29 research outputs found
Sea lice on wild juvenile Pacific salmon and farmed Atlantic salmon in the northernmost salmon farming region of British Columbia
No full textThe Kitasoo/Xai'xais First Nation established a program to monitor sea lice levels on seaward migrating wild juvenile salmon in their traditional territory which contains the most northerly salmon farming region of British Columbia. A total of 12 locations were routinely sampled during the period between 2005 and 2008 to gain a better understanding of the levels and patterns of sea lice infestation on wild salmonids in the region. Over 5000 juvenile salmon were collected and examined for sea lice. Around 78% were identified as pink salmon, 18% were chum salmon and the remainder classified as ‘other’ salmon (coho and sockeye salmon). Two species of sea lice were observed: Lepeophtheirus salmonis and Caligus clemensi. Over 91% of all the juvenile salmon examined had no sea lice and there was no significant difference in L. salmonis prevalence levels among salmon species. However, chum salmon had significantly lower C. clemensi prevalence levels than either pink or ‘other’ salmon. There were significant annual and regional differences in L. salmonis prevalence on juvenile pink salmon; the lowest prevalence in all sampling zones occurring in 2008, while channels containing salmon farms consistently had higher levels than those without salmon farms. Mean prevalence of L. salmonis in the channels with salmon farms ranged from 2% to 9% which is lower than levels published for the same region in different years or for other areas without salmon farms. C. clemensi prevalence on wild pink salmon was associated with sampling zone and the size of pink salmon; larger juvenile fish were more likely to be infected than smaller fish. During the period of wild juvenile salmon migration, the mean abundance of motile stages of L. salmonis on farmed salmon ranged from 0.13 to 0.79 lice per fish but there were no significant differences among years. In comparison, C. clemensi abundance levels on farms were significantly higher in 2005. Factors contributing to variations in these observations are discussed.Source type: Electronic(1
The involvement of amygdala neurons and amygdaloid dopaminergic and glutamatergic receptors in the acquisition and reinstatement of fear-potentiated startle in rats.
No full textThe basolateral amygdala (BLA) contains NMDA, AMPA, and dopamine (DA) D1 and D2 receptors and neurobiochemical events within the amygdala mediate conditioned-fear-learning (CFL) and fear expression. Long-term potentiation (LTP) occurs in the amygdale during Pavlovian fear conditioning and is associated with fear-memory storage. CFL depends on NMDA, AMPA and dopaminergic receptor-mediated processes and enhanced amygdaloidal synaptic transmission facilitates fear-memory retrieval and makes the expression of conditioned fear possible. Since mesoamygdaloid DA receptors contribute to CFL and fear expression, Experiment 1A and 1D examined the impact of intra-BLA infusion of the DA D1 and D2 receptor antagonists SCH 23390 and raclopride L-tartrate on the acquisition of FPS in rats. Rats of the Wistar strain were bilaterally implanted with guide cannulae positioned 1.0 mm above the medial portion of the BLA. Approximately fourteen days later rats were assessed for baseline acoustic startle responding and assigned to drug-treatment groups. Forty-eight hours later rats were infused with either saline or the appropriate dopaminergic antagonist. The intra-BLA infusions occurred before five fear conditioning and testing blocks and were conducted to see if antagonism of DA receptors would prevent FPS acquisition. Retention testing for FPS took place forty-eight hours later. The results demonstrated that blockade of amygdaloid DA D1 and D2 receptors prevented the acquisition of FPS. The pretraining intra-BLA infusions of either raclopride or SCH 23390 disrupted the formation of long-term conditioned fear memories as rats treated with these DA antagonists failed to exhibit FPS on the retention test. Thus, the deficits in FPS displayed by SCH 23390 and raclopride-treated rats are likely due to the impact of these DA antagonists on associative learning and fear-memory consolidation processes. Experiment 2 demonstrated that fear-extinguished rats exposed