caninum, S. neurona and T. gondii, respectively ( Dubey learn more et al., 2001a, Dubey et al., 2007 and Kikuchi et al., 2004). In addition, studies aimed to understand the phenomena related to transplacental transmission of these parasites are increasingly required. Interestingly, serum samples of pre-colostral foals exhibited high

percentage of samples positive for more than one parasite. Previous study states that the antibody avidity is dependent on how long cattle are infected with N. caninum ( Sager et al., 2003). Additionally, different studies demonstrate that antibody avidity depends on the interactions between immune cells, heterogeneity of T and B lymphocytes and maturity of the immune responses acquired with age ( Doria et al., 1978 and Mei and Radbruch, 2012). Relationship between the level of antibodies in mares and a frequency of vertical transmission of protozoa Neospora sp., S. neurona and

T. gondii are still BAY 73-4506 in vivo unclear. Our results indicate that foals from mares that presented higher IgG titers probably were born uninfected ( Fig. 2). These results suggest that the antibody responses in mares may prevent transmission through placenta. This data corroborates with a previous study performed in the same region in Brazil ( Locatelli-Dittrich et al., 2006). However our study assessed only the humoral immune response. Therefore, further studies evaluating the cellular response are needed in order to better understand the vertical transmission of protozoan belong to the family Sarcocystidae, since the cellular response has an important role in the protection against parasites ( Tanaka Sodium butyrate et al., 2000) In summary, we have assessed the serological status of mares and pre-colostral foals to parasite from the Sarcocystidae family, Neospora spp., S. neurona

and T. gondii, which suggested that seronegative mares, or those with low to intermediate antibody levels, have a higher risk of giving birth to seropositive foals. “
“Avian trichomonosis, also known as pigeon trichomonosis or canker, is caused by the flagellated protozoan parasite Trichomonas gallinae. The parasite primarily infects the upper digestive tract of birds and lesions vary from mild ulceration of the mucosa to large caseous masses ( Narcisi et al., 1991). Trichomonosis has been reported in turkeys and chickens ( Stabler, 1954), raptors, columbids, passerines ( Forrester and Foster, 2008 and Stoute et al., 2009), budgerigars ( Mckeon et al., 1997), house finches ( Gerhold et al., 2008) and in wild finches ( Neimanis et al., 2010). Multiple large mortality events have been associated with trichomonosis ( Forrester and Foster, 2008 and Robinson et al., 2010). Previous molecular characterization of T. gallinae isolates in the United States, disclosed multiple genotypes and potential host-parasite associations ( Gerhold et al., 2008, Anderson et al., 2009 and Lawson et al., 2011). Here we describe the lesions and molecular characterization of Trichomonas spp.

Here, the key measure of success is the subject’s accuracy in predicting the US time. To test this hypothesis, we used each subject’s mean timing estimate from instrumental test trials as an index of his or her internal GSK1349572 datasheet prediction of outcome timing. We then examined the classical conditioning trials where the experienced US timing was closest (1/3 trials) to this internal US timing prediction (more accurate trials), and compared VS responses in these trials against those in all other trials (less accurate trials). As predicted, we found larger

responses to more accurate trials (t13 = 2.76, p = 0.016; Figure 5A). Furthermore, such a signal was not present in the VTA (p = 0.919) and direct comparison between VTA and VS revealed a trend for an interaction (ROI × accuracy: F1,52 = 3.57, p = 0.064). Second,

if this VS response is a measure of covert timing performance then, after large VS responses, subjects should not change their timing estimates on subsequent test trials. Again, by analogy to more conventional tasks, high VS BOLD responses are associated with reselecting the same option on the following trial (Li and Daw, 2011). To test this hypothesis, we calculated the change in subjects’ timing guesses between one test trial and the next. We then examined VS responses in the classical conditioning trials that occurred between these test trials. Again we examined trials that led to the smallest (1/3 trials) behavioral change second (smaller update trials), and compared VS responses in these trials against those OSI-744 molecular weight in all other trials (larger update trials). As expected, we found larger responses to smaller update trials (t13 = 2.20, p = 0.046; Figure 5B). Again, such a signal was not present in the VTA (p = 0.22). Our data show that the BOLD signal from the VTA, but not the VS, is consistent with TD reward prediction errors both to conditioned and unconditioned stimuli. However, in situations with uncertain reward timing, TD theory also predicts that activity in the waiting period between CS and US will be depressed

