At least four individuals per species were investigated, with two to three times more males sampled than females. Before discussing the advantages of these techniques, it is

important also to recognize their limitations. Both approaches are restricted to polyadenylated RNAs and to protein-coding mRNAs and could not fully explore the relative levels of alternatively spliced transcripts. The DGE method also required 4,869 genes to be discarded since these are without a site for the DpnII restriction enzyme for any of the three species. Finally, it needs to be recognized that levels of transcripts and proteins tend to be only modestly correlated, if at all ( Ghazalpour et al., 2011), and thus that conclusions based on transcript abundance may not be translated to the protein level. The DGE approach employed two to three million 20 bp tags from the 3′ of transcripts per sample that were mapped to gene models DAPT ic50 within reference genome assemblies. Not surprisingly, perhaps, the DGE method, which is based on the Illumina GAIIx this website next-generation sequencing technology, outperforms two microarray technologies, capturing more genes, more differentially expressed genes, and more conserved modules (defined below).

Konopka et al. (2012) thus concentrate on the DGE results. Babbitt et al. (2010) previously applied DGE to ADAMTS5 frontal cortex samples from three humans, three chimpanzees, and three macaques, and their lists of genes that were differentially expressed between human and chimpanzee are similar to those identified by Konopka et al. (2012). The first major findings of Konopka et al. (2012) are that genes that are differentially expressed in human, with respect to the other two species, are more numerous for the frontal pole than they are for the other two brain regions and that this bias is not observed for the frontal pole samples of chimpanzee or macaque. In the human frontal pole samples, 1,450 genes are differentially expressed, and Konopka et al. (2012) make mention of 23 that contribute to

a variety of neurobiological processes, such as neuron maturation and neurotrophin signaling. Further advances from this study arose from Konopka et al. (2012)’s analyses of gene coexpression networks derived from the three brain regions of the three primates. These networks are constructed from genes whose expression levels are correlated (either positively or negatively) among these samples, with genes that are more highly correlated being more closely neighboring in the network (Oldham et al., 2006). In these experiments, each gene expression level is the sum of its transcripts’ abundances in all cells of each sample. There are two explanations for why two gene expression levels may be positively correlated across samples.

67, χ2 test), and the KO mice were grossly healthy, viable, and fertile. Western blotting with antibodies directed against the C-terminal region of dynamin 3 (Ferguson et al., 2007) confirmed the absence of the protein in brain, testis, and lung;

i.e., the tissues where it is most prominently expressed (Figure 1C). Due to the high levels of dynamin 1, dynamin 3 represents only a minor fraction of the total dynamin in the brain (Ferguson et al., 2007). However, western blotting with an antibody that specifically and equally recognizes both dynamin 2 and 3 (Ferguson et al., 2009) showed that dynamin 3 makes a larger contribution to total dynamin levels in the brain than does dynamin 2, which in turn is expressed at lower concentration in

brain than in other tissues (Figure 1C). In spite of the expression of dynamin 3 in the testis and of its proposed function PD0332991 order in sperm maturation (Vaid et al., 2007), matings between dynamin 3 KO mice yielded pups without any indication of fertility defects (see below). As expected, the immunoreactivity recognized by our anti-dynamin 3 rabbit polyclonal and mouse monoclonal (clone 5H5) antibodies was no longer observed in KO samples (Figures 1A, 1C, and 1E). In contrast the fluorescence produced by a more widely used dynamin 3 antibody that strongly labels dendritic spines (Gray et al., 2003 and Lu et al., 2007) GW3965 in vitro was unchanged in dynamin 3 KO neurons (Figure 1E). Thus, these experiments also do not support the reported preferential postsynaptic localization of dynamin 3 in dendritic spines. Consistent with their overall good health, no defects were observed in the brain of dynamin 3 KO mice at the histological level (data not shown). Likewise, no defects were observed in primary cultures of cortical neurons with respect to gross morphology or distribution of immunoreactivity for synaptic markers, including clathrin coat components (α-adaptin), synaptic vesicle proteins (synapsin; as well

as synaptophysin and synaptobrevin, not shown), and an active zone protein (bassoon) (Figure 1D). Furthermore, electron microscopy analysis of dynamin 3 KO synapses in primary neuronal cultures did not reveal obvious pre- or postsynaptic structural alterations (Figure 1F). For example, synaptic vesicles were abundant and showed a normal homogeneous diameter. To test for a synergistic function of dynamin 1 and 3, mice harboring KO alleles of dynamin 1 and 3 were bred to yield double KO (DKO) mice. Such mice were born but were immediately distinguishable from their littermates because of their limited movement. They failed to nurse and died within several hours after birth (Figure 2A). Thus, they had a more severe phenotype than dynamin 1 single KO mice that can survive for up to 2 weeks (Ferguson et al., 2007).

