Postnatal depression has been found to be more common among recent migrants to Australia (Williams and Carmichael 1985; Brown and Lumley 2000), Pacific Island mothers in Auckland, New Zealand (Abbott and Williams 2006), Canadian immigrants, asylum seekers and refugees (Stewart et al. 2008; Dennis et al. 2009), London ethnic minorities (Onozawa et al. 2003), and Latinas or Hispanic U.S. mothers (Beck et al. 2005; Diaz et al. 2007). The significance of these findings is complicated by the wide international Inhibitors,research,lifescience,medical cross-cultural variation

definitions and understandings of postnatal depression and depressive symptoms. Halbreich and Karkun (2006) undertook a review of 143 studies from 40 countries and found a Inhibitors,research,lifescience,medical wide range in reported rates. The authors concluded that the variability might

be due to cross-cultural variables, reporting style, differences in perception of mental health and its stigma, differences in socioeconomic environments and biological vulnerability factors. Of significance in our study is the possibility that migrant mothers are socially isolated or segregated within the South West Sydney community. The fifth identified dimension, family size, was a complex combination of variables Inhibitors,research,lifescience,medical including Danusertib number of children under five, household size and weak negative loading of suburb duration, and “no regret leaving the suburb.” Taken together, they represent mothers with larger families who have been in

their suburb for some time and do not want to leave. It was not surprising, therefore that this dimension might protect mothers from depressive symptoms as it has been frequently reported that lack of social support is an Inhibitors,research,lifescience,medical important predictor of maternal depression (Beck 2001). The vector for the variable maternal expectations was intermediate between the infant behavior-related variables and the variables for emotional, practical, Inhibitors,research,lifescience,medical and social support, suggesting some correlation with those vectors. The length of the vector suggested that the variable was important and independent from the identified latent variables. An association between maternal expectation’s and depressive symptoms is consistent with previous studies (Beck 2002). Methodological limitations The size (15,389) of this cross-sectional study of the Astemizole EPDS administered to postnatal women is unique. The cross-sectional design, however, has limitations particularly in relation to drawing causal inferences from the regularities observed. Selection bias may have occurred from refusal and nonresponse in the study population. The self-report nature of the survey is particularly problematic with altered responses depending on mother’s mental state. There was a systematic nature to the missing EPDS data.

The BIS values (25, 50, and 75 percentile)

at the predetermined time points are presented as a Box Plot (figure 2). Table 2 Number and percentage of the patients with a bispectral index above 60 Discussion In spite of the remarkable trend toward the use of regional anesthesia in Western Europe and USA, many C/S patients still undergo the operation under general anesthesia elsewhere in the world.13-16 Some of these patients are frightened of the prospect of a needle in their back or wakefulness during major abdominal surgery.16 Regional anesthesia is liable to be very problematic, unfeasible, or contraindicated Inhibitors,research,lifescience,medical in some other patients with special medical problems.17-25 The rates of awareness and occurrence of unpleasant dreams during general anesthesia for C/S in

different studies have been reported between 0.13-7% and 17%, respectively. These figures are Inhibitors,research,lifescience,medical clearly higher in other cases, probably leading to severe psychological sequelae.26,27 The use of clinical signs is not Inhibitors,research,lifescience,medical of much help to the anesthetist in precisely assessing the level of hypnosis through general anesthesia. However, the use of relevant variables such as unresponsiveness, HR, BP, and the anesthetic method has proven WEEL inhibitors library useful enough to explain the causes of awareness.28,29 Clinical signs to infer the depth of anesthesia, which rely on changes in the autonomic nervous system, are obscured by concurrent drugs such as adrenergic blockers, coexisting diseases such as hypertension, and side effects of agents given during surgery such as tachycardia associated with isoflurane. Moreover, hypovolemia, hypoxia, hypercapnia, or inadequate analgesia rather Inhibitors,research,lifescience,medical than inadequate anesthesia may lead to

such manifestations. Because many purposeful movements are due to reflexes at the level of the spinal cord, they cannot essentially denote that the patient is awake.30 BIS monitoring provides Inhibitors,research,lifescience,medical an EEG–derivative index, a numerical array from 1 to 100 that has been reported to correlate with Tolmetin the central nervous system (CNS)-depressant effects of anesthetic drugs. This monitoring tool is sensitive to the hypnotic effects of inhaled anesthetics as well as Propofol in a dose-dependent manner. It is also deserving of note that the BIS is not sensitive enough for the assessment of analgesia and evaluation of the effect of opioids during general anesthesia.19,31-33 Sodium thiopental requirement is decreased during pregnancy.34 The present study was started with 4 mg/kg Sodium Thiopental, but the administration of this dose to the second patient was accompanied by aggressive movements of all the extremities and severe bucking with intubation. Therefore, 5 mg/kg of Sodium Thiopental was preferred for the remaining 58 patients afterward.