by continual small negative prediction errors, as each successive time bin fails to deliver a reward. This depression should be proportional to the predicted reward level and be more depressed for larger or higher probability predicted rewards. To examine this hypothesis, we modeled a constant ongoing negative reward prediction error in the time between CS and US in our variable timing trials (Figure 6A). In the VTA, parameter estimates were both negative on average (one sample t test: t27 = −4.4, p < 0.001) and exhibited a trend toward being more negative in proportion to the CS reward probability (t27 = −1.5, p = 0.08; Figure 6B). Neither of these effects held true in the VS (p = 0.23, 0.75). Formal testing between structures revealed that this ongoing depression of activity was significantly greater in the VTA than the VS (two sample t test: t27 = −2.4, p = 0.

Penn et al. (2012), take a rigorous approach to address the composition of AMPAR complexes at synapses. There remain however great challenges in relating molecular events inside the cell to synaptic outcomes. Numerous genetic and optical approaches are needed to address the subunit-specific composition of receptor complexes not only at synapses but also within the biosynthetic and secretory pathways. Optical approaches aimed at determining subunit composition of synaptic iGluRs are being developed. For example, the use of single particle tracking photoactivation localization microscopy in concert with viral glycoproteins has begun to redefine our understanding of membrane receptor dynamics and their

movement trajectories within the cell (Hoze et al., 2012). However, these techniques at present do not allow subunit/splice variant composition of AMPARs BI 2536 mouse to be defined. Development of quantitative imaging and biochemical techniques will be required to SAR405838 nmr discern the oligomerization processes and the factors that regulate their dynamics. Further, these techniques would allow us to better understand the role of endocytosis in synaptic transmission and perhaps whether recycling endosomes represent a secondary level of

subunit-specific processing. These issues are critical to resolve because, unlike in politics, “flip-flopping” appears to be a good thing in neurons. The authors were supported by grants from NIH and the MSTP (C.L.S.). “
“Understanding the neurobiology of schizophrenia is like charting a course on a map—a map, that is, with a very fuzzy idea of a destination, many potential starting points, and far too many opinions about waypoints to visit in between (Figure 1). The destination is the disorder itself, rendered fuzzy by its profound heterogeneity. For starting points, we have its myriad potential causal factors, be they genes such as DISC1 or the 22q11.2 microdeletion, or early environmental factors such as prenatal infection or malnutrition. The waypoints

are the equally varied pathophysiological theories, ranging from too much dopamine to too little GABA and encompassing just about everything in between. MTMR9 In such a morass of a landscape, how is a neuroscientist supposed to navigate toward a better understanding of schizophrenia? We would argue that one needs first to fill in the map—to sketch out which paths lead to which destinations. Or to put it in into scientific terms, one needs to make and test hypotheses about how specific causes lead to specific pathophysiologies; how specific pathophysiologies lead to the symptoms of schizophrenia and how these causes and pathophysiologies interact. This approach is, at is sounds, a tremendous endeavor, but it is necessary in order to populate our map with valid pathways. And it just may yield novel ways of thinking about schizophrenia. The paper by Phillips et al. (2012) in this issue of Neuron does just that.

In principle, teaching and practice follows a gradual, part-to-whole, and easy-to-difficult progression with an emphasis on movement repetition, variation in practice, and integration of program core components. As with the training approach, teaching and practice of the program emphasizes key movement points, including ankle sway in multiple directions, dorsiflexion/plantarflexion,

firm surface contact using the toes, trunk-driven rotational movement, weight shift, multiplanar active head movement, and concurrent cognitive tasks involving recalling, switching, verbalizing, spatial orientation, and natural breathing that follows the rhythm of the movements. The program follows the principles of Epigenetic inhibitor motor control and learning16 in that the moves are (1) performed while seated, standing, or stepping, with varying speeds, ranges of motion, sensory inputs, and bases of support; (2) taught in various patterns (blocked vs. random vs. variable) and/or under dual-task conditions (by adding secondary cognitive tasks); and (3) practiced and reinforced using varying cues (ranging from the instructor’s auditory and visual cues to internalized

