The phase encoding design was similar to procedures widely used for retinotopic mapping (Bandettini et al., 1993 and Schneider

et al., 2004). A transparent wedge within a dark foreground rotated around a central fixation point. The underlying checkerboard was only visible through the transparent wedge, giving the appearance of a rotating checkerboard wedge (Swisher Cabozantinib in vitro et al., 2007). The wedge rotated either clockwise or counterclockwise and spanned 1°–15° in eccentricity with an arc length of 75°. The chromaticity and luminance of each check of the colored checkerboard alternated at a flicker frequency of 4 Hz. To ensure proper fixation, subjects performed a luminance detection task on the fixation point. Luminance changes of the fixation point

occurred every 2 to 5 s for the duration of 0.09 s. SM and control subjects performed with an accuracy of 93% and 91% ± 7%, respectively. Each run was composed of eight 40 s cycles of the rotating wedge. Runs alternated between clockwise and counterclockwise wedge rotation, with a total of 12 runs per scanning session. Using fMR-A paradigms, High Content Screening we investigated neural representations of different types of objects including 2D objects, 3D objects, and line drawings of objects as well as size and viewpoint invariance (Figure 2). For each fMR-A study, 51 gray-scale images of 2D objects, 3D objects, or line drawings were used. The objects were subdivided into a matrix of equally sized rectangulars (25 along the horizontal dimension and 25 along the vertical dimension). Subsequently, the rectangulars were randomly re-arranged resulting in 51 scrambled images per study. The stimuli subtended approximately 18° × 18° of visual angle centered over a fixation point on a gray background. 2D and 3D objects were generated

with MATLAB software (The MathWorks; Natick, MA); line drawings were chosen from the ClipArt Gallery (http://office.microsoft.com/). For the size-invariance study, the 2D objects were changed in size, resulting in 16 different sizes of each object over a range of 6.75° × 6.75° to 18° × 18°. For the viewpoint-invariance study, the 3D objects were rotated around the y axis, resulting in 16 different viewpoints Rolziracetam of each object covering a range of ±75°. In the adapted condition, the same object was presented 16 times. In the non-adapted condition, 16 different objects were presented once. Similar stimulus sets and fMR-A paradigms have been successfully used in our previous study ( Konen and Kastner, 2008). Each fMR-A study consisted of three scans, each of which contained epochs of intact and scrambled object presentations. Each epoch lasted for 16 s and was alternated with equally long blank periods. In each epoch, 16 intact or scrambled objects were presented for 750 ms each interposed with 250 ms blank periods. Each scan started and ended with a blank period of 16 s.

However, these seminal studies used electrical stimulation—nonspecifically activating multiple cell types and axons of passage—making BIBW2992 molecular weight it difficult to determine the critical neural circuit element with confidence. In another seminal study from the 1990s, elegant in vivo intracellular recordings in anesthetized animals first characterized the role of hippocampal, prefrontal cortical, and amygdalar inputs to the NAc, demonstrating distinct properties of electrical stimulation in each upstream region (O’Donnell and Grace, 1995). O’Donnell and Grace established the unique ability of hippocampal inputs to the NAc to induce changes in membrane

potential, commonly referred to as “up and down states”—medium spiny neurons were pushed into step-function-like states in which the cells were slightly depolarized and more excitable in response to prefrontal cortical inputs (O’Donnell and Grace, 1995). Distinct from the bistable responses elicited by fornix stimulation, electrical stimulation of the amygdala

produced longer-lasting depolarization with greater onset latency, and electrical stimulation of the prefrontal cortex elicited a fast, but transient, depolarization (O’Donnell and Grace, 1995). Until the development of optogenetic projection-specific targeting approaches, we did not have the ability to manipulate axons originating in specific regions during freely moving behaviors nor to stimulate axons arriving from a known source in acute slice preparations (Tye et al., 2011; Stuber et al., 2011). Optogenetic-mediated projection-specific targeting leverages the genetically encodable capability of these selleck light-sensitive proteins and allows for the selective activation of specific populations

of cells and axons. However, caveats still include the possibility of depolarizing axons of passage that do not form synapses in the illumination field or the induction of backpropagating action potentials (Petreanu et al., 2007), also known as antidromic stimulation, which may scale with stronger illumination parameters, opsin expression levels, and the specific characteristics of the preparation. These early studies in optogenetic projection-specific targeting used local pharmacological manipulations, blocking glutamate receptors in the postsynaptic ADP ribosylation factor target region to demonstrate that the behavioral changes observed were indeed due to local effects—ruling out the possible contribution of axons of passage or antidromic activation to the light-induced behavioral change (Tye et al., 2011; Stuber et al., 2011). Stuber and colleagues investigated two of the same projections, specifically testing the ability of amygdalar and prefrontal cortical inputs of the NAc to support ICSS, by expressing channelrhodopsin-2 (ChR2), a light-activated cation channel, in glutamatergic pyramidal neurons of the amygdala or prefrontal cortex and implanting an optical fiber into the medial shell of the NAc.

