Extremely Dilution of Strychnos Nux vomica Mitigates Alcohol-Induced Reduction in Enthalpies Associated With Free Water Molecules in a Fish Brain

Introduction Alcohol intoxication affects aquaporins in the glial cells of brain resulting in oedema. Nux vomica, a homeopathic drug of plant origin, is known to counteract alcohol effect. The objective of this present study is to find out the level of free water molecules in the brain of a teleost fish under ethanol intoxication. The second objective is to determine whether Nux vomica could restore the level of free water in the alcohol treated fish. Materials and methods One group of fish was exposed to 456 mM ethanol for 30 min, another exposed first to a solution of Nux vomica 200c for 20 min and then to 456 mM ethanol for 30 min. The third group served as an untreated control. The mid brain of each fish was kept in an aluminium sample pan and its free water level was assessed by differential scanning calorimetry (DSC). Results All alcohol treated fish showed significant reduction in the level of free water molecules as compared to the untreated control. Treatment with Nux vomica increased the level of free water in the brain significantly as compared to the untreated alcoholic group. Conclusion Alcohol intoxication reduces free water molecules in the fish brain. Nux vom might have acted on aquaporins in the glial cells thereby increasing the level of free water in the brain.

Increased brain growth in escaped rainbow trout

Recent examples of rapid brain size plasticity in response to novel laboratory environments suggest that fish brain size is a flexible trait, allowing growth or shrinkage of brain tissue based on short term needs. Nevertheless, it remains to be seen if plasticity of fish brain size is relevant to natural environmental conditions. Here, using rainbow trout escaped from a farming operation as a natural experiment, we demonstrate that adult fish brain size can change rapidly in response to life in a natural lake environment. Specifically, escaped trout had on average 15% heavier brains relative to body size than captive trout after living for about 7 months in the lake. Because relative brain size of most escaped trout fell above the range of variation seen within the captive trout population, we conclude that increased brain size was achieved by plasticity after escape. Brain morphology analysis showed that the most anterior regions (olfactory bulbs and rest of telencephalon) contributed most to the increase in overall brain size in escaped trout. Relative size of the heart ventricle, another organ which can be subject to plastic changes under variable environmental conditions in fish, did not differ between escaped and captive trout. Massive and selective brain growth under the changed environmental conditions associated with escape from holding pens highlighted the plastic potential of fish brain size and suggests that a shift to increased complexity of life in the wild setting of a lake imposed greatly increased cognitive requirements on escaped trout.

Role of the G protein-coupled receptors GPR84 and GPR119 in the central regulation of food intake in rainbow trout

We evaluated the role of GPR84 and GPR119 in food intake regulation in fish using rainbow trout (Oncorhynchus mykiss) as a model. In a first experiment, we assessed the effects on food intake of intracerebroventricular treatment with agonists of these receptors. In a second experiment, we assessed in hypothalamus and hindbrain the impact of the same treatments on mRNA abundance of neuropeptides involved in the metabolic control of food intake (npy, agrp1, pomca1, and cartpt) as well as in changes in parameters related to signalling pathways and transcription factors involved in the integrative response leading to neuropeptide production. Treatment with both agonists elicited an anorectic response in rainbow trout attributable to changes observed in the mRNA abundance of the four neuropeptides. Changes in neuropeptides relate to changes observed in mRNA abundance and phosphorylation status of the transcription factor Foxo1. These changes occurred in parallel with changes in phosphorylation status of Ampkα and Akt, mRNA abundance of mTOR as well as in signalling pathways related to PLCβ and IP3. These results allow us to suggest that 1) at least part of the capacity of fish brain to sense MCFA like octanoate depends on the function of GPR84, and 2) the capacity of fish brain to sense NAE or triglyceride-derived molecules through binding of these ligands to GPR119.

