Effects of predation and social interaction on spatial learning and brain cell proliferation in weakly electric fish, Apteronotus leptorhynchus

Previous studies have determined that the stress of predation inhibits brain cell proliferation in two species of weakly electric fish, including, Apteronotus leptorhynchus. In this thesis, three experiments examined how predator stimuli and social interaction affect brain cell proliferation and spatial learning in A. leptorhynchus. The three questions that were explored were: 1) Is the decrease in brain cell proliferation seen after tail amputation in weakly electric fish due to the actual predation injury event or the subsequent regenerative process of their tail? 2) Does social interaction influence the effect of predator stimuli on brain cell proliferation? 3) Do predator stimuli in the form of chasing affect the spatial learning ability of the fish? In the first experiment the action of amputating the tail of the fish caused a drastic significant decrease in brain cell proliferation as compared to the fish allowed long-term recovery (17-18d) and the intact fish. This indicates that the actual predation injury event causes the decrease in cell proliferation, not the regenerative process of the tail. In the second experiment social interaction mitigated the negative effects of stress on brain cell proliferation. Finally in the third experiment the decrease in brain cell proliferation associated with chasing had no apparent effect on the spatial learning behavior of the fish

The Degeneration of the Human Mind: An Analysis of Alzheimer’s Disease, A Kuhnian Perspective

In 1906, a German physician, Dr. Alois Alzheimer, specifically identified a collection of brain cell abnormalities (and the formation of plaque in the brain) as a disease, which forever changed the way scientists view degenerative cognitive disorders. Today, this brain disease bears his name, and is one of the most common diseases among the aging population. The discovery of Alzheimer’s Disease (AD) can be seen as a revolutionary, paradigmatic shift in regards to scientific discovery from a Kuhnian perspective. In that vein, the discovery presents philosophical implications for the notion of personhood and how those suffering from AD are treated in society

Effect of photosensitizers photosens, photodithazine and hypericin on glioma cells and primary neuronal cultures : a comparative analysis

The aim of the study was to compare the effect of photosensitizers photosens, photodithazine, and hypericin on primary brain cell cultures, and assess their toxic effect on tumor and normal nervous cells in order to choose the optimal photodynamic agent for glioma therapy. Materials and Methods. The cytotoxicity of photosens (NIOPIK, Russia), photodithazine (Veta-grand, Russia) and hypericin (Merck KGaA; Sigma-Aldrich, Germany) was assessed on primary brain cell cultures obtained from C57BL/6 mice (gestation day 18). On day 14 of cultivation, the tested photosensitizers were added to a culture medium at concentrations of 0.1, 1, 10, 50, and 100 mu M. Then the cultures were placed in a CO2-incubator in the dark. The viability of primary neuronal cultures was estimated on days 3 and 7 after photosensitizer application. Using confocal microscopy, we analyzed the rate of entry and subcellular localization of the tested agents in the primary neuronal cells. Statistical analysis was performed in SigmaPlot 11.0 (Systat Software Inc., USA) using ANOVA. Results. We analyzed the absorption and fluorescence spectra of the tested photosensitizers. Photosens and photodithazine showed the presence of absorption maximum in short- and long-wave spectral ranges. Hypericin was characterized by a complex spectrum with many peaks in both blue-violet and orange-red spectral ranges. Cell viability analysis revealed that high concentrations of photosensitizers caused a pronounced toxic effect on nervous cells. The most marked effect was shown for photodithazine. Photosens exhibited the lowest accumulation rate in primary neuronal cells. Photosens and hypericin were found to have a high phototoxic effect on glioma, and demonstrated low dark toxicity for normal brain cells. Conclusion. The photosensitizers hypericin and photosens are the least toxic for nervous tissue, though effectively penetrating in tumor cells. These properties enable to consider them as prospective photodynamic agents for clinic

Excitable Media Seminar

The simulation data presented here, and the conceptual framework developed for their interpretation are, both, in need of substantial refinement and extension. However, granting that they are initial pointers of some merit, and elementary indicators of general principles, several implications follow: the activity patterns of neurons and their assemblies are\ud interdependent with the extracellular milieu in which they are embedded, and to whose time varying composition they contribute. The complexity of this interdependence in the temporal dimension forecloses any time and context invariant relation between what the experimenter may consider stimulus input and its representation in neural activity. Hence, ideas of coding by (quasi)-digital neurons are called in question by the mutual interdependence of neurons and their\ud humoral milieu. Instead, concepts of 'mass action' in the Nervous system gain a new perspective: this time augmented by including the chemical medium surrounding neurons as part of the dynamics of the system as a whole. Accordingly, a meaningful way to describe activity in a neuron assembly would be in terms of a state space in which it can move along an infinite number of trajectories.\u