self-commanded cues). LY2157299 order Introduced in 2003,5 the 8-form routine (originally named Easy Tai Chi) was initially evaluated in a randomized controlled trial in which older adult participants were assigned to either a Tai Ji Quan group or a low-impact group exercising three times per week for 24 weeks. 9 At the end of 24 weeks, it was shown that, relative to those in the low-impact exercise condition, Tai Ji Quan participants showed improvements on four clinical physical performance measures: single-leg stands (right: p < 0.001; left: p < 0.001); chair rise (p = 0.003); and 50-foot speed walk (p = 0.003). These promising results provided ever a scientific basis and clinical impetus for continued refinement efforts for the training protocol (under the revised

name Tai Chi: Moving for Better Balance 12). With a strong focus on balance, gait, and mobility, Li et al. 12 emphasized training for movement symmetry, active head movement, bilateral weight-shifting, control of movement of the center of body mass within its full limits of stability, and variable walking/stepping, all of which are essential ingredients for posture control and locomotion. In a community-based dissemination study with a pre–post-design,13 the application of the revised routine showed encouraging results. At the end of a 12-week intervention, participants exhibited significant pre- to post-intervention improvements in forward functional reach (32.31 cm pre-test, 34.39 cm post-test; p < 0.0001), TUG test (7.40 s pre-test, 7.17 s post-test; p < 0.0004), chair stands (10.60 s pre-test, 10.07 s post-test; p < 0.0006), and 50-foot walk speed (12.78 s pre-test, 12.14 s post-test; p < 0.001).

Previous studies suggested that a glutamatergic-purinergic signaling pathway prevents hypoosmotic swelling of Müller cells in the rodent retina Bleomycin order by vesicular release of glutamate (Wurm et al., 2008 and Wurm

et al., 2010; Figure 4A). Therefore, we tested whether this pathway was defect in BoNT/B-expressing Müller cells. Müller cells from Tam-injected bigenic mice, which expressed the BoNT/B transgene as indicated by the presence of EGFP (Figure 4B), had similar cross sectional areas as cells from Tam-injected monogenic mice (Figure 4C). However, these cells swelled in hypotonic solution, while Müller cells from monogenic animals maintained their cell volume (Figure 4D) indicating a toxin-induced defect in volume regulation. If the Everolimus chemical structure swelling of toxin-expressing Müller cells was due to the block of glutamate release, coapplication of glutamate should prevent the swelling of these cells. As shown in Figure 4D, this

was indeed the case thus confirming the involvement of exocytotic glutamate release in volume regulation. Vascular endothelial growth factor (VEGF), which activates the volume-regulating cascade upstream of glutamate release (Wurm et al., 2008), failed to abolish swelling of Müller cells from bigenic mice (Figure 4D), whereas it prevented hypotonic swelling of Müller cells from monogenic mice due to barium-induced block of inwardly rectifying potassium channels (Wurm et al., 2008) (Figure 4D). Toxin expression in Müller cells may have provoked reactive gliosis and thereby perturbed glial volume regulation (Pannicke et al., 2004, Pannicke et al.,

2005 and Sene et al., 2009). However, levels of glial fibrillary acidic protein (GFAP) were similar in retinae from Tam-injected mono- and bigenic mice (data not shown). Additional hallmarks of Müller cell reactivity are a downregulation of potassium inward currents and an increase in membrane capacitance (Pannicke et al., 2005). Our patch-clamp recordings revealed comparable amplitudes of inward currents and even a significant (p < 0.02; Student's t test) decrease in membrane capacitance in acutely isolated Müller cells from Tam-injected bigenic (2.4 ± 0.7 nA; 40 ± 12 pF; n = 33 cells from 8 mice) compared to monogenic mice (2.2 ± 0.6 nA; 49 ± 12 pF; PAK6 n = 29 cells, 7 mice). The VEGF-induced glutamate release from Müller cells also induces swelling of neurons in the ganglion cell layer independently from a hypo-osmotic challenge (Wurm et al., 2008). To test whether this effect was eliminated by glial toxin expression, we measured the size of neuronal somata that were close to endfeet of toxin- and EGFP-expressing Müller cells from Tam-injected bigenic mice (Figure 4E). Indeed, these neurons did not show VEGF-induced swelling, whereas the effect was present in cells from Tam-injected monogenic animals (Figure 4E, F). As for Müller cells, the mean cross sectional area of untreated neurons was similar in mono- and bigenic mice (Figure 4C).