to unsignalled footshocks displayed a reinstatement of FPS, but the exact neurobiochemicaI events involved in FPS reinstatement have not been elucidated. In contrast, fear-extinguished rats that received no unsignalled footshocks exhibited no FPS during final testing. Since unsignalled footshocks produced robust FPS reinstatement, Experiments 3A to 3D independently examined the effects of NMOA, AMPA, and DA D2 and D1 receptor antagonists on this phenomenon. Over a period of ten days, rats with cannulae targeting the BLA were base lined, fear-conditioned, pretested, fear-extinguished and then infused with either raclopride L-tartrate (8.0µg, 4.0 µg and 2.0µg), SCH 23390 (4.0 µg), (±)-2-amino-5-phosphonopentanoic acid {(APS); 2.5 µg and 1.25 µg}, 6-Cyno-7-nitroquinoxaline-2,3-dione disodium {(CNQX); 5.0 µg and 2.5 µg), or phosphate buffered saline (PBS) before exposure to five unsignalled footshocks. FPS reinstatement was assessed 24 hours later. Results from these experiments demonstrate that PBS-infused rats showed FPS reinstatement, whereas rats infused with AP5, CNQX, or the two higher doses of raclopride failed to exhibit FPS reinstatement. Intra-BLA SCH 23390 infusions did not appear to disrupt the reinstatement of FPS in Experiment 3B, however obstructed guide cannulae may have affected these results. In Experiment 3C, intra-BLA AP5 infusions made just before unsignalled footshock presentation, prevented rats from exhibiting FPS reinstatement during final testing. A similar effect on FPS reinstatement was produced by CNQX application to the BLA of rats in Experiment 3D. The overall findings of Experiment 3 suggest that DA D2 receptor antagonism and the glutamatergic receptor antagonists (AP5 and CNQX) impaired amygdaloid fear-memory reconsolidation and retrieval processes by preventing the re-excitation of neurons and pathways that had become established during fear-conditioning. It is speculated that these drugs may have interfered with excitatory synaptic transmission processes and neurobiological intracellular cascades within the amygdala and thus prevented FPS reinstatement from occurring. Two expression-control experiments (Experiments 4 and 5), revealed that the observed blockade of FPS reinstatement in Experiment 3 could not be attributed to the drugs simply blocking fear expression since infusion of raclopride, AP5, or CNQX into the BLA of non-extinguished rats 24 hours before final testing did not prevent rats from expressing FPS. Electrical stimulation (ES) of the human amygdala and temporal lobe region produces emotionally charged memory flash-backs and behaviours indicative of a central fear-state. ES of the rat amygdala is known to elevate acoustic startle amplitudes and enhance emotionality in rats and kindling of the rat amygdala exaggerates FPS and produces a variety of autonomic and behavioural
fear responses. In rats, conditioned fear and LTP are induced by ES of amygdaloid afferents so it is possible that electrical excitation of BLA neurons can trigger FPS reinstatement. Experiments 7A and 7B were conducted to test the hypothesis that ES of BLA neurons can restore FPS responding in fear-extinguished rats. Thus, rats with bipolar electrodes implanted unilaterally in the BLA were baselined, fear conditioned, pretested and then assigned to one of five groups matched on FPS. Rats then received fear-extinction or no-extinction training, followed 48 hours later by either 100 unsignalled electrical stimulations of the BLA or no stimulation. Experimental groups included; [Extinction + Stimulation (N=12), Extinction + No stimulation (N=12), No Extinction + No stimulation
(N= 12), No Extinction + Stimulation (N=11) and Extinction + Stimulation out of context (N=12)]. FPS reinstatement was assessed 24 hours later and BLA AD-current threshold were recorded four days after FPS reinstatement testing was completed. Experiment 7A demonstrated that all experimental groups exhibited FPS except the Extinction + No stimulation control group which displayed a robust extinction effect. Most importantly, the Extinction + Stimulation group exhibited statistically significant FPS reinstatement after ES of the amygdala. Experiment 7B demonstrated that ES of the amygdala in a context different to the startle apparatus also produced FPS reinstatement in fear-extinguished rats.
