, 2009). Streptococcus mutans is an opportunistic pathogen considered as one of the principle etiological

agents of dental caries. Natural genetic transformation of this bacterium was shown to be modulated by a quorum sensing (QS) signaling system comprised of a ComDE two component signaling system, which responds to a peptide signaling molecule designated the competence stimulating peptide (CSP) (Li et al., 2001). In addition to eliciting the competence phenotype, the CSP signaling pathway also contributes to proper biofilm formation, bacteriocin production and stress Selleck Staurosporine tolerance in S. mutans (Senadheera & Cvitkovitch, 2008). Intriguingly, the CSP-induced genetic Dasatinib transformation pathway also modulates cellular lysis in a fraction of the population in S. mutans cultures (Qi et al., 2005; Perry et al., 2009). Development of genetic competence is directly correlated with activation of an alternate sigma factor, ComX, which depends on ComE activity and that of another regulatory protein, ComR that responds to an internalized signaling peptide called XIP (Mashburn-Warren et al., 2010). Recently, it was demonstrated that ComX was

expressed only in a fraction of the CSP-induced population, which resulted in the bifurcation of the population into fractions undergoing competence or cell death (Mashburn-Warren et al., 2010; Lemme et al., 2011). Although transcriptome analysis has shown the regulation of nearly 240 genes by ComX (Perry et al., 2009), most of these putative “late competence

genes” modulating competence and cell lysis remain uncharacterized to date. Here, we studied a ComX-regulated gene designated the competence induced protein A (cinA) in S. mutans. Recently, Okinaga et al. (2010) showed that the HdrRM system regulated expression of cinA via ComX in S. mutans. While cinA’s putative functions have not been closely examined in S. mutans, in Streptococcus pneumoniae, its ortholog belongs to the ComX-activated “late competence” Protein tyrosine phosphatase regulon (Masure et al., 1998; Mortier-Barriere et al., 1998). In pneumococci, cinA is part of the rec locus, which includes recA that facilitates homologous recombination between single- and double-stranded DNA during genetic transformation (Kowalczykowski, 1994; Camerini-Otero & Hsieh, 1995). While CinA in S. pneumoniae was shown to facilitate transport of RecA to the membrane during genetic transformation (Masure et al., 1998), studies in Bacillus subtilis suggested that CinA is not specific to competence, but instead is a nucleoid-associated protein that serves a general role in cells entering stationary phase (Kaimer & Graumann, 2010). Here we report that cinA transcription is modulated by ComX in response to CSP, and that cinA is required for optimal genetic transformation in S. mutans.

(2009)Eur. J. Neurosci. 29, 1921–1930], the neuronal representation of sound intensity is significantly affected. Rate–intensity functions of inferior colliculus neurons were recorded in anaesthetized adult rats that were exposed to intense noise at postnatal day 14, and compared with those obtained in age-matched controls. Although the response thresholds were similar in the exposed selleck chemical and control rats, the neurons in the exposed animals had a longer first-spike latency, a narrower dynamic range, lower maximum response magnitudes and a steeper slope

of the rate–intensity functions. The percentage of monotonic neurons was significantly lower in the exposed animals. The observed anomalies were confined to the mid- and high-frequency regions, whereas no significant changes were found in the low-frequency neurons. The altered parameters of selleck chemicals llc the individual rate–intensity functions led also to differences in the cumulative responses. We conclude that a brief noise exposure during the critical period leads to a frequency-dependent

alteration of the sound intensity representation in the inferior colliculus of adult rats. The results suggest that such impairments may appear in individuals with normal hearing thresholds, but with a history of noise exposure very early in childhood. “
“Extracellular spiking activity and local field potentials (LFP) were recorded via tetrodes at the output of the antennal lobe (AL) in the honeybee brain during olfactory conditioning. Odors induce reliable rate responses that consist of either phasic-tonic responses, or complex responses with odor-specific profiles. In addition, odors evoke consistent responses of LFP oscillations in the 50-Hz band during the phasic ON-response to odor stimulation, and variable LFP responses at other frequency bands during the sustained response. A principal component analysis of the ensemble activity during differential conditioning consistently indicates

the largest changes in response to the learned odor (conditioned stimulus; CS+). Relative LFP power increases for CS+ in the Racecadotril 15–40-Hz frequency band during the sustained response, and decreases for frequencies above 45 Hz. To quantify the relationship between these population responses given by the ensemble spiking activity and LFP, we show that for CS+ the learning-related changes in the degree of the phase-locked spiking activity correlate with the power changes in the corresponding frequency bands. Our results indicate associative plasticity in the AL of the bee leading to both enhancement and decrease of neuronal response rates. LFP power changes and the correlated changes in the locking between spikes and LFP at different frequencies observed for the learned odor serve as further evidence for a learning-induced restructuring of temporal ensemble representations.

