Additionally, those who are very deconditioned could start RT wit

Additionally, those who are very deconditioned could start RT with a “very light” to “light” intensity

(40%–50% 1-RM) to improve strength, power, and balance.27 It is advised that women unfamiliar with RT consult a fitness professional prior BMN 673 nmr to beginning a program. It is suggested that one must use progressive overload to stimulate muscular adaptations to resistance exercise. Typical recommendations for progression of RT is to first increase repetitions, followed by an increase in weight (0.5 kg for upper body, 1 kg for lower body) per week. For optimal results from a resistance program, the focus should be on full-body, compound movements (bench press, squat, pull-ups, etc.). Furthermore, adherence to group-based RT programs Everolimus molecular weight tends to be higher among older women than home based programs. 88 and 89 Additionally, Elsangedy and colleagues 71 recently found that women who self-selected resistance

exercise intensity fell below current ACSM guidelines. Consequently, the participation in a supervised or group-based resistance exercise program may improve women’s adherence and health benefits stemming from a higher intensity attained. Finally, the authors propose circuit training, which incorporates both RT and aerobics, as an attractive alternative for weight training. One of the major benefits to circuit training is that it can illicit the same positive physiological responses as traditional RT, thus providing a time-efficient alternative to improve muscular strength and functional fitness. 90 The ACSM recommendations for flexibility are to aim for greater than 2–3 days per week, ultimately aiming for daily training. Static stretching should be held 10–30 s at a point of mild discomfort, although stretches lasting 30–60 s may provide additional benefits. Two to four repetitions per exercise are recommended, aiming for at least 60 s of stretching for each major muscle-tendon

unit (Table 3).27 The recommendations we have provided are general. The frequency, intensity, PAK6 type, and duration of exercise one is able to achieve and maintain will vary from person to person. Thus we suggest that an individualized approach be utilized. While some activity is better than none, individuals aiming to improve CV health, muscular strength and endurance, and functional mobility should strive to meet the minimum recommendations we have provided. “
“Across the world a demographic shift is occurring; the number of older adults (individuals ≥65 years) is expected to nearly triple from 2010 to 2050.1 Consequently, for the first time ever, the total number of older adults in the world will be greater than the number of young children (≤5 years).1 Moreover, it is predicted that women will continue to outnumber and outlive men.

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Live imaging confirmed that transport of labeled vesicles was blo

Live imaging confirmed that transport of labeled vesicles was blocked by BFA see more (data not shown). As Schwann cells do not myelinate in the

presence of BFA (data not shown), we established microfluidic chambers, which allowed neurons to be treated separately from Schwann cells. In these cultures, neuronal cell bodies and their distal neurites are grown in separate compartments, connected by processes that extend through microgrooves (Taylor et al., 2005); Schwann cells were added to the neurite compartment and maintained under myelinating conditions (Figure 2D). The compartment containing the cell bodies was treated either with vehicle control (DMSO) or with BFA continuously, beginning with the onset of myelination. Cultures were then fixed, and domain markers were analyzed in the Schwann cell-neurite compartment. As shown in Figure 2E, and quantified in Figure 2F, treatment with BFA blocked accumulation of sodium channels and ankyrin G, but not that of adhesion molecules (i.e., NF186 and Caspr). Like the transected Nmnat1-protected axons, the effects of BFA were most pronounced Selleckchem 5 FU on ankyrin G accumulation; occasional sodium channel clusters devoid of ankyrin G were observed (Figure S2C). These findings strongly support the notion that ion channels and their

cytoskeletal scaffold require transport from the soma, whereas adhesion molecules (i.e., NF186, NrCAM) accumulate at the node from local (i.e., transport-independent) stores. To investigate whether these distinct routes of accumulation correlate to differences in the planar mobility of these components, we analyzed the diffusion of each of these proteins in the axon membrane. We first nucleofected neurons with GFP-tagged NF186 (Dzhashiashvili et al., 2007), NrCAM, NaV1.2, KCNQ3, and ankyrin G constructs. We analyzed NaV1.2, which is expressed transiently at forming PNS nodes (Boiko et al., 2001 and Rios et al.,

