g., increases followed by decreases) in extracellular DA that take place over minutes, it is perhaps most useful to employ the term “fast phasic” to talk about the rapid changes in DA-related activity that can be measured with electrophysiology or voltammetery, and “slow phasic” in reference to the changes that take place over the slower time scale measured

with microdialysis methods (e.g., Hauber, 2010; Segovia et al., 2011). Electrophysiology studies have shown that presentation of novel or unexpected food reinforcers is accompanied by transient increases in the activity of putative ventral tegmental DA neurons, but that this effect goes away with regular presentation, or repeated exposure through training (Schultz et al., 1993; Schultz, 2010). Employing voltammetry Romidepsin methods to measure fast phasic changes in DA release, Roitman et al. (2004) showed that, in trained animals, exposure to a conditioned stimulus signaling that lever pressing would result in sucrose delivery was accompanied by an increase in DA transients, however, the actual

presentation of the sucrose reinforcer was not. A similar finding was reported years ago by Nishino et al. (1987), who studied free-operant fixed ratio lever pressing in monkeys and observed that activity of putative ventral tegmental DA neurons was increased during lever pressing in trained animals but actually decreased during reinforcer presentation. Unpredicted food delivery, as well as presentation of cues that predicted food delivery, increased fast phasic signaling as measured by voltammetry in Selleckchem VX809 the nucleus accumbens core (Brown et al., 2011). DiChiara and colleagues showed that exposure to novel palatable foods transiently

increased extracellular DA in nucleus accumbens shell as measured by microdialysis, but that this response rapidly habituated (e.g., Bassareo et al., 2002). A recent microdialysis paper demonstrated that presentation of high carbohydrate food reinforcers to previously exposed rats did not produce any change in extracellular DA in accumbens core or shell (Segovia et al., 2011). In contrast, both the acquisition and maintenance of fixed ratio lever pressing was associated with increases in DA release (Segovia et al., 2011). A similar pattern was shown when markers of DA-related signal transduction (c-Fos and DARPP-32) were very measured (Segovia et al., 2012). Taken together, these studies do not support the idea that food presentation per se, including that of palatable foods, uniformly increases accumbens DA release across a broad range of conditions. Nevertheless, considerable evidence does indicate that increases in DA transmission are associated with presentation of stimuli associated with natural reinforcers such as food, or the performance of instrumental behavior; this has been seen in studies involving microdialysis (Sokolowski and Salamone, 1998; Ostlund et al., 2011; Hauber, 2010; Segovia et al., 2011), voltammetry (Roitman et al., 2004; Brown et al.

Research has linked essentialistic representations of social groups to stigmatizing processes in domains like race, gender, sexual orientation, mental illness, and obesity (Dar-Nimrod and Heine, 2011). The concurrence of the concepts of brain and identity in contemporary society may make popular neuroscience a potent engine for essentialism, and its influence on intergroup relations should be a future focus of empirical investigation. Finally, the “brain as

biological proof” theme demonstrates how neuroscience can be recruited as a rhetorical tool to advance certain agendas. The media data provide a naturalistic analog to experimental findings Ku-0059436 manufacturer that brain-based information confers a scientific aura Proteasome inhibitor that obscures an argument’s substantive content (Weisberg et al., 2008). The ability to simulate coherent “scientific” explanations through cursory reference to the brain meant that neuroscience was exploited for rhetorical effect. Due to the size and range of the media sample, it was impossible to directly compare media coverage with the corresponding neuroscience research to precisely establish the extent they diverged. However, it seemed clear that research was being applied out of context to create dramatic headlines, push thinly disguised ideological arguments, or support particular policy agendas. The thematic representation of neuroscience in the media we

present offers a potentially useful resource for neuroscientists engaged in public communication of their research. If scientists are aware of the issues and contexts into which their research might be subsumed, they can explicitly address what their research implies (or does not imply) for these areas. Rather than

a one-way flow of information in which scientists passively impart “the facts” in a press release, the public engagement process thus becomes a dialogue in which scientists interact with, influence, and are influenced by society. Awareness of the public impact of neuroscientific out information should also be encouraged within the policy sphere. Incorporation of neuroscientific evidence into policy debate should be closely monitored to ensure that the contribution is substantive rather than purely rhetorical and that neuroscientific evidence is not used as a vehicle for espousing particular values, ideologies, or social divisions. Neuroscience does not take place in a vacuum, and it is important to maintain sensitivity to the social implications, whether positive or negative, it may have as it manifests in real-world social contexts. It appears that the brain has been instantiated as a benchmark in public dialogue, and reference to brain research is now a powerful rhetorical tool. The key questions to be addressed in the coming years revolve around how this tool is employed and the effects this may have on society’s conceptual, behavioral, and institutional repertoires.