3% Triton X-100, three changes, 5 min each; (6) ExtrAvidin-Peroxidase (1:1000; Sigma) in PBS containing 0.3% Triton X-100 for 30 min at RT; (7) PBS containing 0.3% Triton X-100, five changes, 5 min each; and (8) working learn more solution of the metal-enhanced diaminobenzidine (DAB) substrate kit (Thermo Scientific). After six rinses in distilled water, sections were mounted on untreated clean glass slides and covered with mounting medium Inhibitors,research,lifescience,medical (Aquatex; Merck, Darmstadt, Germany) and a glass cover slip. Photomicrographs were obtained using a light microscope (BZ-8000; Keyence, Osaka, Japan). Negative controls were obtained by preadsorbing antibodies with an excess (30 mM) of

the synthetic peptides. Multiple-label immunofluorescence Sections (16 μm) were prepared by the same method as for immunoperoxidase staining and sequentially incubated overnight at 4°C with rabbit anti-Gpnmb antibody (1 μg/mL) and mouse monoclonal antibodies in the blocking Inhibitors,research,lifescience,medical buffer; the details and final concentrations are given in Table 1. After rinsing, sections were incubated for 1 h at RT with a mixture of appropriate fluorescence-conjugated secondary antibodies (Table 1) in the blocking solution. Sections were examined

under a Inhibitors,research,lifescience,medical Keyence BZ-9000 microscope using OP-66836 BZ filter GFP-BP (excitation, 440–470 nm; emission, 535–550 nm), OP-66838 BZ filter TexasRed (excitation, 540–560 nm; emission, 630–660 nm), and OP-66834 BZ filter DAPI-BP (excitation, 340–360 nm; emission, 450–460 nm). Table 1 List of antibodies used in this study Staining with isolectin B4 (IB4) Sections were incubated with biotin-conjugated IB4 (1:100; Sigma) during primary antibody incubation and with Texas Red-conjugated streptavidin (1:100; GE Inhibitors,research,lifescience,medical Healthcare) during secondary antibody reaction. Results Gpnmb mRNA expression in rat brain To examine whether Gpnmb mRNA was expressed in

rat CNS, we first performed RT-PCR Inhibitors,research,lifescience,medical analysis. Primers were designed to distinguish between the amplified product from cDNA and an amplified product derived from contaminating genomic DNA. As shown in Fig. 1A, sense and antisense primers were made to recognize exons 6 and 11, respectively. PCR products from cDNA and genomic DNA were predicted to be 993 bp and 4.4 kb, respectively. Furthermore, specificity of PCR products was confirmed by Southern blot analysis using an internal probe (Fig. Linifanib (ABT-869) 1A). Gpnmb mRNA expression was detected in all brain regions examined; GAPDH cDNA was used to confirm the integrity of RNA preparations (Fig. 1B). Figure 1 Reverse transcription-polymerase chain reaction (RT-PCR) analysis of Gpnmb mRNA in CNS of adult rats. (A) Schematic representation of the recognition sites of Gpnmb-specific PCR primers (arrows), the predicted sizes of the amplification products, and … Antibody validation To examine Gpnmb expression at the protein level, we generated a polyclonal antibody against rat Gpnmb by immunizing rabbits with a synthetic peptide corresponding to the C-terminal region.