2003) and is more readily expressed after transfection of neurons than NaV1.6 (Lee and Goldin, 2009). Each of these constructs was diffusely expressed along unmyelinated axons and localized appropriately to heminodes (Figure 3A) and nodes (insets, Figure 3A) MycoClean Mycoplasma Removal Kit of Ranvier with myelination. We next measured the mobility of these nodal components in individual, unensheathed neurites by FRAP (fluorescence recovery after photobleaching) (Snapp et al., 2003). Representative results from photobleaching experiments are shown in Figure 3B; intensity measurements (Figure 3C) and a summary of the calculated mobilities (Figure 3D) are also shown. In general, NF186 and NrCAM were uniformly mobile with diffusion coefficients for NF186 of 0.338 ± 0.022 μm2/s (mean ± SEM, n = 12) and for NrCAM of 0.198 ± 0.016 μm2/s (n = 6); in both cases, the fluorescence recovery was nearly complete, indicating that the population is fully mobile. In contrast, the mobility of ion channels NaV1.

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Indeed, the finding that deafening alters the spontaneous action

Indeed, the finding that deafening alters the spontaneous action potential output of HVCX neurons OSI-744 ic50 in anesthetized birds hints that the output of this cell type may also be altered during singing. Although the exact role of HVCX neuron output in singing awaits full elucidation,

a recent study in Bengalese finches implicates the singing-related action potential activity of these cells in the encoding of syllable sequences (Fujimoto et al., 2011), a song feature that is sensitive to feedback perturbation, including deafening (Sakata and Brainard, 2006 and Woolley and Rubel, 1997). Ultimately, long-term measurements of the effects of deafening on the singing-related activity of HVCX neurons await the development of in vivo functional imaging techniques or improvements to single-unit recording methods in songbirds. All procedures were in accordance with a protocol approved by the Duke University Institutional Animal Care and Use Committee. See also Supplemental Experimental Procedures. Male zebra finches (85 to 150 dph) were anesthetized by isoflurane inhalation (2%) and deafened by bilateral cochlear removal. Complete removal of each cochlea was confirmed by visual inspection under a microscope. Standard parametric and nonparametric statistical analyses were used for all comparisons (alpha = 0.05); reported errors are SEM unless otherwise noted. Undirected

song was recorded continuously starting at least 2 days before deafening until at least 1 week postdeafening. To assess Palbociclib price song degradation, spectral features of song were quantified by measuring the Wiener entropy and entropy variance (EV) of each syllable in a bird’s song using Sound Analysis Pro (Tchernichovski et al., 2000). Thirty examples of each syllable were measured on each day of song, and values from two predeafening days were pooled to obtain a baseline distribution of entropy and EV values for each syllable. The onset of song degradation for each bird was defined as the day on which the distribution of values for either the entropy or EV of any syllable

differed significantly from the baseline distribution and remained significantly different on all subsequent days (one-way ANOVA). Syllable sequence changes were measured using sequence consistency (adapted from Scharff and Nottebohm, 1991). The onset of temporal change Endonuclease to song was defined as the first day on which the mean sequence consistency was less than the lower bound of the 95% confidence interval for the mean sequence consistency measured on the last predeafening day. Birds were anesthetized with isoflurane inhalation (2%) and placed in a stereotaxic apparatus. Injection sites were localized using stereotaxic coordinates and multi-unit neural recordings. A glass pipette attached to a Nanoject II (Drummond Scientific) was used to deliver GFP-lentivirus (eGFP expressed under the control of the Rous Sarcoma Virus LTR [FRGW]) to HVC or neuronal retrograde tracers to Area X and RA (lentivirus: 32.

