The effects on very early events in expression are surprising in light of the fact that U(L)31 is designated a late gene and pU(L)31 is not a virion component. We show herein that while most pUL31 is expressed late in infection, low levels of pU(L)31 are detectable as early as 2 h postinfection, consistent with an early role in HSV-1 infection.”
“Principal cells of the lateral superior olive (LSO) compute interaural intensity differences by comparing converging excitatory and inhibitory inputs. The excitatory input carries information from the ipsilateral ear, and the inhibitory input carries

information from the contralateral ear. Throughout life, the excitatory input pathway releases glutamate. In adulthood, the inhibitory input pathway releases glycine. During a period of major developmental refinement in the LSO, however, synaptic terminals of the immature inhibitory input pathway release Selleckchem 5-Fluoracil not only glycine, but also GABA and glutamate. To determine whether glutamate released by terminals in either pathway could spill over to activate postsynaptic N-methyl-D-aspartate (NMDA) receptors under the other pathway, we made whole-cell recordings from learn more LSO principal cells in acute slices of neonatal rat brainstem bathed in the use-dependent NMDA receptor antagonist MK-801 and stimulated in the two opposing pathways. We found that during

the first postnatal week glutamate spillover occurs bidirectionally from both immature excitatory terminals and immature inhibitory terminals. We further found that a population of postsynaptic NMDA receptors

is shared: glutamate released from either pathway can diffuse to and activate these receptors. We suggest that these shared receptors contain the GluN2B subunit and are located extrasynaptically. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Koi herpesvirus (KHV) has recently been classified as a member of the family of Alloherpesviridae within the order Alanine-glyoxylate transaminase of Herpesvirales. One of the unique features of Herpesviridae is latent infection following a primary infection. However, KHV latency has not been recognized. To determine if latency occurs in clinically normal fish from facilities with a history of KHV infection or exposure, the presence of the KHV genome was investigated in healthy koi by PCR and Southern blotting. KHV DNA, but not infectious virus or mRNAs from lytic infection, was detected in white blood cells from investigated koi. Virus shedding was examined via tissue culture and reverse transcription-PCR (RT-PCR) testing of gill mucus and feces from six koi every other day for 1 month. No infectious virus or KHV DNA was detected in fecal secretion or gill swabs, suggesting that neither acute nor persistent infection was present.

However, many GPCRs, when activated or blocked by drugs, elicit both beneficial and adverse pharmacology. Recent work has Protein Tyrosine Kinase inhibitor demonstrated that in some cases, the salutary and deleterious signals linked to a specific GPCR can be selectively targeted by “”biased ligands”" that entrain subsets of a receptor’s normal pharmacology. This review briefly summarizes the advances and current state of the biased ligand field, focusing on an example: biased ligands targeting the angiotensin II type 1 receptor. These compounds exhibit unique pharmacology, distinct from classic agonists or antagonists, and one such molecule is now in clinical development for the treatment of acute heart failure.

(C) 2013 Elsevier Inc. All rights reserved.”
“Spinal muscular atrophy (SMA), a fatal genetic motor disorder of infants, is caused by diminished full-length survival of motor neuron (SMN) protein levels. Normally involved in small nuclear ribonucleoprotein (snRNP) assembly and pre-mRNA splicing, recent studies suggest that SMN plays a critical role in regulating apoptosis. Interestingly, the anti-apoptotic Bcl-x isoform, Bcl-xL, is reduced in SMA. In a related finding, Sam68, an RNA-binding protein, was found to modulate splicing of SMN and Bcl-xL transcripts, PCI-32765 chemical structure promoting SMN Delta 7 and pro-apoptotic Bcl-xS transcripts. Here we demonstrate that Bcl-xL expression

increases SMN protein by similar to 2-fold in SH-SY5Y cells. Conversely, SMN expression increases Bcl-xL protein levels by similar to 6-fold in SH-SY5Y cells, and similar to 2.5-fold in the brains of transgenic mice over-expressing SMN (PrP-SMN). Moreover, Sam68 protein levels were markedly reduced following SMN and Bcl-xL expression in SH-SY5Y cells, suggesting a feedback mechanism co-regulating levels of both proteins. We also found that exogenous SMN expression increased full-length SMN transcripts, possibly by promoting exon 7 inclusion. Finally, co-expression