For example, Selleck Navitoclax MinCEc causes enlargement of chloroplasts in higher plants (Tavva et al., 2006), a MinD homologue from Arabidopsis thaliana complements the minicell phenotype of E. coliΔminDE mutant (Zhang et al., 2009), MinD and MinE from Neisseria gonorrhoeae can oscillate in E. coli (Ramirez-Arcos et al., 2002) and gonococcal MinCD is able to elongate N. gonorrhoeae and E. coli cells (Szeto et al., 2001). So far there has

been no reference to the functional exchange of Min systems between Gram-negative and Gram-positive bacteria. The results presented in this study extend previous findings about the heterologous functioning of Min proteins and shows for the first time that the E. coli Min system can partially substitute the Min system when introduced into B. subtilis cells. The authors thank Emília Chovancová EX 527 supplier for technical assistance, all members of the laboratory for consultations and help, David H. Edwards for strain 1920,

David Rudner for pED962 plasmid, Daniel B. Kearns for strain DS3185 and Juraj Labaj for help with graphics. This work was supported by Grants 2/7007/27 from Slovak Academy of Sciences, by grants from the Slovak Research and Development Agency under contract No. APVT-51-0278 and No. LPP-0218-06, by grant from the European Science Foundation ESF-EC-0106, and by grant 066732/Z/01/Z from The Wellcome Trust. “
“Validation of bactericidal profiles owing to a deficiency of target bacterial molecule provides opportunities to discover antimicrobial drug candidates. In this study, we constructed genetic-engineered Escherichia coli strains, in which the target gene expression is conditionally regulated by a tryptophan promoter, while the target protein expression is regulated by N-end rule-based proteolysis. Among 10 genes, whose correspondent proteins are target candidates of antibiotics for community acquired respiratory tract infection, it was clearly

demonstrated that the suppression of DnaB,GlmU, or DnaX results in a bactericidal profile, while the suppression of FabB,PyrG,DnaG,Der,PyrH,Era, or IspA leads to a bacteriostatic profile. This study is the first to predict the antibacterial inhibition profiles of Der,DnaG,DnaX,Era,GlmU,IspA,PyrG, Fenbendazole and PyrH, and confirms previous findings for DnaB and FabB. The results suggested that the system constructed in this study is a novel and useful tool to validate whether the target bacterial molecule has appropriate properties as a target of antimicrobial agents. The ability to induce bactericidality is one of the crucial profiles for an antimicrobial drug, as eliminating pathogens in hosts is difficult with bacteriostatic drugs alone. In fact, the frequency of recurrences of the primary infection in community acquired respiratory tract infections (RTIs) is higher especially in immunocompromised patients, when treated with bacteriostatic as opposed to bactericidal antibiotics (Douidar & Snodgrass, 1989; von Rosenstiel & Adam, 1994).

For example, selleck inhibitor MinCEc causes enlargement of chloroplasts in higher plants (Tavva et al., 2006), a MinD homologue from Arabidopsis thaliana complements the minicell phenotype of E. coliΔminDE mutant (Zhang et al., 2009), MinD and MinE from Neisseria gonorrhoeae can oscillate in E. coli (Ramirez-Arcos et al., 2002) and gonococcal MinCD is able to elongate N. gonorrhoeae and E. coli cells (Szeto et al., 2001). So far there has

been no reference to the functional exchange of Min systems between Gram-negative and Gram-positive bacteria. The results presented in this study extend previous findings about the heterologous functioning of Min proteins and shows for the first time that the E. coli Min system can partially substitute the Min system when introduced into B. subtilis cells. The authors thank Emília Chovancová learn more for technical assistance, all members of the laboratory for consultations and help, David H. Edwards for strain 1920,