The effects of minimal footwear on running form and injury are poorly Selleckchem Crenolanib understood, but studies of western runners who have transitioned to minimal shoes suggest that they are more likely to RFS than actual barefoot runners,20 and 21 with the possible effect of increasing the likelihood of certain injuries.22 and 23 This study aims to add to our understanding of the effects of footwear on variation in running form by examining a population of runners who traditionally wear minimal footwear: the Tarahumara Native Americans from the Sierra Madre Occidental of northwestern Mexico (also known

as the Sierra Tarahumara). The Tarahumara (self-identified as the Rarámuri) are one of several Native American groups that are famous for their

tradition of running long distances in very rough terrain. Oral history and ethnographic accounts report that the Tarahumara used to run down prey such as Talazoparib research buy deer and antelopes through endurance running.24, 25 and 26 This style of hunting, known as persistence hunting, takes advantage of two unique human abilities: to cool by sweating, and to run long distances at speeds that make quadrupeds gallop. Since quadrupeds cool by panting but cannot simultaneously pant and gallop, persistence hunting through endurance running can drive animals into a state of hyperthermia over long distances in hot, arid conditions.27, 28, 29 and 30 The Tarahumara do not train in a conventional sense by running on a regular basis, but instead engage in long distance running several times a year by participating in the rarajipari, an ancient ball game in which teams run long distances, often 75 km or more, while kicking and then chasing a small wooden ball. Tarahumara women compete in a slightly different long distance race known as

the ariwete, which uses a hoop rather than a ball, and typically involves distances of 40 km or less. The antiquity of the rarajipari Tryptophan synthase and ariwete are unknown, but the rarajipari is recorded by the earliest accounts of the Tarahumara, and probably dates back for many thousands of years. Recently, the Tarahumara have also started to compete in ultramarathons. Although the Tarahumara rarely if ever practice persistence hunting today, some older individuals report having done so when they were young, and long distance running remains an important part of their culture through rarajiparis, ariwetes, and ultramarathons. These races have become well known because of the best-seller Born to Run, 31 but it is worth emphasizing that the Tarahumara are just one of many Native American groups that excelled at long distance running. 32 A second reason to study variation in running kinematics among the Tarahumara is that they traditionally run in minimal footwear.

The findings of Wang et al. take us another step toward a better understanding

of the role of NMDARs and phasic firing of DA neurons in the memory and learning functions of the brain. They also generate more questions. More detailed study of the relationship between firing modes, plasticity, and learning, coupled with direct measures of phasic dopamine release in target areas, promises to further elucidate the neural Pexidartinib datasheet correlates that differentiate various modes of learning behavior. “
“Neuroscientists are in a difficult bind when it comes to studying and reporting male-female differences. On the one hand, many features of the brain and behavior do vary by sex, and so researchers—whether studying humans or other animals—should include both male and female subjects and analyze their data with sex as a possible covariate. Just as medical research for too long overlooked women’s health issues, Selleckchem CH5424802 current research cannot ignore sex differences in behavior

or brain anatomy, physiology, and neurochemistry, especially considering the different prevalence of many psychiatric and developmental disorders in males and females (Cosgrove et al., 2007). On the other hand, research findings about sex differences have been distorted and exploited by nonscientists to an extraordinary degree—perhaps second only to research on weight loss. Beginning with the wildly popular 1992 book Men Are from Mars, Women Are from Venus, public discourse has been saturated with faulty factoids about men, women, Dichloromethane dehalogenase boys, and girls that have settled deeply into society’s collective understanding of gender roles. From education and parenting to corporate leadership and marital harmony, so-called scientific findings about the male and female brain have been used to validate various stereotypical practices that are discriminatory to both sexes. Consider that over 500 public schools in the U.S. now administer single-sex academic classes, fueled in large measure by claims about sex differences

in the brain and neuropsychological function, according to the website of the National Association for Single-Sex Public Education (http://www.singlesexschools.org). For example, a recent application for a public charter school in Palm Beach County, Florida that centered on single-sex instruction for kindergarten through eighth grade (Rogers, 2011) states under its “Guiding Principles” that “the brain develops differently,” which is then further explained, “In girls, the language areas of the brain develop before the areas used for spatial relations and for geometry. In boys, it’s the other way around.” The next heading is titled “The brain is wired differently” and continues, “In girls, emotion is processed in the same area of the brain that processes language. So, it’s easy for most girls to talk about their emotions.