Together, these data imply that mGluR-induced OPHN1 mediates LTD by promoting MAPK Inhibitor Library high throughput the internalization of AMPARs. Further support for these results, and mechanistic insight into how OPHN1 induction could regulate AMPAR endocytosis during mGluR-LTD, were provided by our finding that OPHN1 interacts with N-BAR domain-containing Endo2/3 core components of the postsynaptic clathrin-dependent endocytic machinery (Chowdhury et al., 2006). Interestingly, our data show that mGluR stimulation enhances OPHN1 association with Endo2/3 in a protein synthesis

dependent manner. And importantly, disruption of the OPHN1-Endo2/3 interaction impedes both mGluR-elicited persistent decreases in surface AMPARs and LTD. Notably, these effects are not attributable to some general disruption of AMPARs or the machinery that controls their trafficking, because disruption of the OPHN1-Endo2/3 interaction does not affect basal AMPAR levels or basal synaptic function. Thus, these data imply that the downregulation of surface AMPARs during mGluR-LTD requires OPHN1 induction and its ability to bind Endo2/3. Likely, OPHN1 induced upon mGluR activation, via the regulation of Endo2/3′s activities, increases the rate of AMPAR endocytosis. While our data demonstrate a requirement for

OPHN1 synthesis in mGluR-LTD, previous studies have shown that newly synthesized Obeticholic Acid cell line Arc protein is also required for this process (Waung et al., 2008), implying that both mGluR-induced OPHN1 and Arc, and perhaps other proteins, such as MAP1B and

STEP (Davidkova and Carroll, 2007 and Zhang et al., 2008), are likely to contribute jointly to LTD, and, moreover, that mGluR1/5 must coordinate the various translational control mechanisms involved. Of particular interest is that Arc also interacts with Endo2/3 and this interaction is important for the role of Arc in AMPAR trafficking (Chowdhury et al., 2006). Of note, OPHN1 and Arc interact with different regions of Endo2/3, with OPHN1 binding to the SH3 domain of Endo2/3, and Arc to the C terminus of the N-BAR domain of Endo2/3 (Chowdhury et al., 2006). Isotretinoin Therefore, it is possible that newly synthesized OPHN1 and Arc cooperate at the level of Endo2/3 to promote mGluR-driven AMPAR endocytosis, either by regulating distinct aspects of Endo2/3 function or by promoting/engaging a common mechanism, at least under wild-type conditions. Importantly, a different mode of mGluR-LTD regulation seems to occur upon loss of FMRP. Indeed, previous studies demonstrated that mGluR-LTD in Fmr1 KO mice is distinctly different from that in wild-type mice. For instance, whereas mGluR-LTD in wild-type mice is protein synthesis dependent, it persists in the absence of protein synthesis in Fmr1 KO mice ( Hou et al., 2006 and Nosyreva and Huber, 2006).

97, stimulated 8.28, Palbociclib p < 0.001). Response magnitude, however, was reduced by stimulus exposure (Figure 7E, two-way ANOVA main effect of stimulation, F[1,1502] = 59.7, p < 0.001; means in bins

1–9 naive 9.87% ± 0.16%, stimulated 8.31% ± 0.14% dF/F). As in Figure 5F, there was a significant main effect of fidelity on response strength—in both the naive and stimulated groups, the neurons that responded with the highest fidelity (ten out of ten trials) had the largest changes in fluorescence (Figure 7E, F[9,1502] = 27.95, p < 0.001). To examine the effect of passive stimulation on total network activity, we plotted the fraction of neurons in the total population as a function of their mean magnitude of fluorescent change (Figure 7F). Exposure to a nonreinforced stimulus increased total activity by 32.5% (failures included) relative to naive controls (Figure 7F, naive dF/F = 4.64% ± 0.13%, stimulated dF/F = 6.15% ± 0.24%; p < 0.0001). Taken together, our data indicate that exposure to a nonreinforced stimulus has no effect on population sparsification, but does enhance response fidelity at the expense of

response strength. The goal of this study was to determine how associative fear learning shapes the local population response to the associated conditional stimulus in primary sensory cortex. To do this, we developed a paradigm in which controlled whisker stimulation in freely exploring mice could be paired with a foot shock. Mice in which foot shock was paired with whisker stimulation learned the association Metformin supplier only between the two stimuli and retained the memory for weeks, and possibly longer. This learning was reflected in the neural responses in the region of barrel cortex mapping the trained whisker. Fewer neurons responded to stimulation of the trained whisker, yet their responses were stronger than those in control mice in which whisker stimulation was explicitly unpaired with foot shock. The emergence of sparse population coding

and increased response strength after learning likely improves the metabolic efficiency of cortical processing. The increase in response strength improves robustness in terms of signal to noise, but is metabolically expensive. The enhanced sparsification of the population response likely compensates for the increased metabolic demand of the improved robustness, while simultaneously decreasing network crosstalk (Olshausen and Field, 2004). Supporting this view, we found that net activity—the average activity across all neurons, inclusive of failures—was reduced after associative fear learning. Importantly, these changes were unique to associative learning. In mice that were merely exposed to the CS, response fidelity increased, but the strength of a given neuron’s response decreased.