The Effect of Hypoxia on Brain Cell Proliferation in Weakly Electric Fish, Petrocephalus degeni

Oxygen levels tend to remain at a steady state concentration in the Earth’s atmosphere, yet in some bodies of water, they can fluctuate and decrease drastically. Many organisms that inhabit the swamps, lakes, streams, and parts of the ocean where this occurs have evolved adaptations to manage this environmental uncertainty and continue normal oxygen consumption. The Lwamunda swamp in Uganda is chronically hypoxic, yet it is home to many species, including the electric fish Petrocephalus degeni. P. degeni are unusual by nature of their immense brain, and the Lwamunda swamp appears ill-suited for maintaining this large, metabolically active organ. To determine the possible mechanisms P. degeni employ for survival and brain maintenance in this hypoxic swamp, 33 individuals were collected aiming to analyze their brain cell proliferation. One-third were immediately sacrificed, and two-thirds were transported to a laboratory and divided into hypoxic and normoxic environments for two weeks. All brains were collected, and new brain cell proliferation was quantified using PCNA immunohistochemistry. P. degeni from the hypoxic lab condition showed significantly fewer PCNA+ cells than their conspecifics in normoxic water, and individuals harvested directly from the field showed the overall highest density of PCNA+ brain cells. Our results suggest that hypoxia and captivity negatively impacted brain cell growth in P. degeni. The activation of hypoxia-inducible factors (HIFs) likely mediated this reduction in brain cell proliferation and the corresponding oxygen demand. Despite showing a reduction in new brain cell growth, P. degeni remains capable of surviving and maintaining their large brain in extremely hypoxic conditions

Social buffering of brain cell proliferation and behavioral responses to tail injury in weakly electric fish, Apteronotus leptorhynchus

Social interactions can mitigate the damaging effects of threatening stimuli, a phenomenon termed ‘social buffering’. In two different forms of social buffering, social interactions reduce stress-induced decreases in brain cell proliferation and enhance recovery from somatic injury. However, the positive effects of social interactions on the brain cell proliferation response to somatic injury have not been extensively examined. Here, I investigated the social buffering of the brain cell proliferation response to tail injury in an electric fish, Apteronotus leptorhynchus. I ask three major questions: 1) Does social interaction mitigate the decrease in brain cell proliferation caused by simulated predatory tail injury?; 2) Does the timing of social interaction relative to injury alter this social buffering response?; and 3) Does tail injury modify affiliation with a non-injured social partner? I mimicked predatory injury through experimental tail amputation, exposed fish to paired interactions that varied in timing, duration, and recovery period, and measured cell proliferation (PCNA+ cell density) in the forebrain and midbrain. I also measured social affiliation based on the position of fish in retreat sites located near or distant to a stimulus fish. Social interaction either before or after tail amputation mitigated the negative effects of tail injury on brain cell proliferation. This buffering effect was specific to the forebrain and occurred after short-term (1 d) or long-term (7 d) recovery periods following tail amputation. However, social interaction both before (4 d) and after (7 d) tail amputation produced an even greater buffering effect in localized regions of the forebrain and midbrain. Similarly, fish exposed to social interaction both before and after tail amputation sought close affiliation with non-injured stimulus fish, but this effect did not occur in fish exposed to social interaction only after injury. Thus, despite the social buffering response on brain cell proliferation, it remains unclear whether fish modify their affiliation behavior in response to tail injury

Anatomical Characterization of the Type-1 cannabinoid receptors in specific brain cell populations of mutant mice

151 p.The Cannabinoid Type I receptor protein (CB1) expression in the hippocampus of rescue mice modified to express the gene exclusively in specific brain cell types: such as dorsal telencephalic glutamatergic neurons, or GABAergic neurons have been analysed. Furthermore, aiming at knowing the exact anatomical distribution of the astroglial CB1 receptors with respect to the excitatory and inhibitory synapses, the CB1 receptor expression in astrocytes of mouse expressing CB1 receptor only in astrocytes and mutant mouse expressing the protein hrGFP into astrocytes (that allows for better detection of the astrocytic processes) have been also investigated. The results showed that the majority of the hippocampal synapses surrounded by CB1 receptor immunopositive astrocytes in the 400-800 nm range are of excitatory nature. Moreover, the CB1 receptor rescue mutant mice characterized in this Doctoral Thesis have proven 1) to express CB1 receptors in specific brain cell types; 2) the re-expression is limited to the particular brain cell populations; 3) the endogenous levels of CB1 receptors are maintained in the brain cell types re-expressing the receptor. Which makes this mutant mice excellent tools for functional and translational investigations on the role of the CB1 receptors in the normal and diseased brain