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All patients were operated at the Academic Medical Center Amsterd

All patients were operated at the Academic Medical Center Amsterdam, a tertiary academic referral center. All patients gave informed consent for the procedure. Patients often were examined on multiple visits before consideration of surgical intervention to confirm the persistence of the symptoms and to provide detailed information to each patient regarding the potential risks of the procedure. Data were retrieved from an electronic patient file containing www.selleckchem.com/products/VX-809.html structured operation notes and reports of all visits. Operations were performed with the Alcon Accurus or Alcon Constellation machine (Alcon Laboratories, Fort Worth, Texas, USA) and a BIOM wide-angle viewing system (Binocular Indirect Ophthalmol Microscope; Oculus Inc,

Wetzlar, Germany). For the Accurus 25-gauge procedures, learn more infusion

pressure was set at 30 mm Hg, vacuum was set at 500 mm Hg, and cutting rate varied between 1000 and 1500 cuts/minute. For the Constellation 25-gauge procedures, infusion pressure was 25 mm Hg, vacuum was 300 mm Hg, and cutting rate varied between 2500 and 5000 cuts/minute. For all 20-gauge procedures, infusion pressure was set at 20 mm Hg and vacuum was set at 300 mm Hg, with cutting rate varying between 1000 and 2500 cuts/minute. If the posterior hyaloid was attached, a PVD always was induced. Vitreous was removed up to the vitreous base. We did not use visualization aids during the PVD induction. Shaving of the vitreous base was performed only around retinal breaks. An extensive internal search was performed in all cases using visualization with the BIOM system and scleral indentation, and the location of retinal breaks were drawn in

the chart. All peripheral lesions that resembled breaks or areas of traction were treated with external cryotherapy. Parameters ADAMTS5 retrieved were patient characteristics, preoperative and postoperative VA, preoperative phakic status, combined phacoemulsification, comorbidity, active PVD induction, intraoperative peripheral retinal breaks or traction areas, application of cryocoagulation, and tamponade type. Statistical analysis was performed using SPSS software for Windows version 16.0 (SPSS Inc, Chicago, Illinois, USA) for chi-square test, Wilcoxon signed-rank test, Mann–Whitney U test, and Kruskal-Wallis analysis. For analysis, VA was converted to logarithm of the minimal angle of resolution (logMAR) values, whereby counting fingers was converted to 1.40 logMAR and hand movements was converted to 2.70 logMAR. A total of 116 eyes from 97 patients were included. All cases had a history of persistent floaters for at least 6 months. Mean follow-up was 10.1 months (range, 3 to 57 months). Mean patient age was 58.7 years (range, 26 to 86 years). Most operations were performed under local anesthesia. General anesthesia was used only in patients who made a specific request. The posterior hyaloid was still attached in 30 (25.9%) cases. In all of these, we actively induced a full PVD.

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All synaptotagmin-controlled fusion reactions appear to require c

All synaptotagmin-controlled fusion reactions appear to require complexin as a cofactor (e.g., see Reim et al., 2001, Cai et al., 2008, Jorquera et al., 2012 and Cao et al., 2013). It seems likely that all Ca2+-triggered exocytosis depends on synaptotagmin Ca2+ sensors and complexins and that different synaptotagmins contribute to the specificity of exocytosis pathways. Ultrafast neurotransmitter release in response to an action potential can only be achieved by tethering Ca2+ channels to docked c-Met inhibitor and primed synaptic

vesicles at the active zone. A large protein complex whose central components are three multidomain proteins called RIM, RIM-BP, and Munc13 mediates the docking and priming of synaptic vesicles at the active zone and recruits Ca2+ channels to docked and primed vesicles (Kaeser et al., 2011). Thus, a single protein