David Rudner for pED962 plasmid, Daniel B. Kearns for strain DS3185 and Juraj Labaj for help with graphics. This work was supported by Grants 2/7007/27 from Slovak Academy of Sciences, by grants from the Slovak Research and Development Agency under contract No. APVT-51-0278 and No. LPP-0218-06, by grant from the European Science Foundation ESF-EC-0106, and by grant 066732/Z/01/Z from The Wellcome Trust. “
“Validation of bactericidal profiles owing to a deficiency of target bacterial molecule provides opportunities to discover antimicrobial drug candidates. In this study, we constructed genetic-engineered Escherichia coli strains, in which the target gene expression is conditionally regulated by a tryptophan promoter, while the target protein expression is regulated by N-end rule-based proteolysis. Among 10 genes, whose correspondent proteins are target candidates of antibiotics for community acquired respiratory tract infection, it was clearly

demonstrated that the suppression of DnaB,GlmU, or DnaX results in a bactericidal profile, while the suppression of FabB,PyrG,DnaG,Der,PyrH,Era, or IspA leads to a bacteriostatic profile. This study is the first to predict the antibacterial inhibition profiles of Der,DnaG,DnaX,Era,GlmU,IspA,PyrG, Protein kinase N1 and PyrH, and confirms previous findings for DnaB and FabB. The results suggested that the system constructed in this study is a novel and useful tool to validate whether the target bacterial molecule has appropriate properties as a target of antimicrobial agents. The ability to induce bactericidality is one of the crucial profiles for an antimicrobial drug, as eliminating pathogens in hosts is difficult with bacteriostatic drugs alone. In fact, the frequency of recurrences of the primary infection in community acquired respiratory tract infections (RTIs) is higher especially in immunocompromised patients, when treated with bacteriostatic as opposed to bactericidal antibiotics (Douidar & Snodgrass, 1989; von Rosenstiel & Adam, 1994).

4). The last two results suggested a σE-dependent regulation of the sbmA promoter. In contrast to the above results, eliminating σE

would reduce the expression of sbmA. Although rpoE is essential, it could be deleted from the strain SC122 (Rouviere et al., 1995) in the presence of an uncharacterized suppressor mutation (Alba et al., 2001), obtaining the CAG22222 strain. This allows a comparison of the specific activity of the ΔsbmA∷lacZY fusion (transduced in the two above-mentioned strains) in the presence and absence of σE. The stationary-phase activity of ΔsbmA∷lacZY fusion seen in the wild-type rpoE+ context (NC122 strain) was almost completely abolished in an rpoE background (NC322 strain) (Fig. 5). On the other hand, the induction of the ΔsbmA∷lacZY fusion activity by ethanol addition was also observed in the NC122 fusion strain and was reverted in the absence of rpoE (NC322 strain) EPZ015666 chemical structure (data not shown). The last result confirms the σE-mediated induction of sbmA by this extracytoplasmatic stress. In order to evaluate the influence Atezolizumab ic50 of σE on the tolC mutation-dependent upregulation

of sbmA, the tolC rpoE double mutant of the ΔsbmA∷lacZY fusion was constructed. To this end, a P1 transduction was performed with a tolC∷Tn10 mutant, as a donor, and NC122 and NC322 strains, as recipients, obtaining the NC222 and NC422 strains, respectively. Figure 5 shows that the increase in the β-galactosidase activity of ΔsbmA∷lacZY fusion produced in a tolC context (NC222 strain) disappears when rpoE is absent (NC422 strain). Altogether, these Carbohydrate results strongly support the idea that the transcriptional induction of sbmA by tolC mutation is completely σE dependent. It is well known that tolC mutants are pleiotropic and extremely sensitive to detergents and dyes, mainly due to the inability to pump out noxious compounds. In this mutant, a membrane permeability defect

was also demonstrated that involved a modification in the OmpF/OmpC ratio, pushing this in favor of OmpC (and MicF) (Misra & Reeves, 1987). Recently, we demonstrated that the tolC mutation severely reduces high-level resistance to tetracycline (de Cristobal et al., 2008). These results have indicated that TolC is critical for E. coli survival in an environment with noxious compounds. We also found that the inactivation of sbmA alone partially inhibited high-level tetracycline resistance. Moreover, the sbmA tolC double mutation had an additive effect, resulting in almost complete suppression of the phenotypic expression of Tn10 tetracycline resistance. In this paper, we showed that there is an sbmA-positive regulation in response to the absence of tolC, mediated by σE activation. This upregulation could be caused by the alteration in outer membrane permeability.