Each candidate site was initially tested PFT�� purchase whether it was permissive for

UAG suppression by the orthogonal tRNACUALeu/leucyl-tRNA synthetase (LeuRS) pair, which incorporates the natural amino acid leucine (Leu). Each Kir2.1  TAG gene was transfected into HEK293T cells along with the tRNACUALeu/LeuRS   ( Figure 2B). The gene for green fluorescent protein (GFP) engineered with an amber stop codon at Tyr182 (GFP_Y182  TAG) was cotransfected ( Wang et al., 2007). GFP fluorescence would indicate the successful suppression of the UAG stop codon by the orthogonal tRNA/synthetase. The function of individual Kir2.1TAG channels was then determined by whole-cell patch-clamp recordings from GFP-positive cells. For example, a green-positive HEK293T cell transfected with Kir2.1_C169  TAG and the tRNACUALeu/LeuRS produced a basally active inwardly rectifying current that was inhibited by extracellular Ba2+ (IKir), similar to wild-type Kir2.1 channels ( Figure 2C). Of the eight candidate sites, IKir currents measured at −100 mV from HEK293T cells expressing Kir2.1_I143TAG, Kir2.1_C149TAG, Kir2.1_C169TAG, or Kir2.1_I176TAG were significantly larger than those from untransfected cells ( Figure 2D), indicating successful suppression and incorporation of Leu. If a functional Kir2.1 channel could be generated through Leu incorporation at the TAG site, then it seemed likely that the

same site would be compatible for the larger Uaa Cmn. We therefore tested Kir2.1_I143  TAG, Kir2.1_C149  TAG, Kir2.1_C169  TAG, and Kir2.1_I176  TAG for functional incorporation of Cmn ( Figures 2E–2H; Figure S1C). HEK293T cells were transfected with cDNAs for the Kir2.1TAG channel, tRNACUALeu/CmnRS GSK 3 inhibitor and the GFP_Y182TAG reporter ( Figure 2B), and incubated in Cmn (1 mM) aminophylline for 12–24 hr. Functional incorporation of Cmn was expected to lead to either a basally active IKir or an IKir that is revealed upon brief (1 s) light illumination (385 nm at 40 mW/cm2). For HEK293T cells expressing Kir2.1_I143TAG or Kir2.1_I176TAG,

we could detect no IKir before or after light illumination, indicating either no amber suppression or a nonfunctional channel after Cmn incorporation ( Figure 2E; Figure S1C). By contrast, HEK293T cells expressing Kir2.1_C149TAG displayed a large IKir that was unchanged by light illumination ( Figure 2F), suggesting that incorporation of Cmn at C149 did not significantly occlude the pore. It is striking that HEK293T cells expressing Kir2.1_C169TAG displayed little IKir at negative membrane potentials that increased significantly upon light illumination ( Figures 2G and 2H). These results suggested that incorporation of Cmn at C169 largely occludes the channel pore and that the blocking particle is released following brief light stimulation, indicating the successful construction of a photoactivatable Kir2.1 channel. We next examined the light sensitivity features of Kir2.1_C169TAGCmn (referred to as PIRK) channels expressed in HEK293T cells.