1 Experimentally induced diabetes in animals has provided considerable insight into the physiological and biochemical derangement of the diabetic state. Significant changes in lipid metabolism and its structure also occur in diabetes.2 Such structural

changes are clearly oxidative in nature and associated with development of vascular disease in diabetes.3 In experimental diabetic rats, increased lipid peroxidation has also found to be associated with hyperlipidemia.4 Concurrently, liver and kidney that participate in the uptake, Epigenetics inhibitor oxidation and metabolic conversion of free fatty acids, synthesis of cholesterol, phospholipids, and triglycerides, are also severely affected during diabetes.5 Many indigenous Indian tropical medicines have been found useful in successfully managing the diabetes. Caralluma attenuata weight (Family: Asclepiadaceae) is a herb growing wild in dry hill slope regions of southern India. Indigenously it is known as ‘Kundaetikommu’, and is eaten raw as a cure for diabetes and the juice of the plant along with black pepper is recommended in the

treatment of migraine. 6 This plant was found to be a rich source of glycosides and known for its anti-hyperglycemic activity. 7 The hypoglycemic effect of whole plant C. attenuata was investigated in both normal and alloxan Palbociclib mouse induced diabetic rats. 8 The knowledge and experimental data base of herbal medicine can provide new functional leads to reduce oxyclozanide time, money

and toxicity – the three main hurdles in drug development. It is rightly said that ‘laboratories to clinics’ becomes ‘clinics to laboratories’ – a true reverse pharmacology approach. The present investigation was undertaken to study the potential effect of the antidiabetogenic activity of CAEt with a view to provide scientific evidence on modern lines and the study is also important for being the first biochemical study on the effects of CAEt in the management of type-I diabetes mellitus. Male Wistar rats (210–250 g) were purchased from the animal house of National Laboratory Animal Centre, Lucknow, India. They were maintained in standard environmental conditions and had free access to feed and tap water ad libitum during quarantine period. The animals were kept fasting overnight but allowed free access to the water. All studies were performed in accordance with the guidance for care and use of laboratory animals, as adopted and promulgated by the Institutional Animal Care Committee, CPCSEA, India (Reg. No. 222/2000/CPCSEA). Fresh whole plants of C. attenuata were collected from Ghatkesar, Andhra Pradesh, India. The plant material was identified taxonomically and authenticated by taxonomist in National Botanical Research Institute, Lucknow.

032; p = 0.691). Next, to determine whether activity-dependent production of NO in DMH neurons relies on an increase in intracellular Ca2+, which is often secondary to the activation of NMDARs (Bains and Ferguson,

1997, Nugent et al., 2007 and Szabadits et al., 2011), we conducted two independent experiments. First, we delivered HFS in the presence of AM251 and the NMDAR antagonist APV (50 μM). Under these conditions, HFS failed to elicit LTPGABA (94% ± 10.7% of baseline, n = 7, p = 0.436; Figure 3B). In the second experiment, the postsynaptic www.selleckchem.com/erk.html cell was loaded with the Ca2+ chelator BAPTA (10 mM), and HFS was delivered. This manipulation also completely abolished LTPGABA in the presence of AM251 (99% ± 14.8% of baseline, n = 5, p = 0.944; Figure 3C), indicating that a rise in postsynaptic Ca2+ is necessary for NO-mediated potentiation of GABA synapses. The effects of NO on GABA release VX809 require the activation of presynaptic soluble guanylate