complex www.selleckchem.com/products/pf-06463922.html organizes release sites (Figure 1; reviewed in Südhof, 2013). RIM (for Rab3-interacting molecule; Wang et al., 1997) binds to small Rab3 and Rab27 GTP-binding proteins that are localized on synaptic vesicles, thereby docking the vesicles (Gracheva et al., 2008, Kaeser et al., 2011, Han et al., 2011 and Fernández-Busnadiego et al., 2013). RIM also binds to Munc13 (no relation to Munc18; Brose et al., 1995 and Betz et al., 2001), thereby activating Munc13 (Deng et al., 2011). Munc13 is a priming factor (Augustin et al., 1999) that catalyzes the conformational switch of syntaxin-1 from closed to open, promoting SNARE complex assembly (Richmond et al., 2001 and Ma et al., 2013). RIM binding to both Munc13 and Rab3/27 is mediated by a composite

N-terminal domain that contains a Munc13-binding zinc finger surrounded by Rab3-binding α helices (Dulubova et al., 2005 and Lu et al., 2006). Ca2+ channels need to be localized adjacent to docked and primed vesicles for fast coupling of an action potential to Ca2+-triggered exocytosis. Ca2+ channels are generally positioned less than 100 nm away from docked vesicles (Eggermann et al., 2012). RIM and the RIM-interacting molecule RIM-BP (Wang et al., 2000) both bind to Ca2+ channels in addition to binding to each other (Kaeser et al., 2011). Deletion of RIM in mice (Kaeser et al., 2011, Kaeser et al., 2012 and Han et al., 2011) and found of RIM-BP in flies (Liu et al., 2011) causes a loss of Ca2+ channels from presynaptic active zones and a decrease in Ca2+ influx. These data show that RIM and RIM-BP collaborate to recruit Ca2+ channels to release sites. Thus, in a parsimonious design, a single protein complex that contains RIM as a central element mediates the colocalization of all critical proteins to the active zone. This protein complex localizes synaptic vesicles, Ca2+ channels, and vesicle priming factors next to release sites, thereby allowing fast coupling of an action potential to neurotransmitter release (Figure 1C).

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Although the functional analysis of cortico-thalamo-cortical comm

Although the functional analysis of cortico-thalamo-cortical communication is still in its early days, there is accumulating evidence in support of an essential involvement

of “higher-order” thalamus in cortical processes. Responses of pulvinar and PoM neurons depend on input from cortex, have latencies in the same range as cortical neurons, and inherit properties resulting from cortical computations such as receptive field layout or the sensitivity for direction of motion in the case MK-2206 supplier of pulvinar (Berman et al., 2011). Conversely, two recent studies demonstrated in both the visual as well as the somatosensory domain that cortical activity critically depends on the intactness of higher-order thalamic nuclei such as the pulvinar (Theyel et al., 2010; Purushothaman et al., 2012). Considering all these features together, it is not surprising that cortico-thalamo-cortical loops have been implicated as central ingredients of higher cognitive functions. In the visual system, Talazoparib manufacturer several theories on the mechanisms of spatial attention discuss an involvement of pulvinar gating (Olshausen et al., 1993). Evidence from electrophysiological, imaging, and lesion studies together lend some support to this view, as, for example, monkeys with pulvinar lesions commonly display behavioral

changes ranging from increased reaction times to neglect-like symptoms (Petersen et al., 1987; Wilke et al., 2010). However, how pulvinar activity contributes to attentional processes in the intact animal and controls selective routing

of cortical activity remains unknown. A new study published in Science by Saalmann et al. (2012) aims to fill this gap by investigating the role of pulvinar neurons in coordinating synchronization of cortical signals in the alpha range (8–12 Hz) during visual spatial attention. Saalmann et al. (2012) performed multisite electrophysiological recordings and sampled neural activity from two adjacent midlevel cortical areas of the occipito-temporal stream, thought to be involved in the processing of visual shape and object information and a region in the ventro-lateral part of the pulvinar that they had identified using diffusion tensor imaging (DTI). To control attention, Saalmann ADP ribosylation factor et al. (2012) trained two monkeys to report the shape of a visual target stimulus presented among an array of distracters. The position of the target was cued by a preceding stimulus flashed for 100 ms at the target location followed by a brief delay period before target onset. Saalmann et al. (2012) demonstrate a cue-triggered enhancement of pulvinar responses, which is strongest during the cue presentation and sustained to a smaller extent during the delay period, most likely reflecting attentional engagement. The study does not document the cue effects on the firing rates of the cortical neurons, making it difficult to decide whether attention modulates cortical and thalamic responses to the same extent.