of SMN and Bcl-xL triclocarban produced an additive anti-apoptotic effect following PI3-kinase inhibition in SH-SY5Y cells. Our findings implicate Bcl-xL as another potential target in SMA therapeutics, and indicate that therapeutic increases in SMN may arise from modest increases in total SMN. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“In order to investigate the unique contribution of individual wine grape (Vitis vinifera) berry tissues and water-deficit to wine quality traits, a survey of tissue-specific differences in protein and selected metabolites was conducted using pericarp (skin and pulp) and seeds of berries from vines grown under well-watered and water-deficit stress conditions. Of 1047 proteins surveyed from pericarp by 2-D PAGE, 90 identified proteins showed differential expression between the skin and pulp.

We used the subsequent memory paradigm, in the context of event-related functional

magnetic resonance imaging, in 27 PTSD patients to identify the brain regions involved in the AZD9291 solubility dmso encoding of fearful and neutral faces. Symptom severity was assessed by the Clinically Administered PTSD Scale (CAPS) scores. It was found that memory performance was negatively correlated with CAPS scores. Furthermore, a negative correlation was observed between CAPS scores and ventral medial prefrontal cortex (vmPFC) activity elicited by the subsequently forgotten faces. Finally, symptom severity predicted the contribution of the amygdala to the successful encoding of fearful faces. These results confirm the roles of the vmPFC and the amygdala in PTSD and highlight the importance of taking into account individual differences when assessing the behavioural and neural correlates of the disorder. (C) 2008 Elsevier Ltd. All rights reserved.”
“Background:

Hyperhomocysteinemia is thought to be an independent risk factor for cardiovascular disease, but the association between renal dysfunction and homocysteine may not have been fully taken into account. We performed a meta-analysis of studies that report correlations between glomerular filtration rate (GFR) and homocysteine plasma levels. Methods: Using a prespecified research strategy, we identified 41 studies involving 26,617 participants that reported Pearson or Spearman correlation coefficients for the association between 1/GFR and homocysteine. The summary correlation coefficients with 95% CI were obtained by pooling the logarithmic Z values derived found from the individual trial correlation selleck screening library coefficients. Subgroup analysis was performed to compare results for measured GFR using clearance methods and various estimates of GFR. Results: The pooled correlation coefficient between homocysteine and 1/GFR was 0.37 (CI 0.32-0.40, p < 0.0001). The correlation coefficient

based on various estimates of GFR was 0.33 (CI 0.29 – 0.38, p < 0.0001), and for measured GFR it was 0.45 (CI 0.39 – 0.51, p < 0.0001). The correlation coefficient was higher when GFR was measured using clearance methods compared with various estimates GFR (1.36 [CI 1.13-1.65], p = 0.0014). Conclusions: Homocysteine plasma levels significantly depend on renal function. This correlation is even more robust when GFR is measured using clearance methods. Therefore, in order to assess whether homocysteine is an independent cardiovascular risk factor, accurate adjustments for renal dysfunction are essential. Copyright (C) 2008 S. Karger AG, Basel.”
“Increased variability in reaction time (RT) has been proposed as a cardinal feature of attention deficit hyperactivity disorder (ADHD). Increased variability during sustained attention tasks may reflect inefficient fronto-striatal and fronto-parietal circuitry; activity within these circuits is modulated by the catecholamines.

1038/ki.2010.322; published online 8 September 2010″
“Antimyeloperoxidase antibodies can cause crescentic glomerulonephritis and pulmonary hemorrhage. Anlotinib cost Toll-like receptors (TLRs) respond to infectious agents activating host defenses, whereas infections potentially initiate disease and provoke relapses. Neutrophils were found to be key effector cells of injury in experimental models, as disease does not occur in their

absence and injury is enhanced by lipopolysaccharide (LPS). In this study, highly purified LPS (a pure TLR4 ligand) acted with antimyeloperoxidase antibodies to synergistically increase kidney and lung neutrophil recruitment and functional injury; effects abrogated in TLR4-deficient mice. Increased kidney TLR4 expression after stimulation predominantly occurred in glomerular endothelial cells. Enhanced glomerular OSI-744 mw neutrophil recruitment correlated with increased kidney mRNA expression of CXCL1 and CXCL2 (homologs of human CXCL8), whereas their preemptive neutralization decreased neutrophil recruitment. Disease induction in bone marrow chimeric mice showed that TLR4 in both bone marrow and renal parenchymal cells is required for maximal neutrophil recruitment and glomerular injury. Further studies in human glomerular cell lines stimulated with LPS found that glomerular endothelial cells were the prominent sources of