cyclase (sGC), with a subsequent rise in cyclic GMP (cGMP) (Nugent et al., 2007). Consistent with these observations, we failed to elicit LTPGABA (87% ± 6.7% of baseline, n = 6, p = 0.053; Figure 3C) in the presence of both AM251 and the sGC inhibitor, ODQ (10 μM). When taken together, these findings are consistent with the hypothesis that GABA synapses are potentiated by NO recruited in a heterosynaptic fashion by the activation of NMDARs. We next examined whether these synapses were sensitive to pharmacological manipulations using exogenous ligands that either activate CB1Rs or liberate NO directly. Bath application of the CB1R agonist WIN 55,212-2 (5 μM) elicited

a robust depression in evoked IPSC amplitude (51% ± 7.0% of baseline, n = 10, p = 0.0001; Figure 4A). This was accompanied by an increase in the PPR (baseline: 0.887 ± Bay 11-7085 0.110; post-drug: 1.087 ± 0.112; p = 0.020; Figure 4A) and CV (baseline: 0.394 ± 0.058; post-drug: 0.707 ± 0.174; p = 0.001; Figure 4A), suggesting that these effects are localized at the presynaptic terminal. This is consistent with its action elsewhere in the hypothalamus (Hirasawa et al., 2004, Huang et al., 2007, Oliet et al., 2007 and Wamsteeker et al., 2010) and throughout the brain (Kano et al., 2009). To determine whether the NO donor SNAP (200 μM) modulates GABA release in the DMH, we assessed its effects on evoked IPSCs. SNAP caused a rapid increase in IPSC amplitude (145% ± 14.7% of baseline, n = 13, p = 0.0003, Figure 4B) and a decrease in PPR (baseline: 0.757 ± 0.074; post-drug: 0.655 ± 0.056; p = 0.042; Figure 4B) and CV (baseline: 0.343 ± 0.037; post-drug: 0.284 ± 0.031; p = 0.039; Figure 4B). This is also consistent with previous reports that NO increases GABA release in the CNS (Bains and Ferguson, 1997, Di et al., 2009, Horn et al., 1994, Nugent et al., 2007 and Stern and Ludwig, 2001). Together, our findings confirm that GABA synapses in the DMH are sensitive to manipulations that directly activate CB1Rs or deliver NO to the tissue.

, 2009). These emerging views about the neural basis of drug addiction, and its potential

treatment, have moved well beyond Ku-0059436 purchase the original story offered by the DA hypothesis of “reward. After decades of research, and continuing theoretical developments, there has been a substantial conceptual restructuring in the field of DA research. Considerable evidence indicates that interference with mesolimbic DA transmission leaves fundamental aspects of the motivational and hedonic response to food intact (Berridge, 2007; Berridge and Kringelbach, 2008; Salamone et al., 2007). Behavioral measures such as progressive ratio break points and self-stimulation thresholds, which were once thought to be useful as markers of the “reward” or “hedonia” functions of DA, are now considered to reflect processes involving exertion of effort, perception of effort-related or opportunity costs, and decision making (Salamone, 2006; Hernandez et al., 2010). Several recent electrophysiology papers have demonstrated responsiveness of either presumed or identified ventral tegmental DA neurons to aversive stimuli (Anstrom and Woodward, 2005; Brischoux et al., 2009; Matsumoto and Hikosaka, 2009; Bromberg-Martin et al., 2010; Schultz, 2010; Lammel et al., 2011). Many investigators now emphasize the involvement of mesolimbic and nigrostriatal DA in reinforcement learning or habit formation (Wise, 2004; Yin

et al., 2008; Belin et al., 2009), rather than hedonia per se. These trends have all contributed to

a dramatic rewriting of the story of dopaminergic involvement in motivation. The term motivation refers Z-VAD-FMK mw to a construct that is widely used in psychology, psychiatry, and neuroscience. As is the case with many psychological concepts, the discussion of motivation ADP ribosylation factor had its origins in philosophy. In describing causal factors that control behavior, the German philosopher Schopenhauer (1999) discussed the concept of motivation in relation to the way that organisms must be in a position to “choose, seize, and even seek out the means of satisfaction.” Motivation also was a vital area of interest during the initial development of psychology. Early scientific psychologists, including Wundt and James, included motivation as a subject in their textbooks. Neobehaviorists such as Hull and Spence frequently employed motivational concepts such as incentive and drive. Young (1961) defined motivation as “the process of arousing actions, sustaining the activity in progress, and regulating the pattern of activity.” According to a more recent definition, motivation is “the set of processes through which organisms regulate the probability, proximity and availability of stimuli” (Salamone, 1992). Generally speaking, the modern psychological construct of motivation refers to the behaviorally-relevant processes that enable organisms to regulate both their external and internal environment (Salamone, 2010).