183 (Wilcoxon test: p = 0.782). In control rats injected with vehicle the average mEPSC amplitude was similar in the contra and ipsilateral Selleck Trametinib cortices (Contra: 11.10 ± 0.10 pA, n = 11 cells; Ipsi: 10.94 ± 0.08 pA, n = 16 cells, five rats; Wilcoxon test: p = 0.2375) (Figure 7E) in all animals tested (p = 0.73) (Figure 7E) indicating that visual stimulation

per se, does not produce plastic changes in mEPSC amplitude. The distribution of mEPSCs in the ipsilateral (nonstimulated) cortex was similar to the distribution of the contralateral mEPSCs (Wilcoxon test: p = 0.4298) (Figure 7E), and also similar to the distribution of ipsilateral mEPSCs from rats treated with methoxamine or isoproterenol, supporting the idea that neuromodulators promote changes in activated synapses only. Finally, we examined the role of NMDA receptors and tested the effects of systemic injection of the competitive antagonist CPP (15 mg/kg FK228 cell line i.p 20 min prior monocular stimulation), a dose that blocks experience-dependent plasticity without affect visual responses (Frenkel et al., 2006 and Sato

and Stryker, 2008). The CPP injections consistently abolished the differences in mEPSC amplitude between the contra- and ipsilateral cortices in rats treated with methoxamine (n = 5; Wilcoxon test: p = 0.8489) or isoproterenol (n = 5; Wilcoxon test: p = 0.9686) (Figure 7F), which is consistent with a role of NMDAR in the visually induced plasticity promoted by neuromodulators. A two-way ANOVA test confirmed the significance of the differences in mEPSC amplitude across treatments (F(9,196) = 10.4139, p < 0.001) (Figure 7G). The frequency of the mEPSCs, on the other hand, was not affected (two-way isothipendyl ANOVA, F(9,196) = 0.9163, p = 0.512) (Figure 7H). Altogether the results indicate that activation of α and β adrenoreceptors can be used to globally

potentiate and depress synapses in a controlled manner. The results described above (Figure 7) suggest that monocular stimulation induced LTD throughout the contralateral cortex when delivered in conjunction with methoxamine, and induced LTP when delivered with isoproterenol. To further examine this idea we tested whether the treatment with neuromodulators and monocular stimulation, as it induced plasticity in vivo, occludes subsequent pairing-induced LTD or LTP in vitro. In control rats (stimulated but injected with vehicle, n = 5 rats) (Figure 8B) both hemispheres expressed comparable magnitude of LTP (p = 0.23) and LTD (p = 0.56). In stimulated rats injected with methoxamine (n = 7 rats) (Figure 8C) LTD was robust in the ipsilateral hemisphere (nonstimulated cortex) but absent in the contralateral one (p < 0.0001), consistent with the idea that LTD was already induced in these synapses. Interestingly, pairing at 0mV potentiated synapses in the contralateral, but not in the ipsilateral, hemisphere (p < 0.0001).

In many cases, a functional role has been demonstrated on the basis of pharmacological blockade, knockout, or knockdown. For example, Craner et al. (2005)

demonstrated that sodium channel blockade with TTX attenuates phagocytosis by 40% in cultured microglia. They also showed that the phagocytic capacity of microglia derived from med mice, which lack Nav1.6 channels ( Kohrman et al., 1996), is 65% lower than that of microglia from wild-type (WT) mice. Black et al. (2009) observed that the clinically used sodium channel blocker phenytoin significantly reduces the phagocytic activity of microglia by 50%–60% ( Figure 2). These studies also showed that TTX and phenytoin Vorinostat in vivo attenuate the release of the proinflammatory cytokines interleukin 1-α (IL-1α), IL-1β, and tumor necrosis factor α (TNF-α) from stimulated 5-FU molecular weight microglia while having minimal effects on the release of IL-2, IL-4, IL-6, IL-10, monocyte chemotactic protein 1 (MCP-1), and transforming growth factor α (TGF-α). Phenytoin and TTX also significantly decrease ATP-induced migration of microglia. Supporting a role for Nav1.6 in the pathway leading to microglial migration, the level of ATP-induced migration of microglia cultured from med mice is significantly lower than that of cells from littermate WT mice ( Black et al., 2009). Another line of evidence of a novel contribution

of sodium channels—in this case the “cardiac” Nav1.5 channel—to the function of nonexcitable cells was provided by Carrithers et al. (2007), who demonstrated the expression of Nav1.5 within phagosomes of activated human macrophages by immunocytochemistry and immunogold electron microscopy (Figure 3). The expression of Nav1.5 was restricted to late endosomes of these cells and was not detected in early endosomes or on the macrophage plasma membrane. Evidence of a role for Nav1.5 in macrophage function was provided by the demonstration that TTX at 10 μM (a concentration that blocks Nav1.5) and gene knockdown of Nav1.5 with small hairpin RNA (shRNA) inhibit phagocytosis by these cells. Using time-resolved