This small, lipophilic, unionized compound is therefore expected to cross cell membranes freely via passive diffusion driven by a concentration gradient. Afoxolaner pharmacokinetic properties

have been tested in a number of BKM120 research buy in vivo studies and follow the expectations for a Biopharmaceutics Classification System (BCS) Class II compound. For BCS Class II compounds, if dissolution is complete and the drug is in solution, high bioavailability is expected due to the high permeability. High permeability compounds readily access enzymes within the hepatocytes and therefore may be eliminated primarily by metabolism. These compounds also tend to distribute into tissues (Wu and Benet, 2005). Afoxolaner distributes into tissues, Vd of 2.68 ± 0.55 L/kg, as

expected for a lipophilic compound ( Toutain and Bousquet-Melou, 2004). The single exponential decay of afoxolaner in plasma during the terminal phase from Day 2 to 3 months suggests that no special tissue depots are present in the dog. This conclusion is consistent with the physical chemical properties of afoxolaner, which favor passive diffusion into and out of tissues. Active transport, if occurring, was not saturated under the conditions/dose levels tested. GSK126 clinical trial Afoxolaner has a low systemic clearance of 4.95 ± 1.20 mL/h/kg, determined following IV administration. The low clearance is much less than the hepatic blood flow in dogs (1854 mL/h/kg), as reported in Davies and Morris (1993) and is responsible primarily for the long half-life of afoxolaner in dogs. Clearance may be closely dependent on either free drug concentrations, where significant protein binding (>99.9% for afoxolaner) limits the drug available for renal and hepatic elimination, or on the intrinsic ability of hepatocytes to metabolize the drug (Rowland and

Tozer, 1995). Plasma, urine and bile were collected before to establish the primary route for elimination. Afoxolaner concentrations in the bile were high, and the biliary clearance was on average 1.5 mL/h/kg. This clearance is about 30% of the total clearance measured in PK Study 2, with individual dogs ranging in biliary clearance from 10 to 44% of the total clearance. Afoxolaner reabsorption was experimentally hindered by the biliary collection in this study, therefore, 30% is considered an upper limit of the total afoxolaner biliary clearance from the body. Using the estimated urine afoxolaner values that were below the limit of quantitation (<1.25 ng/mL), renal clearance of the parent compound was calculated to be less than 0.01% of the total clearance. The afoxolaner plasma concentrations from fed and fasted dogs are within the biological or inter-animal variability as shown by the standard deviations of the two groups. The differences were not therapeutically relevant or statistically significant (α = 0.05). As reported, the terminal plasma half-lives were 15.2 ± 5.1 and 15.5 ± 7.

Blots were developed by chemiluminescence reagent (West-zol, Intron) exposure to photographic film and quantified. Independent experiments were conducted at least three times. Under pentobarbital sodium (40 mg/kg) anesthesia, DiI (Molecular Probes; 1 μl, 25 mg/0.5 ml in ethanol) was injected into the VPL region of the thalamus (Bregma: −1.2 ± 0.2 mm, midline: 1.9 ± 0.2 mm, depth: 3.2 ± PFI-2 0.2 mm) using a glass micropipette (20 μm tip diameter) which was guided to the target area using a stereotaxic apparatus (Narishige, Tokyo, Japan). Two silk sutures (7-0;

Ailee, Busan, Korea) were tied loosely around the full circumference of the sciatic nerve 2–3 mm apart and secured with a reef knot; intraneural blood flow was not impeded. For reversal of chronic mechanical allodynia, BCTC was intrathecally injected at 28 days after