25, p = 0.036), and the transverse temporal region (t[21] = 2.79, p = 0.011). Accumbens favored win information, showing significant win-tie decoding (55% accuracy, on average, t[21] = 3.77, p < 0.001) but not tie-loss (51% average accuracy, t[21] = 1.17, p = 0.13). Caudal ACC also favored win-tie over tie-loss discriminations (56% versus 52% accuracy), but still showed a significant (p < 0.05, uncorrected) tendency to decode tie-loss (t[21] = 1.74, p = 0.048). Transverse temporal region showed an ability to decode tie versus loss

information (t[21] = 3.21, p = 0.002) but not win versus tie (t[21] = −0.28, p = 0.6). In a similar searchlight analysis, we contrasted the ability of each voxel to decode wins-ties and ties-losses. We found eight small clusters that differed significantly in their IWR-1 mouse ability to perform these two classifications (Table S6; figures not shown because these small clusters did not show up well when projected to the surface). Regions that did better on win-tie than tie-loss (p < 0.001, k = 10) were in the right basal ganglia (medial globus pallidus), Luminespib clinical trial the left ACC, and left middle frontal gyrus. Regions performing better

on ties-losses were the left amygdala and regions in the right IPL, left medial temporal, left fusiform and left middle temporal gyrus. In total, clusters showing these differences only encompassed 136 voxels, far fewer than those with significant three-way win-tie-loss classification (equal to only 0.4% of the number of voxels able to decode win-tie-loss). Of 34,520 above-chance voxels in three-way win-tie-loss classification, only 25 voxels showed a significant difference between win-tie and tie-loss classification

(42 without cluster correction). Therefore, signals related to both reinforcements and punishments were remarkably ubiquitous, and there was very little difference between encoding of the two. The addition of tie outcomes in Experiment 2 afforded the ability to distinguish signals related to reinforcement and punishment from those related to salience. One possible explanation for the ubiquitous reward signals in Experiment 1 is that one of the two outcomes about in the matching pennies game is more attention-demanding or salient (Maunsell, 2004, Bromberg-Martin et al., 2010, Chun et al., 2011 and Litt et al., 2011). By contrast, during rock-paper-scissors, the “tie” outcome should be less salient and arousing than both wins and losses. We evaluated the salience hypothesis by using a pair of classifiers. First, we trained classifiers to discriminate wins from ties (win-tie classifier), then evaluated whether they tended to classify unseen losses as wins or ties. Next, we also trained classifiers to discriminate ties from losses (tie-loss classifier), then evaluated whether they tended to classify unseen win trials as ties or losses.

Unlike most other mutagens, the molecular lesions caused by EMS are essentially random, ensuring that most genes of interest will be targeted and that multiple lesions will be found in each gene. Whole-genome sequencing now allow us to reliably and efficiently map EMS induced lesions at very reasonable costs ( Blumenstiel et al., 2009 and Wang et al., 2010) (H.J.B., unpublished

data). The identification of novel genes that affect specific biological processes in a specific tissue are based on creating mosaic animals (Xu and Rubin, 1993). Flp-mediated mitotic recombination screens check details result in the generation of homozygous mutant tissue in an otherwise heterozygous animal, limiting the effect of a possible detrimental or lethal mutant phenotype at an earlier developmental stage. Advantageously, such screens can often be designed as F1 screens where single progeny of mutagenized flies can be directly screened, mutations isolated, and balanced to generate stable stocks if the screen does not jeopardize viability and fertility of the heterozygous animals that carry clones. These screens are most conveniently performed with

EMS. Forward genetic Flp/FRT screens are based on creating clones in specific cells, tissue or organs using specific click here Flp drivers ( Figure 6). Flp expression results in homozygous mutant tissue associated with a phenotypic outcome that can be scored easily. The most widely used driver is an eye specific driver, ey-Flp ( Newsome et al., 2000), or ey-GAL4; UAS-Flp ( Stowers and Schwarz, 1999). To obtain clones that are large enough it is important to use a driver that is expressed early in development. Moreover,

clone size can be enhanced with the use of homologous chromosomes that carry a recessive cell lethal mutation, or a Minute. The large clones in the eye have allowed screening for morphological defects of eye cells Tolmetin ( Newsome et al., 2000), simple behavioral paradigms such as phototaxis ( Verstreken et al., 2003), electrophysiological function using electroretinograms ( Ohyama et al., 2007), or bristle abnormalities on the head cuticle ( Tien et al., 2008). These screens can be also combined with different MARCM strategies (see above). Forward genetic screens generally require a strategy to genetically and/or molecularly map the mutation. In the case of transposons, the insertion site is often known or can be easily mapped (Hui et al., 1998 and Bellen et al., 2011). Mutation mapping becomes more challenging for EMS mutagenesis.

