Maternal behaviours are those that increase offspring survival. Estrogens affect maternal behaviour by activating Estrogen Receptors (ER) in the brain. Maternal brain plasticity was explored by characterizing the effects of exposure to a mixture of environmental pollutants on number of ERs. Following exposure to the toxicants during pregnancy and lactation, brains of female rats were collected, sectioned at 30 μm and immunohistochemistry for ERα performed. Immuno-positive cells in the mPOA, VTA and NAc were counted. A two way ANOVA revealed no main effect of Treatment on the number of immunopositive cells for all three brain regions. However, a significant difference between the High and Low Doses with the high dose reducing the number of ERα+ cells in the mPOA and VTA. Our work showcases the importance of studying the effects of multiple chemical co-exposures on the mother's brain, as maternal brain changes impact maternal behaviour consequently affecting offspring neurodevelopment.

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Previous research investigating the neural circuitry underlying memory consolidation has primarily focused on single “nodes” in the circuit rather than the neural connections between brain regions, despite the likely importance of these connections in mediating different aspects or forms of memory. This focus has, in part, been due to technical limitations; however the advent of optogenetics has altered our capabilities in this regard, enabling optical control over neural pathways with temporal and spatial precision. The current set of experiments took advantage of optogenetics to control activity in specific pathways connecting brain regions in rats immediately after different kinds of learning. Chapter 2 first established the use of optogenetics to manipulate activity in the basolateral amygdala (BLA), which has been shown to modulate memory consolidation for a variety of types of learning likely through its connections to various downstream regions. Using a one-trial inhibitory avoidance task, a simple and robust fear learning paradigm, we found that both post-training stimulation and inhibition of BLA activity could enhance or impair later retention of the task, respectively. Enhancement was specific to stimulation using trains of 40, but not 20, Hz light pulses. Chapters 3 and 4 examined the projections from the BLA to the ventral hippocampus (VH) and medial entorhinal cortex (mEC) as the BLA’s ability to influence the consolidation for many types of memory is believed to be mediated through discrete projections to distinct brain regions. Indeed, the BLA innervates both structures, and prior studies suggest that the mEC and VH have distinct roles in memory processing related to contextual and nociceptive (footshock) learning, such as those involved in contextual fear conditioning (CFC). Optogenetic stimulation or inhibition of the BLA-VH or BLA-mEC pathway after training on a modified CFC task, in which the nociceptive or emotional stimulus (the footshock) and the context are separated, enabled experimental manipulations to selectively affect the consolidation for learning about one component and not the other. Optogenetic stimulation/inhibition was given to each candidate pathway immediately after the relevant training to determine its role in influencing consolidation for that component of the CFC learning. Chapter 3 results showed that stimulation of the BLA-VH pathway following footshock, but not context, training enhanced retention, an effect that was specific to trains of 40 Hz stimulation. Post-footshock photoinhibition of the same pathway impaired retention for the task. Similar investigations of the BLA-mEC pathway in Chapter 4 produced complementary findings. Post-context, but not footshock, stimulation of the pathway enhanced retention. In this particular case, only trains of 8 Hz stimulation were effective at enhancing retention. These results are the first, to our knowledge, to find that BLA inputs to different structures selectively modulate consolidation for different aspects of learning, thus enhancing our understanding of the neural connections underlying the consolidation of contextual fear conditioning and providing a critical foundation for future research.

Dehumanization is a process whereby people fail to view others as human beings. Instead, the others are perceived as nonhuman animals or objects, unworthy of the same moral treatment. Dehumanization has previously been studied in a variety of different scholarly domains without adhering to a uniform theoretical framework. This literature review contrasts research on fully humanized perception, with research on dehumanized perception, and proposes neural areas which are likely to be involved. Not every aspect of dehumanization can be understood at the neurological level. To understand what factors lead up to, and modulates dehumanization, other perspectives might also be necessary. Dehumanized perception is coupled with reduced activity in the social cognitive brain network, a wide network which encompasses several cortical and subcortical areas. This disengages prosocial abilities and allows for other people to be treated like objects and means to an end. One area of special interest is the medial prefrontal cortex (MPFC). It functions as an integration center in the person perception network and is also active when we make moral judgments, empathize, or take the perspective of someone else. For this reason, the MPFC is sometimes used as an index of dehumanized perception.

<p>Syftet med studien är att undersöka fyra stycken kvinnor som är medlemmar i samma mediala grupp. Uppsatsen ämnar undersöka hur de ser på sig själva och sin medialitet utifrån gruppen och samhället de lever i genom deras livsberättelse. Det är en kvalitativ undersökning som genom livshistorieintervjuer samt deltagande observationer studerar kvinnornas berättelser och deras medverkan i gruppen. Slutsatsen visade en ambivalent syn på att de var annorlunda och visade en rädsla och försiktighet mot samhället utanför gruppen som de lever i till vardags.</p>