AMPAR blockade induces two rapid and dissociable forms of synaptic compensation: (1) a postsynaptic increase in expression of GluA2-lacking AMPARs and a corresponding enhancement of mEPSC amplitude that is independent of background spiking activity and (2) a retrograde enhancement of presynaptic function that is driven by the convergence of BDNF-TrkB signaling with AP-triggered Ca2+-influx through P/Q/N-type channels. Whereas the postsynaptic changes are sensitive to activity at either AMPARs or NMDARs, the enhancement in presynaptic function is unique to loss of AMPAR activity. Both pre- and postsynaptic

changes RNA Synthesis inhibitor require new protein synthesis, but appear to depend on distinct dendritically synthesized protein products—GluA1 synthesis is likely to be critical for rapid postsynaptic compensation (Ju et al., 2004, Thiagarajan et al., 2005, Sutton et al., 2006 and Aoto et al., 2008), whereas BDNF synthesis is critical

for orchestrating retrograde compensatory changes in presynaptic function. Many studies have demonstrated postsynaptic forms of homeostatic compensation associated with enhanced expression of AMPARs at synapses (e.g., O’Brien et al., 1998, Wierenga et al., 2005 and Sutton et al., 2006). However, clear evidence for homeostatic regulation of presynaptic neurotransmitter release has also been documented (e.g., Bacci et al., 2001, Murthy et al., 2001, Burrone find more et al., 2002, Bumetanide Thiagarajan et al., 2005, Wierenga

et al., 2006 and Branco et al., 2008). Although methodological factors can contribute to this heterogeneity in expression (Wierenga et al., 2006), previous examples of retrograde effects of postsynaptic manipulations on presynaptic structure (e.g., Pratt et al., 2003) and function (e.g., Paradis et al., 2001, Burrone et al., 2002 and Frank et al., 2006) suggest that intrinsic synaptic properties might also play a role. Indeed, we find that in addition to rapid postsynaptic effects, AMPAR blockade induces rapid (<3 hr) functional compensation in the presynaptic compartment, an effect that is not observed with either acute (3 hr) or chronic (24 hr) AP blockade (see also Bacci et al., 2001). Not only was AP blockade insufficient to produce changes in presynaptic function on its own, it also prevented AMPAR blockade from producing those changes. Hence, the compensatory increase in release probability induced by AMPAR blockade is state dependent, requiring presynaptic spiking and P/Q/N-type Ca2+-channel function during the period of AMPAR blockade for its induction. Our findings complement recent studies regarding retrograde homeostatic regulation of presynaptic neurotransmitter release.

Then, IVs were fitted with a cubic, and the zero crossing (Nernst potential) was determined analytically. Residues of the alignment in Figure 1B were colored with Jalview 2 (Waterhouse et al., 2009) in modified Zappo color scheme (hydrophobic I, L, V, A, and M = pink; aromatic F, W, and Y = orange; positively charged K, R, and H = red; negatively charged D and E = blue; hydrophilic S, T, N, and Q = green;

P and G = magenta; C = yellow). Values are reported as mean ± SEM. We would like to thank H. Okada and W. Chu for help with the cloning and the members of the Isacoff lab for discussion. This work was supported by postdoctoral fellowships for prospective and advanced researchers from the Swiss National VE822 Science Foundation (SNSF; PBELP3-127855 and PA00P3_134163) (T.K.B.) this website and by a grant from the National Institutes of Health (R01 NS35549) (E.Y.I.). “
“Cortical circuits display fine functional and structural organization (Feldmeyer et al., 2002, Lefort et al., 2009 and Petreanu et al., 2009) that is carefully established and tuned by sensory experience (Bender et al., 2003, Buonomano and Merzenich, 1998, Feldman and Brecht, 2005 and Stern et al., 2001). Modification of synapses includes Hebbian plasticity