Another possibility is that a small fraction of the NCA channels could remain localized and functional in the absence of NLF-1.

We favor the second possibility because expressing either buy Forskolin NLF-1 or NCA-1 in the GABAergic motor neurons did not result in any noticeable improvement in the locomotion deficit in nlf-1 or nca(lf) mutants (data not shown). Moreover, this small behavioral difference coincided with a subtle, yet also consistent, reduction in Na+-dependent change in background leak current (ΔI; Figure 4C) and RMP (ΔV; Figure 4F) in the AVA premotor interneurons in nlf-1 when compared to that in nca(lf) mutants. We provide the first direct, physiological evidence for the NCA channel’s role in maintaining neuronal RMP. Thus, in both the nonspiking Wnt inhibitors clinical trials C. elegans and spiking vertebrate neurons, this Na+ leak channel constitutes a conserved mechanism that modulates neuronal excitability. Despite a modest sequence homology between NLF-1 and mNLF-1, and the differences in neuronal properties between vertebrate and C. elegans interneurons, mNLF-1 fully substitutes

for NLF-1 when expressed in C. elegans. mNLF-1 exhibits enriched, broad expression in the mouse brain (http://mouse.brain-map.org). shRNA-mediated knockdown of mNLF-1 effectively, albeit partially reduces the Na+ leak currents in primary cortical neuron cultures. Thus, while mNLF-1’s physiological function awaits further investigation, our current studies imply its role in the folding/trafficking of ADAMTS5 the NALCN Na+ leak channel. The ability of mNLF-1 to substitute NLF-1 in the C. elegans nervous system further highlights the conservation of machineries that modulate membrane physiology. Removing extracellular Na+ leads to a further hyperpolarization of RMP in both nca(lf) and nlf-1 mutants, indicating the presence of additional Na+ channels in modulating neuronal excitability. As the C. elegans genome does not encode voltage-gated Na+

channels, machineries that carry out the remaining Na+ conductance remain to be identified. How the Na+ leak channel affects intact neural circuit activity remains to be explored. Intriguingly, nalcn−/− mice cannot generate respiratory rhythm ( Lu et al., 2007); na flies fail to exhibit motor patterns associated with circadian cycles ( Lear et al., 2005; Nash et al., 2002; Zhang et al., 2010); the knockdown of a snail NALCN homolog compromises respiratory function ( Lu and Feng, 2011); the loss of NCA leads to disrupted rhythmicity in C. elegans locomotion ( Pierce-Shimomura et al., 2008; this study). Collectively, these phenotypes imply a requirement of this channel in neural networks generating rhythmic behaviors. Despite a broad expression in the C. elegans motor circuit, NLF-1 activity in motor neurons was neither necessary, nor sufficient to restore the continuity of locomotion.

, 1997). It has been shown that orientation and direction selectivity are established by different mechanisms. While the initial establishment of orientation selectivity in

cortical neurons is independent of visual experience (see review in White and Fitzpatrick, 2007), several lines of evidence indicate that the emergence of direction selectivity Birinapant in vitro strictly requires visual experience. Thus, direction-preference maps are absent at eye opening and do not develop in ferrets that are reared in darkness (Li et al., 2006). Moreover, visual experience with moving stimuli just after eye opening drives the emergence of direction-selective responses in the ferret visual cortex (Li et al., 2008). However, the connectivity and the mechanisms that are necessary for the emergence of direction selectivity remain unclear. In recent years, rodents and especially mice are becoming an attractive model for the investigation of such mechanisms in vivo. Various transgenic mice lines have been used to study visual system development (Fagiolini Raf inhibitor et al., 2003 and Cang et al.,