8% of a series of 61 patients with RDEB with a mean age of confirmation of diagnosis of 8.7 years99. Osteoporosis and osteopenia: A study of 39 children indicated that patients with RDEB and JEB had lower bone mineral density scores than control children56. In this study, a correlation was noted between low bone mass and reduced body mobility. 7.3.3 Management.  A systematic review of randomized controlled trials of treatments

for inherited forms of EB was published in 2008100. Up to the 1 April 2007, the researchers identified five randomized double-blind placebo-controlled crossover trials. None of the studies showed a benefit of the intervention over placebo100. There is still no reliable trial evidence for interventions in inherited EB. Gene, protein, and cell therapies are being researched, but until reliable evidence becomes available, most treatment of EB is directed towards preventative, supportive, selleck kinase inhibitor symptomatic, and palliative goals. Prevention of blisters:  Protection of the fragile skin of EB is of utmost importance (Images 37–38). A cool environment and skin lubrication can help lessen blister formation. Sheepskin is used for padding car seats, infant seats, and other surfaces. Young children should not been picked up under the arms, but be lifted from the bottom and the back of the neck. Clothing

should be made of soft fabric and simple design26. Management of EB wounds:  Most EB wound care techniques consist of multiple layers of bandages or sterile nonadherent Epacadostat in vivo materials (Images 38–40). Dressings are changed on a daily basis or every second day. Blisters must be drained, ideally under sterile conditions, to prevent them enlarging and giving rise to larger erosions33. Dressings should aim to maintain appropriate moisture, be nonadherent, atraumatic, promote a healthy wound bed, reduce pain, and increase speed of re-epithelialization.

(Image 41) Surgical interventions:  Patients with EB, especially RDEB, often require surgery within the oral cavity, gastrointestinal tract, and on the hands. Among the challenges for anaesthesiologists are microstomia, ankyloglossia, intraoral blistering, and sloughing, and the possible need for tracheostomy. When procedures Casein kinase 1 under general anaesthesia are planned, it is best to coordinate as many interventions as possible to avoid repeated anaesthesia26. Anaesthetic managementC:  Anaesthetic management of patients with EB presents several difficulties as a result of mucosal fragility, severe scarring of all tissues, and oesophageal strictures increasing the risk of regurgitation and aspiration during anaesthesia. Coordinated care with dermatologists, surgeons, and nurses is essential for anaesthesia and perioperative management in patients with RDEB (Table 2).57 Nonsurgical interventions– It is a common practice to mechanically separate the digits with gauze wraps on a daily basis in an attempt to prevent, minimize, or delay the EB-associated pseudosyndactyly.

, 1997). Because oligopeptides are impermeable to biological membranes, dedicated proteins (ABC transporters) are used to secrete the oligopeptides into the growth environment where they function as input for two-component transduction systems. Once they interact with a membrane-bound selleck inhibitor receptor, information is transmitted

via a series of phosphorylation events that ultimately coordinate gene expression. Staphylococcus aureus is a gram-positive human pathogen, which causes a variety of conditions ranging from relatively harmless conditions, such as styes, to those that constitute a medical emergency, such as toxic shock syndrome, which occurs when the bacteria enters the body through a cut, sore, catheter, or breathing tube. Recent emergence of S. aureus strains that are resistant to methicillin, the antibiotic of choice for staph

infections, has become a significant health problem. Staphylococcus aureus exhibits a highly complex adaptive behavior, with gene regulation that is population density, time, and environment specific. A part of this behavior is regulated by at least four two-component systems (Novick, 2003), one of which, termed the agr system, uses a modified octapeptide in signaling (Ji et al., 1995). Since its identification, several genes homologous to those involved in agr signaling have been identified in pathogens including Listeria monocytogenes (Autret et al., 2003), Staphylococcus saprophyticus (Sakinc et al., 2006) and Clostridium perfringens (Ohtani et al., 2009). Like the HLs, selleck products the octapeptides also exhibit competitive

exclusion by inhibiting signaling selleck screening library in foreign strains (Ji et al., 1997). The precise reasoning for this is not well understood; however, it is hypothesized to be a mechanism by which strains can exclude each other from infection sites. Further, it has been shown that the octapeptide signal from Staphylococcus epidermidis inhibits virulence factor expression in S. aureus (Otto et al., 1999) without affecting growth. Therefore, the use of ‘inhibitory’ oligopeptides as treatment for certain gram-positive bacterial infections is a promising route, offering a directed therapeutic with, presumably, small chances of the target bacteria evolving resistance. Pseudomonas quinolone signal (PQS) was recently discovered as a novel, signaling molecule. It was surprising to find PQS, an inhibitor of DNA gyrase and topoisomerase (Pesci et al., 1999; McKnight, 2000), as a potential small-molecule signal due to its hydrophobicity. It has now been shown to have a role in cell-to-cell communication (Déziel et al., 2004) and is secreted in concentrated form via vesicular transport (Mashburn & Whiteley, 2005). This makes the signaling mechanism of P. aeruginosa unique in that it does not rely on diffusion-mediated communication of the small molecule, which remains concentrated within the exported vesicle.