mechanisms where correlated (or uncorrelated) activity leads to structural as well as functional alternations, such as changes in spine morphology (Alvarez and Sabatini, 2007), or synaptic insertion or removal of AMPA receptors (Kessels and Malinow, 2009, Malenka and Bear, 2004, Newpher and Ehlers, 2008 and Nicoll et al., 2006). In parallel to such Hebbian

mechanisms, neurons are also equipped with homeostatic-scaling machinery that may serve to avoid instability problems of network activity (Turrigiano and Nelson, 2004). Such scaling can globally regulate synaptic strength by altering the number of AMPA receptors in individual synapses (Turrigiano et al., 1998). Although a number of molecular and cellular mechanisms underlying these plasticity mechanisms have been identified, how synapses on a dendritic branch cooperate with each other to drive such plasticity is not well understood. Accumulating in vitro and theoretical evidence suggests that there exists biochemical compartmentalization on dendrites that leads to clustered synaptic plasticity (Branco crotamiton and Häusser, 2010, Govindarajan et al., 2006, Häusser and Mel, 2003, Iannella and Tanaka, 2006 and Larkum and Nevian, 2008). For example NMDA receptor-dependent Ca2+ influx caused by a dendritic spike (Golding et al., 2002, Schiller et al., 2000 and Wei et al., 2001), spread of Ras activity during long-term potentiation (LTP) (Harvey et al., 2008), and exocytosis of AMPA receptors into dendritic membrane during LTP (Lin et al., 2009, Makino and Malinow, 2009, Patterson et al., 2010 and Petrini et al., 2009) all occur locally on short stretches of a dendrite and could contribute to synaptic potentiation at nearby synapses.

, 2007 and Volgraf et al., 2006), this class of ion channel has been surprisingly underexploited as a tool to couple recognition of different types HKI-272 chemical structure of chemicals with cellular physiological responses. The existence of many hundreds of divergent IRs of presumed distinct specificity reveals a natural exploitation of this ligand-gated ion channel for chemical sensing (Croset et al., 2010 and Liu et al., 2010). The molecular properties of IRs uncovered here provide a basis for their rational modification to generate custom-designed chemoreceptors of

desired specificity. Such sensors could offer invaluable tools as genetically encoded neuronal activators or inhibitors as well as have broad practical applications, for SAR405838 cost example, in environmental pollutant detection or clinical diagnosis. Standard methods were used for Drosophila genetics, as described together with a

list of strains used, in the Supplemental Experimental Procedures. Standard methods were used in construction of all plasmids; details are provided in the Supplemental Experimental Procedures. Standard methods were employed for immunofluorescence as described, together with all antibodies used, in the Supplemental Experimental Procedures. Extracellular recordings in single sensilla of 2- to 14-day-old flies were performed and quantified essentially as described (Benton et al., 2007 and Benton et al., 2009); details are provided, together with odor sources, in the Supplemental Experimental Procedures. Oocyte preparation and injection was carried out essentially as described (Vukicevic et al., 2006); details are provided in the Supplemental Experimental Procedures. Solutions containing agonists were applied once every minute for 10 s; between applications, the recording chamber was perfused with standard bath solution (110 mM NaCl, 2 mM BaCl2, 10 mM HEPES-NaOH, pH adjusted to 7.4 with NaOH) without agonist.

For current/voltage (IV) curves in the presence of different ions, NaCl was replaced first by 110 mM KCl or 40 mM CaCl2 and the osmolarity was adjusted with sucrose. The Na+ and K+ solutions contained 2 mM Ba2+ as divalent cation. Kaleidagraph (Synergy Software) was used to fit the inhibition curves to the Hill equation: I = I0/[1+([inh]/IC50)nH], where I0 is the current in the absence of inhibitor (inh), IC50 is the inhibitor concentration that induces 50% inhibition, and nH is the Hill coefficient. For IV curve measurements in high extracellular Ca2+, we injected 50 nl of 40 mM BAPTA 1-2 hr prior to the electrophysiological measurements to test the contribution of the Ca2+ currents by endogenous Ca2+-dependent chloride currents. Phenylacetaldehyde and propionic acid were prepared as 1 M stock solutions in DMSO and diluted in bath solution to the desired final concentration. Philanthotoxin 433 tris(trifluoroacetate) (Sigma) was diluted to 1 mM in standard bath solution containing 0.