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For the case of opportunities, exploration is mandated by the (in

For the case of opportunities, exploration is mandated by the (initially unexpected) potential gain, and this may be treated as a form of appetitive see more prediction error known as an exploration bonus. One, presumably model-free, realization of such a bonus is phasic dopaminergic activity (Kakade and Dayan, 2002). Strictly speaking, the

potential gain arises as a result of the expected uncertainty that follows from the unexpected change; how dopamine is coupled to ACh and/or NE in expressing this is not yet clear. The mechanism by which exploration bonuses arise in model-based calculations is also unknown. In terms of potential threats, norepinephrine has long been linked with anxiety (Bremner et al., 1996a, 1996b). Environments associated with excessive unexpected uncertainty are highly stressful, since they lack stable relationships

and pose substantial potential problems for safe exploitation. NE helps organize a massive response to stress, notably in conjunction with cortisol, a steroid hormone that acts as another neuromodulator (Wolf, 2008). This involves everything from changing energy storage and usage, via glucocorticoids (Nieuwenhuizen and Rutters, 2008) (involvement [S] with energy regulation is itself a more general principle of neuromodulation; Ellison, 1979; Tops et al., 2009; Montague, 2006), to changing the actual style of information processing. For instance, goal-directed or model-based calculations, which are typically slow, could be suppressed in favor of habitual or model-free selleck chemicals llc ones, which

are typically faster, though possibly less accurate, especially in the face of the quick changes associated with unexpected uncertainty. It has been suggested that suppression arises via functional inhibition wrought by two particular classes of NE receptor in the prefrontal cortex (α  1 and βˆ) whose affinities make them sensitive to high levels of NE; Arnsten, 2011). This combines two previous general principles—selective affinities of different receptors, and neuromodulatory manipulation of gross of pathways. Information about the circumstance an agent occupies in its environment has to be combined from multiple sources of noisy and partial information and integrated over time as it progressively arises. The same turns out to be true for information stored in working memory, since neural activity has to be communicated to relevant targets progressively, through activity. It also arises for reading information out of synapses, for which presynaptic activity is necessary to extract their values, for instance using generic, background, activity (Mongillo et al., 2008). These processes can all fruitfully be seen as involving statistical inference, based on partial and noisy information, and so are all controlled or influenced by uncertainty (Fiser et al.

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Within a block

Within a block click here of 24 trials, the amount of reward was always large (0.25 or 0.3 ml) for the saccades to one direction and small (0 or 0.03 ml) for the saccades to the other direction. Even in the small-reward trials, the monkeys had to make a correct saccade; otherwise, the same trial was repeated. The reward-position contingency was reversed for the next block of trials without external instructions. We used a pseudorandom reward schedule in which each block was divided into six “subblocks,” each consisting of two large-reward and two small-reward trials presented in a random order. In the following inactivation study, we used a reward-biased visually guided saccade task (Lauwereyns et al., 2002).