For the past two decades, autism research has see more depended on a combination of public and private funding sources. Coordination of these efforts is one responsibility of the US Federal Government’s Interagency Autism Coordinating Committee (IACC), which has responsibility for ensuring optimal utilization of federal funds and providing guidance to private funders. To facilitate these efforts, the IACC depends on the Strategic Plan for Autism Research, initiated in 2009 and updated annually.7 The document purposefully uses plain language to summarize research Inhibitors,research,lifescience,medical directions, in order to fully reflect

the various views of the “stakeholders” in autism research. Research directions are posed as questions requiring answers and range from “When should I be concerned?” through “What caused this to happen and can it be prevented?” and “Where can I turn for services?” The questions serve as Inhibitors,research,lifescience,medical organizing points for a wide variety of research studies, with exciting

developments in many of these areas. We focus here on research into the etiology and treatment of autism, as these areas have demonstrated the most interest and promise in recent years. The etiology of ASD is generally believed to involve a complex interaction of genetic abnormalities and environmental forces. The impact of environmental factors is suggested to be modified by the timing of the exposure,8 Inhibitors,research,lifescience,medical such that individuals might be “protected” Inhibitors,research,lifescience,medical against an environmental hazard, if they have already passed through the developmentally sensitive period of risk. Conversely, exposures during the vulnerable period might have greater “epistatic” impact on individuals with a genetic predisposition to ASD.9 The complex interaction of genes, environment, and developmental sensitivities has

made research into the etiology of ASD more complex than that of other disorders. Genetic abnormalities can currently be detected in a small, but significant fraction Inhibitors,research,lifescience,medical of individuals with ASD. The percentage of gene-related cases will likely increase as gene sequencing technology advances10 and the number of genes associated with autism moves into Olopatadine the hundreds.11 Specific genetic defects are often noted in ASD, such as copy number variations in 16p.11.2 and 15q13.2q13.3.12 In addition, several well-known genetic disorders may present with symptoms of autism. Two such examples are tuberous sclerosis (TSC) and Fragile X. Recent work has shown that the signaling pathways that are mechanistic in these disorders may both relate to metabotropic glutamate receptor 5 (MGLUR), but in opposite directions. That is, MGLUR signaling may be reduced in TSC and increased in Fragile X, and researchers have proposed that augmentation should alleviate symptoms in TSC, while inhibition may be beneficial in Fragile X.

137 Statistically significant improvements were observed in the CGI rating scale and the ABC subscale of Social Withdrawal. The other subscales did not show significant improvements. D-cycloserine was administered at 30, 50, and 85 mg/day for 2 weeks each, with the highest dose leading to a 60% decrease in symptom severity. Adverse effects occurred in 2 subjects and included a transient motor tic and increased echolalia. Memantine Inhibitors,research,lifescience,medical Memantine is an NMDA-receptor antagonist is that FDA-approved for the treatment

of Alzheimer’s dementia, but has been shown in preliminary studies to be effective in the treatment of social impairment and other symptoms in individuals with Inhibitors,research,lifescience,medical ASDs. Research is limited to case reports, a retrospective review, and open-label trials. A case report of a 15-year-old male with OCD, Tourette’s disorder, and Asperger’s disorder demonstrated improved OCD symptoms and social interaction with memantine added to fluoxetine and aripiprazole.138 The

subject became more amenable to social interactions, had improved eye contact, and participated more in school activities. Memantine Inhibitors,research,lifescience,medical was dosed 10 mg/day and adverse effects included increased appetite and weight gain (believed to be attributed to aripiprazole). One case report in an adult described a 23-year-old male with autism who demonstrated improved disruptive behavior, as well as decreased social withdrawal and impulsivity, after treatment with memantine 10 mg at bedtime.139 The patient felt calmer at work and reported no further work-related conflicts, which had become problematic for him. A retrospective review Inhibitors,research,lifescience,medical of 18 Inhibitors,research,lifescience,medical children and adolescents with ASDs, aged 6 to 19 years, treated with open-label memantine, LDK378 in vitro revealed a response rate of 61%, with improvements noted in social withdrawal and inattention.140 One open-label trial of memantine in 14 male subjects with ASDs, aged 3 to 12 years (mean age, 7 years), demonstrated significant improvements on the ABC subscales of Hyperactivity, Lethargy,

and Irritability, as well as on a memory test.141 However, there was no significant difference from baseline on measures of expressive or receptive language or nonverbal IQ. Another open-label trial of 151 individuals found with autism, aged 2 to 26 years (mean age, 9 years), revealed significant improvements in language function, social behavior, and se If -stimulatory stereotypic behaviors.142 Eighty-two percent of the subjects continued on memantine, although 14.5% exhibited worsened behavior. In the studies above, memantine was dosed 2.5 to 30 mg/day. Adverse effects in one study included irritability, rash, emesis, increased seizure frequency, and excessive sedation, although another study did not note any adverse effects.