It is generally thought that RIMs operate as Rab3 effectors. Furthermore, RIMs are substrates of PKA and are thought to play important roles in presynaptic forms of synaptic plasticity

(Wang et al., 1997 and Castillo et al., 2002). Three recent papers (Kaeser et al., 2011, Han et al., 2011 and Deng et al., 2011; the latter two of which can be found in this issue of Neuron) shed new light on the function of RIMs, approaching the problem by genetic elimination (knockout). RIM proteins in mammals are highly diverse. They are encoded by four genes (Rim1–4) that drive the expression of seven known RIM isoforms: RIM1α and 1β; RIM2α, 2β, and VRT752271 nmr 2γ; RIM3γ; and RIM4γ. Unfortunately, RIM1α and RIM2α double knockout mice die immediately after birth ( Schoch et al., 2006), preventing a systematic analysis of the function of RIMs in synaptic transmission. The Südhof group ( Kaeser et al., 2011) has now solved this problem by generating a new mouse line in which both RIM1 and RIM2

genes are flanked by loxP sites (floxed). Because RIM3 and RIM4 are selectively expressed in short γ versions (composed of only a single C2 domain), this allows conditional elimination of all long forms of RIM. Kaeser et al. (2011) have addressed the function of RIMs in an elegant series of biochemical and electrophysiological experiments. The starting point of the analysis was the finding that RIMs directly and specifically interact with P/Q- and N-type Ca2+ channels. www.selleckchem.com/products/i-bet-762.html Kaeser et al. then systematically examined the functional significance of this molecular interaction, measuring synaptic currents in cultured hippocampal neurons. To eliminate RIMs from these synapses, lentiviral infection followed by Cre recombinase expression was used. Multiple pieces of evidence suggested that genetic elimination of RIMs changed the coupling between Ca2+ channels and transmitter release (Table 1). not First, the amplitude of evoked inhibitory postsynaptic currents (IPSCs) was reduced. Second, evoked release was desynchronized. Third, the onset of the blocking effects

of the Ca2+ chelator EGTA-AM was prolonged, suggesting a loosening of the coupling between Ca2+ channels and Ca2+ sensors of exocytosis (Neher, 1998 and Bucurenciu et al., 2008). Fourth, the dependence of release on the external Ca2+ concentration was shifted to higher concentrations. Finally, the amplitude of presynaptic Ca2+ concentration transients measured by fluorescent Ca2+ indicators was reduced. Taken together, these results suggest that conditional knockout of RIMs impairs the tethering of presynaptic Ca2+ channels to the active zone of inhibitory synapses. Han et al. (2011) have used the same mouse line to examine the function of RIMs at the calyx of Held, a glutamatergic synapse in the auditory brainstem accessible to quantitative biophysical analysis of transmitter release. To eliminate RIMs from these synapses, the new RIM1 and RIM2 floxed mouse line (Kaeser et al.

This finding is consistent with a demodulating system. Theoretical work has shown that a demodulating nonlinearity will detect a variety of non-Fourier image features including illusory contours (ICs) (Daugman and Downing, 1995 and Fleet and

Langley, 1994). By extension, our finding that Y cells demodulate interference patterns led us to hypothesize that GSK126 mw they will respond to other non-Fourier image features as well. To test this, abutting grating stimuli that produce ICs detected by some neurons in the primary visual cortex of cats and monkeys were drifted across the receptive fields of three LGN Y cells (Grosof et al., 1993 and Song and Baker, 2007; Figure S4A). Importantly, the spatial parameters of the stimuli were tailored

to the individual Ixazomib datasheet Y cells to ensure that only nonlinear responses could be elicited. Specifically, the carrier SF was selected to be above the linear passband of the neuron’s drifting grating SF tuning curve and near the nonlinear SF preference measured using contrast-reversing gratings. The ICs were also constrained to be oriented orthogonally to the carrier to ensure that spatial harmonics in the stimulus did not fall within the linear passband of the cell. Even with the small sample size, the result of this experiment was clear: the responses of all three Y cells oscillated at the frequency of ICs/sec, indicating that the ICs were detected (Figures S4B and S4C). Responses at this frequency are consistent with the output

