained from Jackson Laboratory and maintained at the Yale PLX-4720 manufacturer animal facility under the guidelines of the Institutional Animal Care and Use Committee. Heterozygous male and female mice were mated to obtain homozygous stargazer mice. Cerebellar granule

cell cultures were prepared from postnatal day 7–8 (P7–8) homozygous stargazer mice and were transfected at 5 days in vitro (DIV5) as described (Cho et al., 2007). Primary cultures of rat hippocampal neurons were prepared essentially as described (Kato et al., 2008). Briefly, hippocampi dissected from E19 Wistar rat embryos were incubated at 37°C for 10 min in a papain solution (in mM): 5 L-cysteine, 1 ethylenediaminetetraacetic acid, 10 HEPES-NaOH Protein Tyrosine Kinase inhibitor (pH 7.4), 100 μg/ml bovine serum albumin, 10 U/ml papain (Worthington), and 0.02% DNase (Sigma). The reaction was stopped by addition of an equal volume of fetal bovine serum. The cells were triturated and washed with Neurobasal (Invitrogen) supplemented with B-27, 100 μg/ml penicillin,

85 μg/ml streptomycin, 0.5 mM glutamine. The cells were plated on 12 mm coverslips coated with poly-D-lysine in 24-well plates at 100,000 cells/well density. cDNA (γ-8, CNIH-2, or γ-8 and CNIH-2)- or CNIH-2 shRNA-Lipofectamine 2000 (Invitrogen) complexes were prepared in Neurobasal medium according to manufacturer’s specifications. Primary neurons (>14 DIV) were incubated with these Lipofectamine complexes in Neurobasal medium in the absence of B-27, penicillin/streptomycin, and L-glutamine for at least 2 hr and then returned to the original conditioned medium. Electrophysiological recordings from primary neurons were performed at least Linifanib (ABT-869) 48 hr posttransfection. Lentiviral particles for shRNAs were infected at multiplicity of infection = 2. Hippocampal pyramidal neurons from 5- to 8-month-old mice were isolated as previously described (Kato et al., 2008). Briefly, a rapidly dissected brain was immersed in ice cold NaHCO3-bufferd saline solution (in mM): 120 NaCl, 2.5 KCl, 1 MgCl2, 1.25 Na2PO4, 2 CaCl2, 26 NaHCO3, and 10 glucose (pH 7.2), osmolarity 300 ± 2 mOsm/l. Coronal hippocampal slices (400 μm thick) were prepared by a Vibroslice (Campden Instruments) in ice cold NaHCO3-bufferd saline solution and then were recovered at room temperature in continuously oxygenated (95% O2, 5% CO2), NaHCO3-bufferd saline solution for 0.5–5 hr.

Dans les « Standards Options Recommandations » de 2003 [2], 20 à

Dans les « Standards Options Recommandations » de 2003 [2], 20 à 50 % des 9007 patients analysés

(sur 36 études) étaient douloureux au moment du diagnostic de cancer et la prévalence de la douleur augmentait au cours de l’évolution de la maladie avec 55 à 95 % de patients douloureux. Dans l’étude de Breivik et al., regroupant 5084 patients cancéreux adultes contactés entre 2006 et 2007 dans onze pays européens (dont 642 France) et en Israël, la prévalence globale de la douleur était de 84 % et de 75 % en France [3]. Parmi ces patients, 56 % avaient une douleur modérée à sévère et pour 573 patients selleck chemicals tirés au sort, 41 % recevaient un traitement opioïde fort, 69 % mentionnaient un retentissement de la douleur sur la qualité de vie et 50 % avaient Temsirolimus ic50 le sentiment que la qualité de vie n’était pas une priorité pour les professionnels de santé. La prévalence de la douleur était particulièrement élevée (plus de 85 %) pour les patients qui avaient un cancer du pancréas, des os, du cerveau, de la tête et du cou et les patients porteurs de lymphome. Une enquête nationale, réalisée en

2010, sous l’égide de l’INCa (Institut national du cancer) en collaboration avec l’Institut BVA, a été menée auprès de 1507 patients atteints de cancer traités en ambulatoire. L’objectif principal était de préciser l’état des lieux concernant les modalités de prise en inhibitors charge de la douleur du cancer en France [4]. Ce document s’inscrit

dans la mise en œuvre du Plan cancer 2009–2013, à savoir « renforcer la qualité des prises en charge pour tous les malades atteints de cancer », et plus précisément la mesure 19.1 du plan cancer : « généraliser l’accès aux mesures transversales lancées par le Plan cancer précédent, améliorant la qualité de toute prise en charge en cancérologie ». Cette enquête visait à décrire la douleur des patients en phase de traitement Casein kinase 1 curatif, en situation de cancer avancé et également à distance des traitements (en phase de surveillance ou de rémission), à individualiser la douleur neuropathique, les crises douloureuses et leurs prises en charge. Sur les 1507 patients interrogés, 28 % étaient en phase de traitement curatif, 53 % en situation de cancer avancé, 18 % en phase de surveillance ou de rémission avec, pour la majorité d’entre eux, un recul de plus d’un an par rapport à la fin de la chimiothérapie. La prévalence déclarée de la douleur dans cette enquête est identique à celle des données de la littérature, la douleur étant présente chez 53 % des patients interrogés. Une douleur chronique (présente depuis plus de trois mois) est rapportée par 30 % des patients douloureux en situation de cancer avancé, mais aussi par 25 % des patients douloureux à distance de tout traitement ou bien en rémission.