fluorometry, Carrithers et al. (2007) also demonstrated from that the sodium channel activator veratridine reduces intraendosomal pH and intraendosomal [Na+] and that 10 μM TTX blocks lipopolysaccharide-induced acidification of the intraendosomal compartment in both purified endosomes and intact macrophages. These results suggest a model in which Nav1.5 channels, located intracellularly within the membrane of late endosomes, provide a route for Na efflux, which counterbalances proton influx, and thereby maintain electroneutrality during acidification, which is one of the final stages of phagocytosis. Noting that pH regulates the current of Nav1.5 (Khan et al., 2006), Carrithers et al. (2007) suggested that the expression and activity of Nav1.

Having established how GCAPs-mediated feedback stabilizes the amplitude of the average

SPR across genotypes with differing selleck kinase inhibitor average R∗ lifetimes, we now consider whether it also contributes to reduction of the trial-to-trial variability of SPR amplitudes in an individual rod, i.e., contributes to SPR reproducibility. SPR reproducibility has long been deemed something of a biophysical mystery: despite being driven by individual stochastically deactivating R∗ molecules, SPRs have highly invariant amplitudes, with coefficient of variation (c.v.; standard deviation divided by the mean) of ∼0.2 in amphibian rods (Baylor et al., 1979; Rieke and Baylor, 1998) and ∼0.3 in mammalian rods (Baylor et al., 1984; Figure 6F). In recent years, empirical and theoretical studies have led to general agreement that multiple phosphorylations of R∗ smooth its stochastic deactivation (Rieke and Baylor, 1998; Mendez et al., 2000; Field and Rieke, 2002; Hamer et al., 2003; Doan et al., 2006). Theoretical simulations

have suggested that stochastic R∗ shutoff is nonetheless the primary source of SPR variability and also that the limited diffusion of cGMP acts to suppress the variability associated with R∗ deactivation (Bisegna et al., 2008; Caruso et al., 2010, 2011). These same theoretical studies have also concluded that calcium-mediated feedback plays little role in the reproducibility of the SPR (Caruso et al., 2011), a conclusion at odds with what might now be expected, given our current Epigenetic inhibitor cell line results with GCAPs-mediated feedback and SPR amplitude stability. To directly assess whether calcium feedback to cGMP synthesis contributes to SPR reproducibility, we recorded hundreds of dim flash responses from wild-type (Figure 6A)

and GCAPs−/− (Figure 6B) rods and calculated the mean and time-dependent no standard deviation of the ensembles of isolated SPRs (“singletons”; gray and pink traces, Figures 6C–6D; Experimental Procedures). In addition to being larger, the response peaks of isolated GCAPs−/− singletons were more variable in amplitude and were more broadly distributed in time. As a result, the time-dependent standard deviation of GCAPs−/− singletons had a larger, broader peak than that of WT singletons (note difference in both x- and y-scaling, Figures 6C–6D). The increase in the GCAPs−/− singleton standard deviation relative to that of WT was larger than the relative increase in singleton mean amplitude, resulting in a larger c.v. of the response amplitude (c.v. = 0.34 ± 0.01, n = 5 for WT and 0.42 ± 0.02, n = 4 for GCAPs−/− rods; p = 0.02; Figure 6F, solid green and blue bars). Thus, although R∗ and G∗-E∗ deactivation are the same for WT and GCAPs−/− rods, reproducibility is impaired in the absence of GCAPs-mediated feedback.

The point where the cannulae penetrated the tissue above the brain was constant, (7.5L, 5P mm) and (12.5L, 5P mm) in stereotaxic coordinates for monkey Y and G, respectively. We lowered the cannulae 9 mm and 10.5 mm on average for monkey Y and G. The depth varied only within ±0.5 mm across sessions. The resulting final position of the cannulae was at approximately 4 ± 0.5 mm from the cortical surface estimated as the depth at which we encountered the first neuronal activity. From the MR imaging of the gadolinium spread, we estimated that the center of inactivation area was at (5L, 1P mm) and (7L, 1A mm) in stereotaxic coordinates for monkey Y and G, respectively. These

values differ from the initial penetration points http://www.selleckchem.com/products/CAL-101.html because the cannulae were not