of a demodulating system and cannot be explained by linear processing since a linear response would oscillate at half this frequency. This result suggests that by demodulating visual signals, Y cells may encode a variety of complex image features. Because the amplitude of Y cell responses to interference patterns depends on both the envelope TF (Rosenberg et al., 2010) and the carrier TF (Figure 2), we next wanted to compare the representations of envelope and carrier TF based on response amplitude. Envelope TF tuning curves were measured with a static carrier for 30 Y cells. These tuning curves were well-described by gamma functions (average oxyclozanide r = 0.94 ± 0.04 SD) which were used to estimate the tuning properties summarized in Table 1. For 24 of these Y cells, we also measured a carrier TF tuning curve that was well-described by a gamma function. The envelope and carrier TF tuning curves of a Y cell along with a population scatter plot of the peak envelope TFs and peak carrier TFs are shown in Figures S5A and S5B. Whereas the peak envelope TFs of these 24 Y cells were narrowly distributed around a low frequency (4.2 cyc/s ± 1.2 SD), the peak carrier TFs were widely distributed around a higher frequency (7.5 cyc/s ± 6.8 SD). The distributions of peak envelope TFs and peak carrier TFs were significantly different (p = 0.005, Mann-Whitney U test), and there was a moderate but nonsignificant correlation between them (r = 0.36, p = 0.08).

, 2009). Overall, these

studies suggest that the highly conserved CAP-Gly domain in dynactin might be fully dispensable for vesicular transport in the cell. Strikingly, however, genetic evidence reveals that the CAP-Gly domain of p150Glued is essential for normal neuronal function since point mutations within this domain cause two autosomal dominant human neurodegenerative disorders: Perry syndrome and distal hereditary motor neuropathy 7B (HMN7B, also known as distal spinal and bulbar muscular atrophy) (Farrer et al., 2009 and Puls et al., 2003). HMN7B is caused by a glycine to serine substitution at residue 59 (G59S), while Perry syndrome is caused by one of five point mutations at residues 71, 72, or 74 (G71R, learn more G71E, G71A, T72P, Q74P) (Figures 1A and 1A′; see Movie S1 available online). The neuronal populations that degenerate in these two diseases are wholly distinct.

HMN7B affects motor neurons, while Perry syndrome primarily affects dopaminergic neurons in the substantia nigra (Puls et al., 2005 and Wider and Wszolek, 2008). It remains entirely unclear how these mutations, only 12–15 amino acids apart, differentially Metabolism inhibitor disrupt CAP-Gly domain function causing two disparate diseases. Here, we report a specific function for the CAP-Gly domain of dynactin in neurons. Our data show that the CAP-Gly domain enhances the distal enrichment of dynactin in the neuron, leading to efficient flux of cargo from the distal neurite. This function is separable from the role of dynactin in promoting bidirectional transport along the axon. Further, we show that the known disease-associated mutations all affect CAP-Gly function but differentially affect dynein-mediated transport along the axon, leading to a potential mechanistic explanation for the differential cell-type-specific degeneration observed in HMN7B and Perry syndrome. Together, these studies establish a role for the highly conserved CAP-Gly domain of dynactin in the efficient initiation of transport in highly polarized cells. These findings therefore provide insight Parvulin into both the regulation of axonal transport in the neuron and the cellular

basis for the neuronal specificity of mutations in dynactin. Multiple splice forms of p150Glued are expressed in brain, including a neuronally enriched p135 isoform that lacks the CAP-Gly domain (Tokito et al., 1996). We asked which p150Glued isoforms are recruited to cargos actively transported through the cell. Quantitative analysis of the p150Glued isoforms that copurified with LAMP1-enriched lysosomal fractions indicated that the full-length polypeptide is preferentially enriched in this fraction (Figures 1B and 1C). As dynein drives the motility of lysosomes along axons (Hendricks et al., 2010), the enrichment of full-length p150Glued that we observe suggests that the CAP-Gly domain may serve a specific function in the active transport of these vesicles.