However, the magnitude of this FPS reinstatement effect was much smaller than that obtained when rats received ES of the amygdala in the startle testing apparatus. The overall finding that ES of the BLA causes FPS reinstatement in fear-extinguished rats suggests that ES of the BLA resensitised fear-memory systems and restored FPS responding. This effect was likely achieved by exciting amygdaloid neurons and pathways containing the memory-trace of the CS-UCS association originally established during Pavlovian fear conditioning. Experiments 8 to 10 used the same protocol as Experiment 7A and investigated whether ES of other brain regions that share reciprocal connections with the amygdala would trigger FPS reinstatement in fear-extinguished rats. Rats in Experiments 8 to 10 had bipolar electrodes unilaterally implanted in the perirhinal/insular cortex (PRh/IC), dorsal periaqueductal gray (dPAG), ventral tegmental area (VTA) and ventral periaqueductal gray (vPAG). Experiment 8 revealed that ES of the PRh/IC produced a positive trend towards FPS reinstatement. Experiment 9 examined the impact of dPAG and VTA ES on FPS reinstatement. This experiment demonstrated that VTA but not dPAG ES produced a FPS reinstatement effect. This finding seems to support the research evidence that highlights the importance of mesoamygdaloid systems in mediating conditioned fear and stress responses. Experiment 10 assessed the impact of vPAG ES on
FPS reinstatement and discovered that stimulation of this region did not trigger a restoration of FPS in fear-extinguished rats but it did seem to elevate overall acoustic startle responding during final testing, This finding would seem to indicate that ES of the vPAG likely increased contextual fear but not cue specific fear since acoustic startle amplitudes during both the noise-alone and the CS + noise conditions were elevated, The key finding that ES of the amygdala produces robust FPS reinstatement provides further proof that the amygdala and its afferent and efferent neural circuits are essential for fear-memory reconsolidation and conditioned fear expression and reinstatement
The involvement of ventral tegmental area cholinergic muscarinic receptors in classically conditioned fear expression as measured with fear-potentiated startle
No full textModernization of the mechanism of social services in Ukraine reforming
No full textThe article considers the mechanism of social services reforming in terms of decentralization of power in Ukraine.
It is proved that the introduction of a new model of social services in Ukraine is impossible without reforming of different sectors of the economic system of the country and the implementation of existing managerial capacity of modern management systems at all levels of government. The model of the social services mechanism reforming, which comprises the complex of instruments and methods of social reforms implementing, is given.
It is shown that the main purpose of such a mechanism introducing should act a maintenance of steady development of social sphere and social services system by strengthening its ability to adapt to constantly changing economic, geopolitical, legal terms within the model that meets the needs and the expectations of the community regarding the quality and scope of social services.
The author believes that presented mechanism should ensure implementation of principles of management and coordination of social services in Ukraine by strengthening the accountability of management (providers, representatives of authorities, responsible for ensuring the people’s rights to receive social services), ensuring consistency reform processes, coordination of actions of these processes, and the flexibility of the whole system.
Given the nature of social sphere and system for providing social services, the author argues that the new role of the state and its competent authorities for the management of this area is to promote the formation of effective models and effective mechanisms to guarantee social rights and freedoms of citizens of Ukraine at their place of residence and direct social services that are not at variance with the economic interests of the state and the players of these services market.
At the same time, the role of local authorities is manifested in the performance of the provider function – conductor, mediator – of social services to the recipient who will receive it – a citizen of Ukraine who has the right to appropriate service receiving. The provider should ensure the effectiveness of the mechanism of social services on the territory entrusted to him, to ensure high quality of these services in accordance with the legal framework that regulates relations in this field.
Such presentation of the role of local authorities (regional administrations, district administrations, local administrations) as providers, intermediaries in the model of social services provision, is determined by emphasis on innovation development of management activities in a decentralized governance model that, according to the best achievements of European and international experience in this field, is a prerequisite for the implementation of positive transformations and reforms in social sphere.