After the central fixation (600 or 1,000 ms), the fixation point turned off and simultaneously the target appeared either to the selleck inhibitor right or left 20° from the fixation point. The monkeys had to immediately make a saccade to the visible target. There was no cue during the fixation period. The reward schedule was the same

as the memory-guided saccade task. We followed Haber et al. (1993) for the anatomical localization of the VP which is located ventral to the AC and anterior to the GPe-GPi. Thus defined location of the VP was estimated on the basis of magnetic resonance (MR) images (4.7 T, Bruker). Single-unit recordings of VP neurons were performed with an epoxy-coated or a glass-coated Tungsten microelectrode (0.8–1.5 MΩ at 1 kHz). The electrode was inserted obliquely Carnitine palmitoyltransferase II (36° from vertical in the frontal plane) into the pallidum (Figure 1C) using an oil-driven micromanipulator (MO-97A, Narishige). The recording sites were determined using a grid system, which allowed recordings

at every 1 mm between penetrations. The unitary activity recorded from the microelectrode was amplified, filtered (200 Hz to 5 kHz), converted into digital data with an online window discriminator, and stored in a computer at the sampling rate of 1 kHz. During recording, the VP is located below the AC, which was identified on the basis of axonal signals such as high-frequency background noises and initially positive spikes. Only stable and well-isolated neurons were included in the present data. After the electrophysiological recording (mapping) of VP neurons in monkey H, we performed inactivation experiments to test a causal relationship between the VP activity and the reward modulation of saccadic performance. To accurately inactivate the brain structure, we used an electrode assembly (injectrode) consisting of an epoxy-coated Tungsten microelectrode for unit recording and a silica tube for drug delivery as described previously (Tachibana et al., 2008). After the precise identification of the aimed structures by unit recording, we injected a GABAA receptor agonist, muscimol (Sigma; 0.88–44 mM; 1–2 μl), into the target structure of each hemisphere.

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25 ± 0 11 versus 1 49 ± 0 12, p = 0 1642; PSD-95-positive, 0 89 ±

25 ± 0.11 versus 1.49 ± 0.12, p = 0.1642; PSD-95-positive, 0.89 ± 0.07 versus 1.01 ± 0.08, p = 0.2809; double-positive, 0.86 ± 0.07 versus 0.93 ± 0.08, p = 0.4911, two-tailed t test; Kif1a−/−: synaptophysin-positive, 1.03 ± 0.09 versus 1.06 ±

0.10, p = 0.8125; PSD-95-positive, 0.74 ± GSK1349572 0.05 versus 0.75 ± 0.05, p = 0.8378; double-positive, 0.70 ± 0.05 versus 0.71 ± 0.06, p = 0.9163, two-tailed t test) ( Figures 5D–5F). These results suggest that KIF1A upregulation is required for BDNF-induced synaptogenesis. Finally, to confirm the role of KIF1A in synaptogenesis, we examined the effects of KIF1A overexpression on cultured hippocampal neurons. Neurons were cotransfected with KIF1A and synaptophysin-green fluorescent protein (syp-GFP), and the density of syp-GFP puncta along dendrites was compared with that of neurons transfected with syp-GFP alone (Figure 6A). Significant increases in the total number and density of syp-GFP puncta along dendrites were observed in cotransfected neurons (syp-GFP alone versus KIF1A+syp-GFP: total number, 55.6 ± 4.6 versus 73.3 ± 5.0, p < 0.05; density [per 10 μm], 0.40 ± 0.02 versus 0.54 ± 0.02, p < 0.0001, post hoc Dunnett's test) (Figures 6C and 6D). Furthermore, there was also a significant increase in the number of syp-GFP puncta colocalized

with PSD-95 in cotransfected neurons (syp-GFP alone versus KIF1A+syp-GFP: 37.1 ± 2.6 versus 47.2 ± DNA Synthesis inhibitor 3.6, p < 0.05, post hoc Dunnett's test) (Figures 6B and 6I). No significant differences TCL were detected in neurons cotransfected with KIF5B and syp-GFP (syp-GFP alone versus KIF5B+syp-GFP: total number, 55.6 ± 4.6 versus 57.2 ± 4.2, p > 0.05; density [per 10 μm], 0.40 ± 0.02 versus 0.42 ± 0.02, p > 0.05; number of colocalized puncta, 37.1 ± 2.6 versus 37.4 ± 2.9, p > 0.05, post hoc Dunnett’s test) (Figures