5-fold larger images. We saw the

same regions selectively activated by Faces, Shapes, and Learned symbols irrespective of stimulus size, order, font, or position (Figure S2). Because of their age, we could not scan the juveniles before we commenced Symbol training, so we cannot rule out the unlikely possibility that the four juvenile monkeys might have exhibited Learned symbol-selective cortical domains without training, though the Paclitaxel cost absence of a Learned symbol-selective region in any of the adults makes this unlikely. Four juvenile monkeys learned to recognize symbols faster than six sexually mature adults and showed faster reaction times than the adults in choosing between symbols, even though the reaction times and learning rates of the adults were comparable to the juveniles when choosing between dot arrays. Functional MRI on the juvenile monkeys showed novel domains that were more active when the monkeys viewed the Learned symbols, compared to visually similar but Untrained shapes, and Faces. The same location in the adults responded as strongly to Untrained shapes Volasertib as to Learned symbols. The anatomical

results indicate that intensive early, but not late, experience can cause the formation of a novel specialized cortical domain, or cause an existing domain to become specialized for the trained shapes. The association of aminophylline a specialized domain with faster learning and responding suggests that having a specialized domain bestows a behavioral advantage. These results raise two important

questions: (1) How could intensive early experience cause the formation of a novel functional domain? Our results are completely consistent with the possibility that early symbol learning modifies the tuning properties of cells in an innately specialized domain (Dehaene and Cohen, 2007). We would like, however, to propose an alternative hypothesis: the emergence, only in the juvenile-trained monkeys, of a domain selective for an artificial object category raises the possibility that early experience plays a causal role in the formation or specialization of functional domains. The functional domains for faces and shapes were not in precisely the same location in each monkey, but the paired pattern of face and shape domains within each of the major subdivisions along inferotemporal cortex was similar in all the monkeys and was similar to what has been previously reported (Bell et al., 2009 and Denys et al., 2004). The experience dependence of the novel functional domain, coupled with the pattern of one pair of face and shape functional domains within each major cortical area, suggests a self-organizing Hebbian mechanism.

The larger increase in apoptotic GCs at 2 hr was partially S3I-201 in vitro but significantly suppressed by disturbing grooming, resting and sleeping behavior during the 2 hr. Gentle handling in nostril-occluded mice did not reduce the amount of food pellet consumed (data not shown). These results indicate that enhanced GC apoptosis occurred in association with postprandial behaviors in sensory-deprived OB. Under unilateral sensory deprivation, enhanced GC apoptosis can occur in association with postprandial extended grooming even without apparent sleep. GC apoptosis in the open side of the OB of the nostril-occluded mice also

showed an increase in GC apoptosis at 1 hr, and this increase was also suppressed by gentle handling (Figure 5G). The presence of olfactory sensory input to the open side of the OB and its absence to the closed side during feeding time was

confirmed by examining the presence and MDV3100 mouse absence of induced arc expression in GCs (Figure S4G; Guthrie et al., 2000). The odor map of the OB shows domain and cluster organization (Mori et al., 2006). The survival rate of adult-born GCs is regulated in local OB areas by local activation with odor learning (Alonso et al., 2006). Does local sensory input regulate the extent of GC elimination during the postprandial period in local OB areas? To address this question, we utilized dorsal zone-depleted mice (ΔD mice), in which olfactory sensory neurons (OSNs) in the dorsal zone (D-zone) of the epithelium were selectively ablated (Kobayakawa et al., 2007). Glomerular structure was lacking in the D-domain of the ΔD mouse OB due to the depletion of OSNs targeting the D-domain (Figure S5A). Other layers were largely maintained, including the granule cell layer (GCL), the majority of cells in which were NeuN-expressing GCs (data not shown). As expected, the number of GCs expressing an immediate early gene c-fos with odor stimulation (Magavi et al., 2005) was drastically reduced in the D-domain (Figure S5B). The quantitative analyses in the paragraph below were over conducted in coronal sections at the central portion in the rostrocaudal axis of ΔD and wild-type mouse OBs, which include a considerable

volume of both the D-domain and ventral domain (V-domain) (Figure S5C). ΔD mice and wild-type mice were subjected to food restriction and examined for caspase-3-activated GCs in the D- and V-domains (Figures 6A and S5D). In the ΔD mouse OB, the density of caspase-3-activated GCs in the D-domain increased 3.2-fold during the postprandial period compared to that before feeding, while that in the V-domain increased 2.2-fold (Figures 6A and 6B). The ratio of caspase-3-activated GC density in the D-domain to that in the V-domain was greater in the postprandial period (2.0 ± 0.2; average ± SEM) than before food (1.3 ± 0.1) (Figure 6D; p = 0.009). In wild-type mouse OB, the density of caspase-3-activated GCs increased during the postprandial period by 2.3-fold in the D-domain and 2.