CXCL8. Thus, our results define a role for TLR4 expression in bone marrow-derived and glomerular endothelial cells in neutrophil recruitment and subsequent functional and histological renal injury in experimental antimyeloperoxidase glomerulonephritis. Kidney International (2010) 78, 1263-1274; doi:10.1038/ki.2010.327; published online 15 September 2010″
“Cardiovascular disease is the leading cause of mortality in chronic

kidney disease (CKD). As matrix metalloproteinases have a major role in atherosclerosis, we hypothesized that alterations in metalloproteinases-8, -10 and their tissue inhibitor-1 can be associated with the severity of atherosclerosis in patients with kidney disease. This was evaluated in a cross-sectional, observational study of 111 patients with stages I-V kidney disease, 217 patients on dialysis and 50 healthy controls. The severity of atherosclerosis was estimated with the atherosclerosis Diflunisal score (AS), combining the results of ankle-brachial index and carotid ultrasound. Serum levels of the two metalloproteinases and tissue inhibitor-1 were measured by enzyme-linked immunosorbent assay and were significantly increased in patients with kidney disease compared with the healthy controls, and higher in patients on dialysis than in earlier stages of CKD. The severity of the AS was also more prevalent in the dialysis group, in which serum levels of both metalloproteinases and tissue inhibitor-1 were significantly higher.

Such individuals should be evaluated for risk of hyperkalemia IWP-2 and should consider use of a non-dihydropyridine calcium antagonist added to the single RAAS agent as an alternative for proteinuria reduction. This provides a safe and effective option for those patients with advanced nephropathic disease who need additional proteinuria reduction. In all cases other than advanced proteinuric nephropathy, there is no evidence of any positive CKD outcome with dual RAAS blockade. Thus, dual RAAS blockade cannot be recommended for all CKD patients. Kidney International (2010) 78,

546-549; doi:10.1038/ki.2010.226; published online 21 July 2010″
“Post-weaning social isolation in rodents induces behavioral alterations, including hyperlocomotion, depression- and anxiety-like behaviors, aggression, and learning buy Ispinesib and memory deficits. These behavioral abnormalities may be related to the core symptoms in patients with neuropsychiatric disorders, such as schizophrenia and depression. In view of the recent studies that the group II metabotropic glutamate receptor (mGluR2/3) is involved in neuropsychiatric disorders, the present study examined the effect of isolation rearing on the binding of the mGluR2/3 antagonist [(3)H]LY341495 to mGluR2/3 in the mouse brain by in vitro autoradiography. The [(3)H]LY341495 binding

in the prefrontal cortex, cerebral cortical layers I-III and hippocampus was significantly increased by rearing in social isolation while the binding in other brain regions was not altered. A saturation binding study of hippocampal membranes from isolation-reared

mice revealed that the B(max) value increased significantly without any changes in the K(d) value. Moreover, the mGluR2/3 antagonist MGS0039 (1.0 mg/kg, intraperitoneally) decreased the immobility time of isolation-reared mice in the forced swim test. These results suggest that isolation rearing causes an increase in mGluR2/3 densities in the prefrontal cortex and hippocampus and that the increased receptor function may contribute to pathogenic mechanisms for depression-like behavior of the isolation-reared mice. (C) 2010 Elsevier Ltd. All rights reserved.”
“Monocyte and macrophage markers are among the most highly overexpressed genes in cpk mouse kidneys with Non-specific serine/threonine protein kinase severely progressive renal cystic disease. We show here that one of these markers, CD14, is abnormally transcribed, activated and shed in cystic kidneys. However, these abnormalities were not associated with an increased number of interstitial CD14-positive mononuclear cells. Instead, we found that most non-cystic and cystic renal tubular epithelia were CD14-positive; even distal nephron-derived principal cells. Cd14 was significantly overexpressed in the kidneys of 5-day-old cpk mice and further increased as the disease progressed.