6C, 6D, and 6I). There were no differences in the number or total length of dendrites contacted by axons of transfected neurons among groups (syp-GFP alone, KIF1A+syp-GFP, and KIF5B+syp-GFP: number of dendrites, 18.3 ± 1.3, 19.1 ± 1.2, and 18.5 ± 1.3, respectively, p = 0.9053; total length [μm], 1,389 ± 111, 1,411 ± 118, and 1,394 ± 109, respectively, p = 0.9894, one-way ANOVA) (Figures 6E and 6F). Also no significant differences were observed in the number of neurons contacted by axons of transfected neurons or in the mean distance from transfected neurons to contacted neurons among groups (syp-GFP alone, KIF1A+syp-GFP, and KIF5B+syp-GFP: number of neurons, 6.95 ± 0.41, 7.10 ± 0.51, and 6.80 ± 0.48, respectively, p = 0.9034; mean distance [μm], 245 ± 20, 249 ± 20, and 238 ± 20, respectively, p = 0.9254, one-way ANOVA) (Figures 6G and 6H). Collectively, these results suggest that increased KIF1A levels promote synaptogenesis via the formation of presynaptic boutons.

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, 2005), a likely possibility is that the internally generated am

, 2005), a likely possibility is that the internally generated amplitude signal described in vS1 cortex ( Fee et al., 1997) is relayed from vM1 cortex. We now come to the crux issue and ask if neurons in vS1 cortex code touch conditioned LBH589 cell line on vibrissa position, i.e., on peripheral reafference. Such conditioning would imply that neurons

in vS1 cortex contain the information necessary to report the location of an object that makes contact with a single vibrissa. These cells could therefore underlie the animal’s ability to report object position (Knutsen et al., 2006, Mehta et al., 2007 and O’Connor et al., 2010a; Figure 2). In principle, neurons can code both touch and position independently. The critical test of whether touch and reafferent signals are merged in vS1 cortex is if the strength of the touch response depends on where the vibrissae are in the whisk cycle. The experimental realization involved recording single units in vS1 cortex Dorsomorphin in vitro while rodents contacted a sensor for

a liquid reward. Both free ranging and body fixed animals were used in a paradigm designed to ensure that the animals contacted the sensor at all possible positions in the whisk cycle across a different set of trials (Figure 8A). This in turn ensured that the strength of the contact response for each unit could be determined as a function of position and, with further analysis (Figure 4), as a function of phase in the whisk cycle. A majority of neurons in L4 and L5a exhibit a prompt response to self-induced contact (Crochet and Petersen, 2006, Curtis and Kleinfeld, 2009 and O’Connor et al., 2010b), not unlike TCL that observed in experiments with mechanical stimulation of a vibrissa in an anesthetized preparation (Armstrong-James et al., 1992, Armstrong-James and George, 1988 and Simons, 1978). The strength of the contact response as a function of the phase in the whisk cycle was found for eight different phase intervals of π/4 radians. Consider the example of Figure 8B. The instantaneous rate varies by nearly a factor of three across the whisk cycle and, in this example,

peaked near the start of protraction from the retracted position. In general, 85% of the units with a prompt touch response showed strong conditioning of the touch response by phase in the whisk cycle. The consensus data indicates that the preferred phases for touch, denoted ϕtouch, matches the preferred phase for whisk, i.e., ϕtouch ≅ ϕwhisk ( Figure 8C). Thus the spike rate upon contact is nominally proportional to a nonlinear function, such as cos [ϕ(t) − ϕwhisk]. These data show that vS1 cortex codes touch contingent upon position in the whisk cycle. We now return to the topic of the coordinate system used to code vibrissae motion (Figure 4A). The videographic analysis of vibrissa movement allowed the instantaneous spike rate upon contact to be plotted against either phase or actual azimual angle (Figure 8A).

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