This finding is encouraging in that rehabilitation could possibly ameliorate deficits. Gaze direction is another modulator of amygdala response. In healthy people, directed fear and averted anger expressions produced greater amygdala response than averted fear and directed anger.

This effect was interpreted to suggest that the amygdala is especially sensitive to threat-related ambiguity. Since poor eye contact is a major feature of impaired social interactions in schizophrenia, gaze direction and evaluation of the patient’s ability to use information in the eyes region seems the most appropriate target for the Inhibitors,research,lifescience,medical next phase of investigation. Although scan-path Inhibitors,research,lifescience,medical studies reported a restricted range of visual scanning in schizophrenia for happy, sad, and neutral

faces, these studies have not indicated a difference between the eyes and the mouth region. However, fear and anger stimuli have not been used. Because amygdala damage leads to avoidance of the eyes region in fearful faces, and the eyes region is important for distinguishing anger from fear, the difficulty of patients in identifying fear could be related to impairment in recognizing changes in the eyes region, thereby diminishing amygdala response to Inhibitors,research,lifescience,medical fear in the eyes relative to the mouth region. As with other bottom-up activation abnormalities, we expect the severity of these abnormalities to be associated with poorer eye contact and affective Inhibitors,research,lifescience,medical flattening. Pharmacology The INCB28060 literature on the possible effects of antipsychotic agents on BOLD signal change is relatively limited.21,22 Few studies have examined neuroleptic-naïve patients, and fewer still applied a pre -post paradigm. Furthermore, small samples and methodologically limited designs have precluded systematic examination of the possible effects of therapeutics. Examples of studies include a working memory evaluation with an n-back paradigm after patients Inhibitors,research,lifescience,medical switched from first-generation antipsychotics

to a second generation agent. Increased dosolateral prefrontal cortex and parietal cortex activity were reported in the patients with the new treatment.23 Similarly, normalization of brain activity was reported in patients treated with long-acting risperidone compared with conventional depot medication while performing an n-back task.24 Normalization of prepulse inhibition was noted in patients treated with olanzapine Calpain and risperidone compared with those on first-generation antipsychotics.25 Studies that examined motor control in relation to medications have also noted improved brain activity in patients treated with second-generation agents compared with first generation antipsychotics. Given the limited number and scope of the available literature, there is no conclusive evidence, and double-blind studies are needed.

5 × 13 × 11 cm, kept at an ambient temperature (21 ± 2°C) and light (light/dark cycle with white lights on from 08:00 to 20:00), with food (Rat and Mouse No. 3 diet, Special Diet Services, Essex, UK) and tap water available ad libitum. Sawdust (Litaspen premium) and nesting materials (Sizzlenest; Datsand, Manchester, UK) in each cage were changed once every 2 weeks, but never on the day before or the day of testing to minimize the disruptive effect of cage cleaning on behavior. All housing and experimental procedures were performed in compliance with the UK Home Office Animals Scientific Procedures Act 1986. Early life stress To model early life

stress, a Inhibitors,research,lifescience,medical MS protocol was used. Males were paired with female breeders for Inhibitors,research,lifescience,medical 2 weeks and then removed. Litters of each strain were randomly allocated to control or maternal separation (MS) groups. For the litters in the MS group, the mother was removed from the litter on postnatal day 9 for 24 h and returned to the housing room, leaving the pups undisturbed. The cages containing the litters were Inhibitors,research,lifescience,medical placed on a heating pad and kept in a PF-02341066 ic50 procedure room to maximize separation from their mother. After 24 h, the dam was returned to the litter and the cage returned to the housing room.

(Control group litters were not disturbed and remained in the housing room with their mothers until they were weaned.) Mice were weaned aged 5 weeks and two pups within each litter were randomly assigned to one of three groups; test-naïve adolescent group (culled at 5 weeks), test-naïve adults (culled at 14–15 weeks), and test adults (tested at Inhibitors,research,lifescience,medical 11–12 weeks, culled at 14–15 weeks). The groups of adult mice were transferred at approximately 9 weeks of age to a separate housing and test facility and pair housed with a same sex sibling. All mice were allowed to habituate for 2 weeks before being either culled or undergoing a battery of behavioral tests and then culled. Behavioral tests A battery of Inhibitors,research,lifescience,medical behavioral tests were conducted in the following order: home cage