First, we review preclinical data supporting the serotonergic raphe nuclei and their forebrain projections as targets of drugs of abuse, with emphasis on the effects of psychostimulants, opioids and ethanol. Next, we examine the role of 5-HT receptors in impulsivity, a core behavior that contributes to the vulnerability to addiction and relapse. Finally, we discuss evidence for serotonergic dysregulation in comorbid mood and addictive disorders and suggest novel serotonergic targets for the treatment of addiction and the prevention of drug relapse.

This article is part of a Special Issue entitled GANT61 purchase ‘Serotonin: The New Wave’. (C) 2011 Elsevier Ltd. All rights reserved.”
“Objective:

Obliterative bronchiolitis is

the predominant histopathologic finding in patients with chronic rejection after lung transplant. see more This fibroproliferative transformation within small airways of lung allograft is poorly understood; however, studies suggest epithelial-mesenchymal transition plays a role. Transplant immunosuppressive therapy has been shown to cause epithelial-mesenchymal transition in renal tubular epithelial cells, with subsequent fibrosis. This study explored whether immunosuppressive therapy contributes to epithelial-mesenchymal transition in airway epithelial cells.

Methods: Bronchial epithelial cell line RL-65 was treated 3 to 5 days with several immunosuppressive agents, including cyclosporine (INN ciclosporin), tacrolimus, azathioprine, mycophenolic acid, sirolimus, prednisone, and transforming growth factor beta

1 as control. We then analyzed cells for presence of mesenchymal morphology and protein markers.

Results: Treatment with cyclosporine, azathioprine, mycophenolate, and sirolimus resulted in elongated and irregular cell shape, and all but azathioprine showed loss of cell-cell adhesions relative to vehicle-treated cells. Expressions of extracellular matrix proteins, fibronectin and collagen, along with mesenchymal marker, vimentin, were significantly upregulated. Immunofluorescence showed loss of E-cadherin at cell membranes and cytoskeletal Bay 11-7085 rearrangements typical of epithelial-mesenchymal transition. These immunosuppressive agents also increased transforming growth factor produced by cells; however, tacrolimus-and prednisone-treated cells maintained epithelial morphology, baseline levels of matrix protein expression, and transforming growth factor production levels.

Conclusions: Overall, we found that certain immunosuppressive agents may contribute to partial epithelial-mesenchymal transition in bronchial epithelial cells, specifically increasing production of excessive extracellular matrix proteins. This may provide novel insights into the pathogenesis of obliterative bronchiolitis after lung transplant.

Among regulatory binding sites on the NMDAR complex is a glycine binding site, distinct from the glutamate binding site, which must be co-activated for NMDAR channel opening. We developed a novel glycine site partial agonist, GLYX-13, which is both nootropic and neuroprotective in vivo. Here, we assessed the effects of GLYX-13 on long-term synaptic

plasticity Capmatinib cost and NMDAR transmission at Schaffer collateral-CA1 synapses in hippocampal slices in vitro. GLYX-13 simultaneously enhanced the magnitude of long-term potentiation (LTP) of synaptic transmission, while reducing long-term depression (LTD). GLYX-13 reduced NMDA receptor-mediated synaptic currents in CA] pyramidal neurons evoked by low frequency Schaffer collateral stimulation, but enhanced NMDAR currents during high frequency

bursts of activity, and these actions were occluded by a saturating concentration of the glycine site agonist D-serine. Direct two-photon imaging of Schaffer collateral burst-evoked increases in [Ca(2+)] in individual dendritic spines revealed 4SC-202 mouse that GLYX-13 selectively enhanced burst-induced NMDAR-clependent spine Ca(2+) influx. Examining the rate of MK-801 block of synaptic versus extrasynaptic NMDAR-gated channels revealed that GLYX-13 selectively enhanced activation of burst-driven extrasynaptic NMDARs, with an action that was blocked by the NR2B-selective NMDAR antagonist ifenprodil. Our data suggest that GLYX-13 may have unique therapeutic potential as a learning and memory enhancer because of its ability to simultaneously enhance UP and suppress LTD. (C) 2008 Elsevier Ltd. All rights reserved.”
“Objective: In patients with ischemic cardiomyopathy and substantial amounts of dysfunctional but viable myocardium, revascularization cannot always improve the left ventricular ejection fraction.