normal but slightly tilted with respect to the horizontal stereotaxic plane for monkey Y and G. The inactivation was contained within the medial wall of the midposterior portion of the IPS. The medial wall of the IPS includes two anatomically distinct areas, the medial intraparietal area (MIP) and the ventral part of area 5 (5v) (Colby et al., 1988; Lewis and MDV3100 mouse Van Essen, 2000; Saleem and Logothetis, 2012). The distinction between MIP and 5v is based on their myeloarchitecture, and the boundary between the two areas reported in the literature ranges from approximately a quarter to half way along the IPS from the posterior end. In the absence of histology, we cannot determine the precise boundary of these two areas and, thus, do not know whether the inactivated area was MIP, 5v, or both. Methisazone In each inactivation session, a stainless steel beveled-tip cannula (28–30 GA, Plastic One) affixed to a microdrive (NLX18, Neuralynx) was acutely lowered to the aforementioned constant location. Then, typically 5 μl (range: 3.5–10) of muscimol solution (5 mg/ml, pH ∼7.4) was injected at 1 μl/min using a 100 μl gas-tight Hamilton syringe and

a micropump system (Harvard Apparatus). The behavioral experiment began 35–60 min after the injection started and lasted up to 3 hr, well within the accepted time for muscimol action (Arikan et al., 2002). These experimental parameters for individual sessions are listed in Table S1. We alternated between inactivation and control sessions. They were typically spaced 24 hr apart. Exceptions were two inactivation sessions with a 2 day separation from the previous control session, and four control sessions with a 3–9 day separation from the previous inactivation sessions. The recovery of function in control sessions was visually noticeable in terms of the reach endpoint accuracy in the interleaved control sessions (Figures S1B, S1C, and S4D). In a subset of control sessions (four sessions for Y, nine sessions for G), 5 μl of saline solution was injected instead of muscimol.

05 two-tailed; Figure 5E). These findings suggest that GABAA-mediated inhibition contributes to the suppression of fimbria-evoked EPSPs following the PFC train but does not account entirely for this suppression. We found that high-frequency PFC stimulation suppresses EPSPs arising from single-pulse fimbria stimulation in VS MSNs. This suppression

was observed at a short latency following the PFC Depsipeptide nmr stimulus (50 ms after the final pulse in a 10 pulse, 50 Hz train delivered to the PFC), but not at a long latency (500 ms) following the PFC train. The suppression of fimbria-evoked EPSPs by the PFC cannot be attributed solely to the depolarization of recorded cells elicited by the PFC train, as fimbria-evoked EPSPs were not attenuated by the depolarization elicited by spontaneous up states or current

injection through the recording electrode. Moreover, burst-like activation of the PFC was necessary to produce suppression of fimbria responses; single-pulse stimulation of the PFC did not reduce the magnitude of the fimbria-evoked EPSP. The suppression of glutamatergic responses by robust PFC activation extended to other afferents as well, as PFC train stimulation attenuated thalamus-evoked responses. Trains of stimuli to the HP did not attenuate PFC-evoked EPSPs, consistent with the proposed gating relationship of the HP with VS MSNs (O’Donnell and Grace, 1995). However, burst-like stimulation of the thalamus was able to attenuate the PFC-evoked response, but this effect was not as dramatic as the near-total suppression of HP and thalamic inputs caused by PFC train stimuli. These check details data suggest that burst-like PFC activity elicits brief heterosynaptic suppression of HP and thalamic Adenosine inputs to the VS. The integration of excitatory inputs in the VS is complex, with several nonlinearities (Goto and O’Donnell, 2002; Wolf et al., 2009). HP afferents are critical for the spontaneous up states observed in anesthetized animals; VS up states are eliminated if the fimbria/fornix is transected or inactivated (O’Donnell

and Grace, 1995) and can be detected simultaneously with HP spindles (Goto and O’Donnell, 2001b). As MSNs fire action potentials only from the up state, the relationship of the HP to the VS has been described as a gating mechanism, in which the VS must receive convergent excitatory input from the HP for other excitatory inputs, including those from the PFC, to be transmitted onward to downstream targets (O’Donnell and Grace, 1995). The critical role of the HP in shaping VS activity is also apparent in the behaving animal. Under resting conditions, the VS shows highly synchronous field potential activity with the ventral HP (Gruber et al., 2009a). Furthermore, place cells are found in the VS (Lavoie and Mizumori, 1994), and their activity is likely driven by HP inputs.