Indices of the DNA repair system in the brain of fish as a biomarker of inorganic mercury burden

Mercury is a widespread heavy metal that causes a stable and prolonged environmental pollution. Low concentrations of inorganic and organic mercury compounds are found in almost all water bodies. The high level of mercury bioaccumulation is a cause of tissue-specific toxicity, including neurotoxicity. Absorbed in nervous tissue mercury can cause brain disorders both in neural and glial cells. The brain of fish is considered one of the most susceptible targets for cytotoxicity of mercury in aquatic ecosystems. Taking into account that different forms of mercury have widespread distribution and exhibit a strong neurotoxic effect, the assessment of mercury cytotoxicity in the brain of fish is relevant and extremely important. Rainbow trout Oncorhynchus mykiss was exposed to mercury chloride in the dose range of 5-20 μg/L for 60 days to study the chronic exposure of low doses. In this paper, we studied the influence of inorganic mercury on oxidative stress, DNA repair proteins – ERCC1 and PARP1 in the trout’s brain. The results obtained have shown that the chronic effect of inorganic mercury causes dose-dependent oxidative stress in the fish brain. In addition, low concentrations of mercury (10 and 20 μg/L) caused a decrease in the content of ERCC1 in the brain of fish. On the contrary, the same doses have caused an increase in PARP1 expression. That is the chronic influence of low concentrations of inorganic mercury has a negative effect in the fish brain. Observed results showed that inorganic mercury has a potential for suppressing DNA repair and, therefore, increases the instability of genome. Thus, ERCC1 and PARP1 can be considered as the sensitive biomarkers of mercury cytotoxicity in the fish brain. A further study of mercury neurotoxicity is needed to find out the hazard of mercury environmental pollution as well as a validation of biomarkers of their impact.

Colourfulness as a possible measure of object proximity in the larval zebrafish brain

The encoding of light increments and decrements by separate On- and Off- systems is a fundamental ingredient of vision, which supports the detection of edges in space and time and makes efficient use of limited dynamic range of visual neurons [1]. Theory predicts that the neural representation of On- and Off-signals should be approximately balanced, including across an animals’ full visible spectrum. Here we find that larval zebrafish violate this textbook expectation: in the fish brain, UV-stimulation near exclusively gives On-responses, blue/green-stimulation mostly Off- responses, and red-light alone elicits approximately balanced On- and Off-responses (see also [2–4]). We link these findings to zebrafish visual ecology, and suggest that the observed spectral tuning boosts the encoding of object “colourfulness”, which correlates with object proximity in their underwater world [5].

The long-chain fatty acid receptors FFA1 and FFA4 are involved in food intake regulation in fish brain

ABSTRACTWe hypothesized that the free fatty acid receptors FFA1 and FFA4 might be involved in the anorectic response observed in fish after rising levels of long-chain fatty acids (LCFAs) such as oleate. In one experiment we demonstrated that intracerebroventricular (i.c.v.) treatment of rainbow trout with FFA1 and FFA4 agonists elicited an anorectic response 2, 6 and 24 h after treatment. In a second experiment, the same i.c.v. treatment resulted after 2 h in an enhancement in the mRNA abundance of anorexigenic neuropeptides pomca1 and cartpt and a decrease in the values of orexigenic peptides npy and agrp1. These changes occurred in parallel with those observed in the mRNA abundance and/or protein levels of the transcription factors Creb, Bsx and FoxO1, protein levels and phosphorylation status of Ampkα and Akt, and mRNA abundance of plcb1 and itrp3. Finally, we assessed in a third experiment the response of all these parameters after 2 h of i.c.v. treatment with oleate (the endogenous ligand of both free fatty acid receptors) alone or in the presence of FFA1 and FFA4 antagonists. Most effects of oleate disappeared in the presence of FFA1 and FFA4 antagonists. The evidence obtained supports the involvement of FFA1 and FFA4 in fatty acid sensing in fish brain, and thus involvement in food intake regulation through mechanisms not exactly comparable (differential response of neuropeptides and cellular signalling) to those known in mammals.