We sought to investigate the interaction between the left ventricular volume and the amount of viable myocardium to predict the left Methylitaconate Delta-isomerase ventricular ejection fraction increase after revascularization.

Methods: Eighty-five consecutive patients with a depressed left ventricular ejection fraction (mean: 27.3% +/- 5.2%) underwent coronary artery bypass grafting after a dobutamine stress echocardiography had determined that they had at least 4 viable segments. Six months after coronary artery bypass grafting, left ventricular ejection fraction and regional wall motion were reassessed.

Results: Although the left ventricular ejection fraction was expected to recover more than 5% in all 85 patients after coronary artery bypass grafting, it did not improve in 15 patients (17.6%) despite the presence of viable segments. The likelihood of the left ventricular ejection fraction recovery decreased proportionally with an increase in the left ventricular end-systolic volume. The nonimprovers had a higher left ventricular end-systolic volume (164.2 +/- 22.4 mL vs 125.6 +/- 23.4 mL, P = .0001).

Several orexin receptor

antagonists have been reported in recent years, but currently there are no imaging tools to probe the density and function of orexin receptors in vivo. To date there are no published data on the pharmacokinetics (PK) and accumulation of some lead orexin receptor antagonists. Evaluation of CNS pharmacokinetics in the pursuit of positron emission tomography (PET) radiotracer development could be used to elucidate the association of orexin receptors with diseases and to facilitate the drug discovery and development. To this end, we designed and evaluated carbon-11 labeled compounds based on diazepane orexin receptor antagonists previously described. One of the synthesized compounds, [C-11]CW4, showed high brain uptake in rats and further evaluated in non-human primate (NHP) using PET-MR Selleck Idasanutlin imaging. PET MEK162 scans performed in a baboon showed appropriate early brain uptake for consideration as a radiotracer. However, [C-11]CW4 exhibited

fast kinetics and high nonspecific binding, as determined after co-administration of [C-11]CW4 and unlabeled CW4. These properties indicate that [C-11]CW4 has excellent brain penetrance and could be used as a lead compound for developing new CNS-penetrant PET imaging probes of orexin receptors.(C) 2013 Elsevier Inc. All rights reserved.”
“Purpose: Senescence related regulatory pathways serve as barriers to cancer immortalization and progression but they are currently not well defined. FILIP1L is a growth inhibitory gene with multiple isoforms whose expression is increased in senescent prostate and prostate cancer cells, and decreased in many cancers. We investigated whether DNA methylation DOK2 regulates FILIP1L in senescence and in prostate cancer development.

Materials and Methods: FILIP1L mRNA expression

was assessed in prostate cancer and associated normal prostate tissues using quantitative polymerase chain reaction. A tissue microarray was constructed using 95 prostate cancer specimens and 45 benign prostate specimens. Vectra (TM) imaging was used to quantitate nuclear and cytoplasmic FILIP1L protein expression. Bisulfite sequencing and Pyrosequencing (R) were used to assess methylation. Prostate cancer cell lines were treated with 2′-deoxy-5-azacytidine and mRNA expression was assessed.

Results: FILIP1L isoform 2 mRNA was increased in replicatively senescent human prostate epithelial cells and decreased in prostate cancer specimens. We verified a reduction in nuclear FILIP1L protein in prostate cancer using tissue microarrays (p = 0.006). A CpG island 5′ of the isoform 2 translational start site was identified that showed hypermethylation in prostate cancer cell lines and tumors compared to normal prostate cells and tissues. Pyrosequencing confirmed FILIP1L hypermethylation in all 14 tumors compared to paired normal tissues (p < 0.0001).

Our work suggested

that Notch pathway could be a critical molecular mediator of BAVM pathogenesis. Here, we investigated the hypothesis that upregulated Notch activation contributes to the pathogenesis of human BAVM. We examined the expression of the canonical Notch downstream Ilomastat chemical structure target Hes1 in the endothelium of human BAVMs by immunofluorescence, and showed increased levels relative to either autopsy or surgical biopsy controls. We then analyzed receptor activity using an antibody to the activated form of the Notch1 receptor, and found increased levels of activity. These findings suggest that Notch activation may promote the development and even maintenance of BAVM. We also detected increases in Hes1 and activated Notch1 expression in our mouse model of BAVM induced by constitutively active Notch4, demonstrating molecular similarity between the mouse model and the human disease. Our work suggests that activation of Notch signaling is an important molecular candidate in BAVM pathogenesis and further validates that our animal model provides a platform to study the progression as well as the regression of the disease. Laboratory Investigation (2009) 89, 971-982; doi:10.1038/labinvest.2009.62; published online 22 June