coli SE11 (Fig. 1c). Analysis of STY1365 predicted product using the tmhmm server showed a single α-helical transmembrane domain (TM) from residues 28 to 47, suggesting a membrane location in accordance to a major feature of holins (Fig.

1b). Promoter activity of STY1365 was evaluated by construction of a targeted transcriptional fusion with the lac operon. β-Galactosidase assays showed that it was optimal at the early log phase (OD600 nm of 0.2), whereas no activity was detected at the stationary phase (RP48 strain, Fig. 2a). These results were supported by RT-PCR from total RNA samples obtained at an OD600 nm of check details 0.2, showing a transcript corresponding to an mRNA of STY1365 (Fig. 2b). Detection of a STY1365 protein product was successfully achieved by Western blotting using a targeted translational fusion of FLAG epitope. A detectable band of ∼17 kDa was mainly obtained from the inner-membrane fraction of S. Typhi grown at an OD600 nm of 0.2, which is consistent with the predicted molecular weight of STY1365 product based on in silico analysis and the size of FLAG tag (Fig. 2c). The latter result supports Z-VAD-FMK nmr that STY1365 ORF is indeed a gene encoding a peptide. Previous studies have shown that the expression

of holin-like genes in E. coli causes growth impairment (Loessner et al., 1999). We evaluated whether STY1365 affects S. Typhi growth. Figure 3 shows that the wild type and the deleted mutant of STY1365 (RP23, white squares) exhibited the same growth curve. However, the complemented mutant ΔSTY1365 strain (RP23/pRP005, black squares), harboring a mid-copy number vector, showed Sucrase a significant retardation exhibiting an extended lag phase. To ensure that this phenomenon was not caused by the copy number of the vector (pRP005), the mutant strain was complemented with a single-copy-number vector (RP23/pRP010, black triangles) showing a behaviour similar to the wild

type and the ΔSTY1365 strain. Nevertheless, when STY1365 cloned in pRP10 was induced by IPTG, the growth curve was similar to RP23/pRP005 (white circles). These results suggest a detrimental effect dependent on STY1365 in the early log phase. No significant differences were observed in strains carrying empty vectors and pCC1 vector induced by IPTG (data not shown). To demonstrate that growth impairment triggered by overexpression of STY1365 is due to alteration in bacterial permeability, S. Typhi strains were treated with crystal violet, a hydrophobic dye that easily enters when the membrane is disrupted (Vaara & Vaara, 1981; Onufryk et al., 2005). In this assay we observed an increased uptake of crystal violet when STY1365 gene product is overexpressed from pRP005 or from pRP0010 induced with IPTG (Fig. 4a).

Mechanisms include hypersensitivity (e.g., with nevirapine, other NNRTIs, darunavir and fosamprenavir) where concomitant rash may occur, mitochondrial toxicity and steatosis (e.g., with d4T, ddI and ZDV), and direct hepatic toxicity (e.g., with ddI and tipranavir) [2,4]. The greatest risk of ARV-induced hepatotoxicity

is observed in those with advanced liver disease. Didanosine (ddI), stavudine (d4T) and ritonavir-boosted tipranavir should be avoided and zidovudine (ZDV) only used in the absence of an alternative option [8–11]; nevirapine should be used with caution. In addition, didanosine is associated with non-cirrhotic portal hypertension [12]. Some retrospective studies AZD8055 order have shown abacavir to be associated with a decreased response to PEG-IFN/RBV therapy in patients treated for HCV genotype 1 infection, possibly due to intracellular reductions in ribavirin level (see Section 8). Several factors (use of non-weight-based RBV dosing and differential baseline HCV viral loads) have made these data difficult to interpret and the findings have recently been disputed [13]. Nevertheless, we advise when abacavir is to be used, ribavirin should be dosed ≥1000 mg or ≥13.2 mg/kg [14–16]. Individuals may develop immune restoration on initiation of ART and need to be carefully monitored for hepatotoxicity click here when ART is commenced or changed