activity, open field, novel object exploration, holeboard, and forced swim test. Specific details of each test are given below. Offspring were aged 11 to 12 weeks at the start of testing (total n = 84). Group PD184352 (CI-1040) sizes were as follows (n = 4–7 litters/group): C57BL/6J control (male n = 14, female n = 8), C57BL/6J separated (male n = 10, female n = 10), DBA/2J control (male n = 10, female n = 12), and DBA/2J separated (male n = 10, female n = 10). Behavioral tests were performed during the light cycle between 09:00 and 18:00 h; except for the home cage in which mice were tested between 01:00 and 02:00 for the dark phase hour. Each apparatus was wiped clean with 1% Trigene® between subjects to avoid olfactory cueing behaviors. Behaviors for all tests were recorded on videotapes for further detailed analysis. Mice were returned to their home cage at the end of each test.

Neuroleptic malignant

syndrome (NMS) is possible with both typical and atypical neuroleptics. Pictilisib purchase treatment of psychosis related to pediatric bipolar disorder No controlled study of pharmacological treatment for pediatric BPAD with psychosis has been published. The only controlled medication treatment study to date for pediatric BPAD included 25 subjects with concomitant substance-abuse problems.117 In this study of lithium monotherapy, bipolar symptoms and substance use decreased significantly Inhibitors,research,lifescience,medical in subjects treated with lithium. Divalproex, lithium, and carbamazepine each showed a large effect size (Cohen’s d>1.00) in an open study 42 children and adolescents (aged 8-18 years) with BPAD based on outcome measures of CGI and Y-M’RS.118 A retrospective chart review Inhibitors,research,lifescience,medical of risperidone in juvenile BPAD indicated improvement in manic and psychotic symptoms.119 Open studies of olanzapine in acutely manic children are promising.120,121 Because of the robust antimanic effect demonstrated

with atypical neuroleptics in adults with BPAD,122 future controlled pediatric Inhibitors,research,lifescience,medical studies of neuroleptics for BPAD are likely. Treatment of pediatric major depression with psychotic features No controlled studies of pharmacological treatment of psychosis associated with pediatric MDD exist. To date, only two controlled studies of antidepressants have shown efficacy in treatment of pediatric MDD. Fluoxetine (5-20 mg) proved superior to placebo in a study of 96 children and adolescents with MDD based on CGI and Hamilton Depression Rating Scale (HAM-D).123 Paroxetine proved superior to placebo in a study of 275 Inhibitors,research,lifescience,medical adolescents with MDD, according to HAM-D and CGI rating.124 An open study of chlorpromazine plus nortriptyline for psychotically depressed adolescents showed some benefit from

the combination,125 however, neither nortriptyline nor chlorpromazine now appear desirable as treatment in pediatric mood disorders or pediatric psychosis because of their side effect profiles. Psychosocial treatment To date, there have been no Inhibitors,research,lifescience,medical published rigorous studies of psychosocial or psychotherapy treatments specific to the psychoses of childhood. Clinical practice standards Urease include detailed education of the patient and parents about the illness, the provision of supportive psychotherapy during the recovery phase of the acute illness, and practical guidance regarding behavior. Continued supportive work interepisode appears to help patients with social and developmental crises. Clinicians also act as advocates with the parents for their patients with schools and other social agencies to ensure that these children and adolescents can continue with their education and that their specials needs are recognized. Families should be given information about the various patient advocacy groups, such as the National Alliance for the Mentally III.

Of particular interest is brain-derived neurotrophic factor (BDNF), one of the most abundant neurotrophic factors in the brain. Ponatinib clinical trial altered neural plasticity in response to stress Recent reports have demonstrated altered molecular and cellular responses

to stress and have contributed to the hypothesis that altered neural plasticity contributes to stress-related psychiatric illnesses. Some examples of stress responses are discussed in this section. Stress alters learning and memory Stress is known to significantly influence learning and memory, and the effects are dependent on Inhibitors,research,lifescience,medical the type, duration, and intensity of the stressor. Emotional arousal can enhance learning and memory via synaptic plasticity of amygdala-dependent pathways, and this Inhibitors,research,lifescience,medical is thought to be the basis for intense, long-term memories of traumatic events and posttraumatic stress disorder.4,5 However, stress can also impair subsequent learning and memory and can even lead to amnesia.6 The influence of stress on hippocampal-dependent learning is complex and dependent on the type of learning task. In studies of LTP, a consistent suppression of neural plasticity is observed after exposure Inhibitors,research,lifescience,medical to stress or adrenal glucocorticoids.6,7 In one of these studies, the suppression of LTP was observed after exposure to an uncontrollable