CCI surgery. Rectal temperature was measured by insertion of a flexible bead probe with a digital thermometer (TC-324B, Warner Instrument Corp., Hamden, CT). All drugs were made as stock solutions and keep at −20°C and diluted as final concentration (1:1,000–5,000). We expressed data as mean ± SEM, unless otherwise indicated. Significances in 50% paw withdrawal thresholds in comparison with preinjection or preinjury levels were calculated by one-way repeated-measure ANOVA followed by Bonferroni’s post-test and Student’s unpaired t test. Detailed methodology can be found in Supplemental Experimental Procedures. Thanks to Dr. Bruce P. Bean (Harvard Medical School) for helpful comments. This work was supported by grant (20110018614) from Chk inhibitor National Research Laboratory Program, grant (2011K000275) from Brain Research Center of the 21st Century Frontier Research Program, grant (2010-0015669) from Basic Research Program, and grant (2011-0030737 to S.J.K.) funded by the Ministry of Education, Science and Technology, the Republic of Korea. “
“Numerous studies have concluded that the thalamocortical (TC) projection, along which sensory information flows into the cerebral cortex, is fixed by the end of development. During a critical period in early postnatal life, monocular

vision loss can trigger robust anatomical plasticity of TC axons in the mouse and cat visual systems (Antonini et al., 1999 and Antonini Tryptophan synthase and Stryker, 1993). Such anatomical changes are thought to be driven, at least in part, by the strengthening and weakening of existing TC synapses, which in slices of somatosensory cortex cannot be induced beyond the first few postnatal weeks, probably due to the known developmental downregulation of NMDA receptors (Feldman et al., 1999). In both the visual and somatosensory systems, sensory experience during adulthood has little or no effect on the receptive fields of neurons in cortical layer 4 (L4) but has robust effects on other layers (reviewed in Feldman and Brecht, 2005, Fox, 2002 and Karmarkar and Dan, 2006).

05, see Experimental Procedures).

Two cells fired independently from the hippocampal θ rhythm (Figure 1A). The four θ-modulated cells fired preferentially between the peak and the descending phase of dCA1 θ (range 187.0–283.7°, where 0° and 360° represent θ troughs; θ phase histograms of single neurons are illustrated in Figure S2). However, statistical analysis showed that these four cells did not form a synchronized population in relation to dCA1 θ (R′ = 1.03, R0.05,4 = 1.09, Moore test). Furthermore, Akt inhibitor the firing of axo-axonic cells did not show statistically significant modulation in phase with dCA1 γ oscillations (p > 0.1, Rayleigh test, n = 6; Figure S3; Table S3). Axo-axonic cells displayed dramatic short-latency excitations in response to noxious stimuli. All axo-axonic cells increased their firing

rates upon hindpaw pinches (+377% of baseline, latency 267 ms, peak 377 ms, n = 6; ranges: 133%–606%, latency 200–400 ms, peak 400–600 ms, respectively; Table 2; individual histograms are shown in Figure S4). This excitation rapidly adapted, and was curtailed at stimulus offset (Figure 5D). Responses to electrical footshocks were similarly pronounced (mean 226% of baseline, latency 50 ms, peak 225 ms, n = 4/4; ranges 133%–606%, 20–100 ms, 20–420 ms, respectively; Figure 1C; Ku-0059436 ic50 Table 2; individual histograms, Figure S5). These neurons exhibited typical axo-dendritic patterns. Their axons formed cartridges. Almost all of large-axon varicosities were in close apposition with ankyrin G-expressing axon initial segments, (n = 6/6 cells), as seen with immunofluorescence (Figure 1D). We analyzed randomly-sampled synapses from two of these cells

using electron microscopy. The vast majority of postsynaptic targets were axon initial segments (95.4%, n = 43 synapses; Figure 1E; Table S1), confirming that these cells were of the axo-axonic type. All axo-axonic cells expressed parvalbumin (PV), sometimes weakly (Figure 1F), but were never calbindin (CB)-positive. Two of 6 neurons densely expressed the GABAAR-α1 subunit TCL on their dendrites (immunohistochemical results are summarized in Table S2). Axo-axonic cells were bitufted. Their dendrites did not branch immediately, were tortuous and sparsely spiny (Figure 1G). Axonal arborizations of all 6 cells were very dense and mostly contained within the dendritic field. Axons were always restricted to the BLA, but could be distributed between lateral and basal nuclei. These results show that the firing of axo-axonic cells of the BLA dramatically increases in response to salient sensory stimuli. However, their spontaneous population activity is not tightly synchronized with hippocampal θ (Figure 5). Next, we studied the firing of parvalbumin-expressing (PV+) basket cells (n = 15). During dCA1 θ oscillations, PV+ basket cells fired at a mean frequency of 11.0 Hz (range 1.8–27.