Accordingly, the coordination of interests plays a key role into the ensuring the success of the institutional stability of the social sector and social services system. Since this area is essentially multifactorial system of social relationships between the forms and types of institutions’ activities, it is a priori can’t be denied the contradictions that arise inevitably and will arise in a progress within it because of various kinds of interests
Performance of the odour span task is not impaired following inactivations of parietal cortex in rats
No full textPeer Reviewe
Maternal Immune Activation during Pregnancy Alters the Behavior Profile of Female Offspring of Sprague Dawley Rats
No full textSex differences are documented in psychiatric and neurological disorders, yet most preclinical animal research has been conducted in males only. There is a need to better understand of the nature of sex differences in brain disease in order to meet the needs of psychiatric patients. We present the behavior profile of adult female offspring produced using a maternal immune activation (MIA) model where pregnant rats receive an immune stimulant and the offspring typically show various abnormalities consistent with psychiatric illnesses such as schizophrenia and autism. The results in female offspring were compared to a previously published cohort of their male siblings (Lins et al., 2018). We examined prepulse inhibition (PPI), sociability, MK-801-induced locomotor activity, crossmodal object recognition (CMOR), and oddity discrimination; behaviors relevant to the positive, negative, and cognitive symptoms of schizophrenia. No between-treatment differences in PPI or locomotor activity were noted. Tactile memory was observed in the control and treated female offspring, visual recognition memory was deficient in the polyinosinic:polycytidylic acid (polyI:C) offspring only, and both groups lacked crossmodal recognition. PolyI:C offspring were impaired in oddity preference and had reduced preference for a stranger conspecific in a sociability assay. Systemic maternal CXCL1, IL-6, and TNF-a levels 3 h after polyI:C treatment were determined, but no relationship was found between these cytokines and the behavior seen in the adult female offspring. Overall, female offspring of polyI:C-treated dams display an array of behavior abnormalities relevant to psychiatric illnesses such as schizophrenia similar to those previously reported in male rats
Performance of the trial-unique, delayed non-matching-to-location (TUNL) task depends on AMPA/Kainate, but not NMDA, ionotropic glutamate receptors in the rat posterior parietal cortex
No full textPeer Reviewe
GluN2B-containing NMDA receptors and AMPA receptors in medial prefrontal cortex are necessary for odor span in rats
No full textWorking memory is a type of short-term memory involved in the maintenance and manipulation of information essential for complex cognition. While memory span capacity has been extensively studied in humans as a measure of working memory, it has received considerably less attention in rodents. Our aim was to examine the role of the NMDA and AMPA glutamate receptors in odor span capacity using systemic injections or infusions of receptor antagonists into the medial prefrontal cortex. Long Evans rats were trained on a well-characterized odor span task. Initially, rats were trained to dig for a food reward in sand followed by training on a non-match to sample discrimination using sand scented with household spices. The rats were then required to perform a serial delayed non-match to sample procedure which was their odor span. Systemic injection of the broad spectrum NMDA receptor antagonist CPP (10 mg/kg) or the GluN2B-selective antagonist Ro25-6981 (10 mg/kg but not 6 mg/kg) significantly reduced odor span capacity. Infusions of the GluN2B- selective antagonist Ro25-6981 (2.5 µg/hemisphere) into medial prefrontal cortex reduced span capacity, an effect that was nearly significant (p = 0.069). Infusions of the AMPA receptor antagonist CNQX (1.25 µg/hemisphere) into medial prefrontal cortex reduced span capacity and latency for the rats to make a choice in the task. These results demonstrate span capacity in rats depends on ionotropic glutamate receptor activation in the medial prefrontal cortex. Further understanding of the circuitry underlying span capacity may aid in the novel therapeutic drug development for persons with working memory impairments as a result of disorders such as schizophrenia and Alzheimer’s disease
Biological clocks and incremental growth line formation in dentine
No full textDentine‐ and enamel‐forming cells secrete matrix in consistent rhythmic phases, resulting in the formation of successive microscopic growth lines inside tooth crowns and roots. Experimental studies of various mammals have proven that these lines are laid down in subdaily, daily (circadian), and multidaily rhythms, but it is less clear how these rhythms are initiated and maintained. In 2001, researchers reported that lesioning the so‐called master biological clock, the suprachiasmatic nucleus (SCN), halted daily line formation in rat dentine, whereas subdaily lines persisted. More recently, a key clock gene (Bmal1) expressed in the SCN in a circadian manner was also found to be active in dentine‐ and enamel‐ secretory cells. To probe these potential neurological and local mechanisms for the production of rhythmic lines in teeth, we reexamined the role of the SCN in growth line formation in Wistar rats and investigated the presence of daily lines in Bmal1 knockout mice (Bmal1 (−/−)). In contrast to the results of the 2001 study, we found that both daily and subdaily growth lines persisted in rat dentine after complete or partial SCN lesion in the majority of individuals. In mice, after transfer into constant darkness, daily rhythms continued to manifest as incremental lines in the dentine of each Bmal1 genotype (wild‐type, Bmal (+/–), and Bmal1(−/−)). These results affirm that the manifestation of biological rhythms in teeth is a robust phenomenon, imply a more autonomous role of local biological clocks in tooth growth than previously suggested, and underscore the need further to elucidate tissue‐specific circadian biology and its role in incremental line formation. Investigations of this nature will strengthen an invaluable system for determining growth rates and calendar ages from mammalian hard tissues, as well as documenting the early lives of fossil hominins and other primates
NMDA receptors in visual and olfactory sensory integration in male Long Evans rats: a role for the orbitofrontal cortex
No full textPeer Reviewe