stressor and correlated with behavioral Inhibitors,research,lifescience,medical performance in a learning and memory task. Giving the animals control over the stress (ie, the stress could be terminated) did not lead to reduced LTP or decreased learning and memory.8 A role for BDNF in the actions of stress on LTP has also been suggested.9 For additional references and discussion of the effects of stress on learning and memory, see the reviews in references 4 to 7. Stress causes atrophy of hippocainpal neurons One of the best-characterized examples of altered structural Inhibitors,research,lifescience,medical plasticity in response to stress is the atrophy of hippocampal neurons, which was first described by McEwen and colleagues (Figure 1.).10 They found that repeated restraint stress results in atrophy of the

dendrites of CA3 pyramidal neurons in the hippocampus, measured as a decrease in the number and length of apical dendrites.11 The reduction in dendritic arborization was found to be dependent on Vasopressin Receptor long-term, repeated exposure to restraint stress (3 weeks) and to be reversible when the animals are removed from stress. The atrophy of CA3 pyramidal cells appears to result from the elevation of adrenal glucocorticoids that occurs during stress because chronic administration of corticosteronc, the active form in rodent, results in a similar decrease in number and length of dendrites.12 The actions of stress and glucocorticoids are blocked by administration of an NMDA receptor antagonist, indicating that this glutamate receptor is required for atrophy of CA3 neurons.

S. P. and P. K. analyzed the data and wrote the article. Conflict of Interest The authors have no conflict of interest to declare. Supporting Information Additional Supporting Information may be found in the online version of this article: Figure S1. Data plotted per animal. Each point at each gap distance is from one animal. The number of attempts for control Inhibitors,research,lifescience,medical (A) and P0 (B) animals. The duration of an attempt in control (C) and P0 (D) animals. Error bars show mean ± SEM. Not all animals crossed

at all gap distances (Control: n = 12; P0: n = 15). Click here to view.(26K, pdf) Click here to view.(142K, png) Click here to view.(596 bytes, txt)
Researchers investigating associative learning in invertebrates have made significant breakthroughs in understanding

Inhibitors,research,lifescience,medical the conditioning process in animals like Aplysia and honey bees (Couvillon and Bitterman 1980; Kandel and Schwartz 1982; Burmeitser et al. 1995). Studying invertebrate learning systems provides the opportunity to ask complex questions in relatively Inhibitors,research,lifescience,medical simple systems, as compared with vertebrates. An area of particular interest is the role of conditioning in learning through changes in behavior. Behavior is modulated by experience, through the acquisition of new information (learning) about the environment. Thus, instinctive behaviors can be modified based on the information provided in the environment. Several invertebrate studies show that these organisms modify Inhibitors,research,lifescience,medical their behavior, especially avoidance behavior. This is seen in mollusks with habituation of the rapid gill withdrawal reflex (Castellucci and Kandel 1974), food aversion with electric shock (Mpitsos and Davis 1973; Mpitsos and Collins 1975), and CO2 poisoning (Gelperin 1975). One

technique to demonstrate learning is using studies of operant learning, specifically the animal’s ability to Inhibitors,research,lifescience,medical complete a task. A key study showed that Carcinus maenas (a crab) are able to perform a lever-press motor task (Abramson and Feinman 1990). Precise manipulation of appendages is a powerful behavior in learning abilities click here because it tests the degree to which manipulative and motor behaviors are part of paradigm motor command. This is especially interesting given our developing knowledge from of neural circuitry and neuronal control in decapods such as crayfish and lobster (Krasne 1969; Davis 1970; Larimer et al. 1971). Learning and memory formation are important in the natural environment and this is especially true for social animals, because many social hierarchies depend on recognition. As seen with many crustaceans, agonistic outcomes between conspecifics create a history of social experience that can influence future behavior (Goessmann et al. 2000; Daws et al. 2002; Bergman et al. 2003). Studies in mollusks have shown that they use sign or goal tracking (Kemenes and Benjamin 1989; Purdy et al. 1999).