[17–18]. See Sections 6 and 8 for recommendations on ARV use when treating HBV and HCV coinfection. In addition, when DAAs are chosen, there are restrictions on choice of first-line ARV due to drug-drug interactions [19–23]. 1  Sulkowski MS, Thomas DL, Chaisson RE et al. Hepatotoxicity associated with antiretroviral therapy in adults infected with human immunodeficiency virus and the role of hepatitis C or B virus infection. JAMA 2000; 283: 74–80. 2  Puoti M, Nasta P, Gatti F et al. HIV-related liver disease: ARV drugs, coinfection, and other risk factors. J Int Assoc Physicians AIDS Care (Chic Ill) 2009; 8: 30–42. 3  Aranzabal L, Casado JL, Moya J et al. Influence of

liver fibrosis on highly active antiretroviral therapy-associated hepatotoxicity in patients with HIV and hepatitis C virus coinfection. Clin Infect Dis 2005; 40: 588–593. 4  Soriano V, Puoti M, Garcia-Gasco P et al. Antiretroviral drugs and liver injury. AIDS 2008; 22: 1–13. 5  Reisler RB, Han C, Burman WJ et al. Tryptophan synthase Grade 4 events are as important as AIDS events in the era of HAART. J Acquir Immune Defic Syndr 2003; 34: 379–386. 6  Labarga P, Soriano V, Vispo ME et al. Hepatotoxicity of antiretroviral drugs is reduced after successful treatment of chronic hepatitis C in HIV-infected patients. J Infect Dis 2007; 196: 670–676. 7  Price JC, Thio CL. Liver Disease in the HIV-Infected Individual. Clin Gastroenterol Hepatol 2010; 8: 1002–1012. 8  Nunez M. Hepatotoxicity of antiretrovirals: incidence, mechanisms and management. J Hepatol 2006; 44(Suppl 1): S132–S139. 9  McGovern BH, Ditelberg JS, Taylor LE et al.

These results, taken together, demonstrate that alterations in TrkB.FL signalling may be regulated via TrkB.T receptors. Upregulation of TrkB.FL Trametinib signalling suppresses epileptiform discharges in the SREDs model. “
“To serve as a robust internal circadian clock, the cell-autonomous molecular and electrophysiological activities of the individual neurons of the mammalian suprachiasmatic nucleus (SCN) are coordinated in time and neuroanatomical space. Although the contributions of the chemical and electrical interconnections between neurons are essential

to this circuit-level orchestration, the features upon which they operate to confer robustness to the ensemble signal are not known. To address this, we applied several methods to deconstruct the interactions between the spatial and temporal organisation of circadian oscillations in organotypic slices from mice with circadian abnormalities. We studied the SCN of mice lacking Cryptochrome genes (Cry1 and Cry2), which are essential for cell-autonomous oscillation, and the SCN of mice lacking the vasoactive intestinal peptide receptor 2 (VPAC2-null),

which is necessary for circuit-level Epacadostat integration, in order to map biological mechanisms to the revealed oscillatory features. The SCN of wild-type mice showed a strong link between the temporal rhythm of the bioluminescence profiles of PER2::LUC and regularly repeated spatially organised oscillation. The Cry-null SCN had stable spatial organisation but lacked temporal organisation, whereas in VPAC2-null SCN some specimens exhibited temporal organisation Fenbendazole in the absence of spatial organisation. The results indicated that spatial and temporal organisation

were separable, that they may have different mechanistic origins (cell-autonomous vs. interneuronal signaling) and that both were necessary to maintain robust and organised circadian rhythms throughout the SCN. This study therefore provided evidence that the coherent emergent properties of the neuronal circuitry, revealed in the spatially organised clusters, were essential to the pacemaking function of the SCN. “
“Abnormal sensitivity to bright light can cause discomfort or pain and evoke protective reflexes such as lacrimation. Although the trigeminal nerve is probably involved, the mechanism linking luminance to somatic sensory nerve activity remains uncertain. This study determined the effect of bright light on second-order ocular neurons at the ventral trigeminal interpolaris/caudalis transition (Vi/Vc) region, a major termination zone for trigeminal sensory fibers that innervate the eye. Most Vi/Vc neurons (80.9%) identified by responses to mechanical stimulation of the ocular surface also encoded bright light intensity. Light-evoked neural activity displayed a long latency to activation (> 10 s) and required transmission through the trigeminal root ganglion.