2005), plasticity (Fagiolini et al., 2004, Syken et al., 2006 and Wang et al., 2010), and function of specific cell types in the visual cortex (Sohya et al., 2007, Kerlin et al., 2010 and Runyan et al., 2010). It is important to remember that unlike in ferrets, cats, and primates, neurons in the primary visual cortex of rodents are not organized into orientation columns. Instead, orientation-selective neurons are distributed in a mixed “salt-and-pepper” manner throughout the primary visual cortex (Ohki Florfenicol et al., 2005 and Van Hooser et al., 2005). Nevertheless,

highly tuned orientation- and direction-selective neurons have been shown to be abundant in the mouse visual cortex (Dräger, 1975, Métin et al., 1988, Sohya et al., 2007, Niell and Stryker, 2008 and Wang et al., 2010). While the emergence of orientation selectivity has been investigated in the rodent visual cortex (Fagiolini et al., 1994 and Fagiolini et al., 2003), the development of direction selectivity has so far received less attention, except in recent studies that investigated the emergence of direction selectivity at the level of the mouse retina. In mice, retinal ganglion cells exhibit strong direction selectivity (Elstrott et al., 2008 and Yonehara et al., 2009). Remarkably, this strong direction selectivity is already present at eye opening (Elstrott et al., 2008, Chen et al., 2009 and Yonehara et al., 2009). Moreover, robust directional responses have been detected in dark-reared mice and in mice lacking cholinergic retinal waves (Elstrott et al., 2008 and Chen et al., 2009), indicating that visual experience and patterned activity are not required for the development of direction selectivity in the mouse retina.

The linear relationship between stimulus intensity commanded by the software and the output luminance of the monitor was confirmed in two ways: (1) with a light meter (Konica Minolta, Model LS-100, Tokyo, Japan) and (2) by performing a fast Fourier transform

on visual stimuli photographed with a Dalsa 1M30 CCD camera (Dalsa Corporation, Waterloo, Ontario, Canada) (Rosenberg et al., 2010 and Zhang et al., 2007). Stimuli were viewed from 40 cm and presented as full screen images on a 40 × 30 cm CRT monitor with a pixel resolution of 800 × 600 and a refresh NVP-BGJ398 nmr rate of 100 Hz. Stimuli consisted of high contrast (80% Michelson) drifting or contrast-reversing sinusoidal gratings as well as three-component interference patterns (Equation 1; Figure 1A). In this equation, ωC is the vector defining the carrier spatiotemporal frequencies, ωE is the vector defining the envelope spatiotemporal frequencies, and χ is the vector defining the space and time dimensions (x,y,t). When measuring interference pattern responses with a drifting carrier, the carrier and envelope TFs were constrained to be whole multiples of each other. Without this constraint, the computation time and memory resources to construct and save the stimuli would have been too prohibitive to tailor the stimuli to the cell being studied. Fixing the carrier and envelope TFs to be whole multiples of each other meant constructing only one cycle of each stimulus (at

most 36 frames) rather than a unique frame for each refresh of the selleck kinase inhibitor monitor (200 frames per stimulus; the 100 Hz and monitor refresh rate times the 2 s stimulus duration). Stimuli were presented statically for either 250 ms or 1 s before drifting for a period lasting 1, 2, or 3 s. Firing rates were calculated over the drift duration. Each stimulus was presented between 4 and 12 times. Baseline activity was measured during the presentation of gray screens whose luminance matched the mean luminance of the other stimuli. equation(1) I(x,y,t)=cos(ωC⋅χ)+0.5⋅cos([ωC−ωE]⋅χ)+cos([ωC+ωE]⋅χ)=cos(ωC⋅χ)⋅[1+cos(ωE⋅χ)] SF tuning was measured using between 5 and 9 stimuli. The SFs of the sinusoidal gratings, which were presented

either in isolation or as components of contrast-reversing gratings or interference patterns, could range between 0.02 and 4.0 cyc/°, but rarely exceeded 3.0 cyc/°. The component SFs of the interference patterns did not exceed 2.0 cyc/°. In the LGN experiments, SF tuning curves were fit with difference of Gaussians (Enroth-Cugell and Robson, 1966). In the cortical experiments, SF tuning curves were fit with log-Gaussians. TF tuning was measured using either 6 or 9 stimuli. The TFs of the sinusoidal gratings, which were either presented in isolation or as components of contrast-reversing gratings or interference patterns, typically ranged between 0 and 25 cyc/s. One component of the interference patterns with a carrier TF of 25 cyc/s was higher (25 cyc/s + the envelope TF).