2009″
“The effects on distortion product otoacoustic emissions (DPOAEs) during the late phase of ischemia/reperfusion injury in the cochlea were studied. Ischemia/reperfusion injury was induced in a gerbil model by

occluding both vertebral arteries for 15 min. Hearing was assessed PF-4708671 ic50 by recording compound action potentials (CAPS) before, during, and 7 days after ischemia. The histological changes in the hair cells were evaluated in specimens stained with rhodamine-phalloidin and Hoechst 33342. first The average increase in CAP threshold 7 days after ischemia was 16.3 +/- 8.0 dB at 8 kHz. In contrast, interruption of the blood supply to the cochlea decreased the DPOAE amplitudes to the noise floor; this usually recovered to the same level as that seen under pre-ischemic conditions 7 days after ischemia. Histologically, the mean respective losses of inner and outer hair cells (IHCs and OHCs, respectively) of the inner ear were 26.5% and 3.3% in the basal turn, respectively. These results indicate that in gerbils OHCs are tolerant to ischemia/reperfusion injury pathologically and physiologically because DPOAE is closely related to the active process of OHCs and is a useful test to examine OHC function. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Mutations in homeoprotein NKX2-5 are linked to human congenital heart disease, resulting in various cardiac anomalies, as well as in postnatal progressive conduction defects and occasional left ventricular dysfunction; yet the function of Nkx2-5 in the postnatal period is largely unexplored.

These findings provide neuropathological evidence for rodents with chronic injection of D-galactose as a promising model for brain aging and age-related neurodegeneration. NeuroReport 19:1611-1615 (C) 2008 Wolters Kluwer Health Lippincott Williams & Wilkins.”
“Duggleby [Duggleby, R.G.,

1979. Experimental designs for estimating kinetic parameters for enzyme-catalyzed reactions. J. Theor. Biol. 81, 672-684] discussed the “”design PSI-7977 ic50 of several replicate measurements of the velocity at as many experimental conditions as there are parameters to be estimated.”" He discussed the application of this method to A -> products, without and with competitive inhibition, and commented briefly on A+B -> products. The availability of computer applications that can solve large sets of simultaneous equations makes it possible to use this method to calculate kinetic parameters for more complicated enzyme mechanisms. This article is concerned with rapid-equilibrium rate equations, but this method can also be used with steady-state rate equations. Computer programs are provided for the calculation

of the three kinetic parameters for ordered A+B -> products from three velocity measurements and for the calculation of the four kinetic parameters for random A+B -> products from four velocity measurements. Computer programs are also provided for competitive inhibition, uncompetitive inhibition, ISRIB and mixed inhibition of ordered A+B -> products. (C) 2008 Elsevier Ltd. All rights reserved.”
“It has been demonstrated that retinal Mueller cells, the predominant Interleukin-2 receptor glial cells, produce neurotrophic factors including

basic fibroblast growth factor (FGF-2), and that electrical stimulation enhances the transcription of FGF-2 in the central nervous system. In this study, the effect of electrical stimulation on the induction of FGF-2 in cultured rat Mueller cells was investigated by quantitative real-time polymerase chain reaction and western blotting. Both the messenger RNA and protein of FGF-2 were significantly upregulated after electrical stimulation compared with that of controls. These results suggest that electrical stimulation may directly induce the production of FGF-2 in the retina. NeuroReport 19:1617-1621 (C) 2008 Wolters Kluwer Health I Lippincott | Williams & Wilkins.”
“The vomeronasal system is segregated from the epithelium to the bulb.Two classes of receptor neurons are apically and basally placed in the vomeronasal epithelium, express G(i2 alpha), and G(alpha x) proteins and VIR and V2R receptors and project to the anterior and posterior portions of the accessory olfactory bulb, respectively. Apart from common vomeronasal recipient structures in the amygdala, only the anterior accessory olfactory bulb projects to the bed nucleus of the stria terminalis and only the posterior accessory olfactory bulb projects to the dorsal anterior amygdala.