Despite advances, stroke remains the largest cause of disability and fourth leading cause of death in the United States. The relationship between changes in human vasculature (atherosclerosis and arteriosclerosis) prior to clinical incident, and other risk factors for stroke remains unclear. This dissertation represents work towards the identification of imaging biomarkers for vascular change, focusing on ultrasound to characterize persons at risk, including differences among race/ethnic groups. This research contained three distinct projects. The first goal was to determine if changes within ultrasonographic measures of carotid vasculature could be found across race/ethnic groups after adjustment for risk factors. The second was to determine if those same measures were related to changes in cerebral white matter known to be associated with ongoing cerebrovascular disease; we compared ultrasound to an MRI marker of subclinical vascular disease, white matter hyperintensity volume (WMHV). Finally, we sought to investigate a known and well-studied ultrasound marker for atherosclerosis, carotid intima-medial thickness, with those same MRI markers of subclinical vascular disease (WMHV). All studies were conducted within an on-going multiethnic cohort that has been followed since 1990, The Northern Manhattan Study. The population is comprised of persons who self-identify as Hispanic (52%), Black (24%), or White (21%), with less than 3% identified as “race/other.” We found race/ethnic differences in carotid arterial stiffness and diameter; carotid diameter increases with age among Hispanics, but not among blacks or whites. A significant correlation was also found between diastolic diameter and subclinical vascular disease, and this relationship was also increased among Hispanics; neither black race nor white race was associated with corresponding increases in both MRI white matter hyperintensity and diastolic diameter. Finally, using a surrogate marker for atherosclerosis, carotid intima-medial thickness (cIMT), we document for the first time, positive associations between cIMT and WMHV. There are important developments still to be made in the field of vascular risk. Use of inexpensive and non-invasive ultrasound technology to approximate ongoing cerebrovascular disease could lead to better understanding of the effect of known risk factors, and could help stroke risk assessment and treatment modification.

Alzheimer’s disease (AD), the most common cause of dementia in the elderly, is a gradually progressive degenerative neurological disorder that is characterized by increasing cognitive impairment, characteristic degenerative pathology and brain atrophy. Studies have shown that the progression of AD pathology in the brain develops in a predictable pattern and the pathological changes that take place in brain begin at the microscopic level long before the first signs of memory loss. Structural Magnetic Resonance Imaging (MRI), which has exceptional soft tissue contrast and detailed resolution, is the best way to noninvasively examine changes which occur early in the course of AD. For this dissertation, our aim is to improve the methods for measuring the atrophy of brain structures in AD, as seen on MRI, and to apply these methods to subjects with cognitive impairment. This study has established a new coordinate template to replace the widely used Montreal Neurological Institute (MNI) template for the atlas-based segmentation procedure. The new template was derived from the same structural image as the one used by the Automated Anatomical Labeling (AAL) procedure. The agreement of the newly developed coordinate template and AAL helps to estimate accurate spatial transformation parameters used in warping the AAL to individual subject images. The new template combines the spatial information of the structural image and the frequency information of MNI template. Based on the same principle, a set of customized templates has been developed. The customized template, associated atlas and customized priors match more closely the aging population than the previous template, so as to improve the atlas-based segmentation of regions of interest in AD assessment. Visual Rating System (VRS) of a single coronal slice (MB slice) in MRI has been another valuable method in the assessment of medial temporal lobe atrophy. An automated procedure has been developed in this study to measure the hippocampal area on the same coronal slice so that the labor of human experts in the VRS assessment of hippocampus will be significantly reduced. Finally the methods and materials (template and atlas) developed in this dissertation were applied to cross-sectional studies of subjects with cognitive impairment. We conducted volumetric analysis on subjects and conclude that the data from the new approaches have higher correlations with clinical data, and therefore can be reliably used as part of an AD assessment tool.

The medial preoptic nucleus (MPN) of the hypothalamus plays a major role in many functions involved in maintaining bodily homeostasis, such as thermoregulation and osmoregulation, as well as in the control of complex behaviours, e.g. sexual behaviour. A fundamental basis for the control and execution of these functions is the synaptic communication between neurons of the MPN. However, the functional properties of the synapses involved are largely unknown. The present thesis is a study of ligand-gated ion channels involved in the pre- and post-synaptic aspects of neuronal communication in the MPN of rat. The aim was to clarify synaptic properties in the MPN, to identify the major channel types involved and to obtain a better understanding of their functional properties. By fast application of agonists to isolated neurons, it was first demonstrated that all neurons responded to glutamate with currents mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and a majority of neurons also with currents mediated by N-Methyl-D-aspartate (NMDA) receptors. All neurons also responded to γ-aminobutyric acid (GABA) and glycine with currents mediated by GABAA receptors and glycine receptors, respectively. These findings show that fast-acting excitatory and inhibitory amino-acid transmitters are most likely important for communication between hypothalamic neurons. Application of agonists to isolated neurons revealed cross-talk, detected as an apparent cross-desensitization, between the responses to GABA and those to glycine. Parallel analysis of current and conductance, using gramicidin-perforated patches to avoid perturbing intracellular chloride concentration, showed that the cross-talk was not dependent on a direct interaction between the receptors as previously suggested, but was a consequence of the change in the intracellular chloride concentration during receptor activation. Strengthened by a computer model, the analysis also showed that the current decay in the presence of GABA or glycine was mainly due to a change in the chloride driving force and that receptor desensitization played a minor role only. The role of thermo-sensitive transient receptor potential TRPV1 channels in the regulation of glutamate- and GABA-mediated transmission was studied in the slice preparation, where much of the synaptic connections between neurons are preserved. It was shown that application of the TRPV1 agonist capsaicin increased the frequency of excitatory AMPA receptor- mediated as well as inhibitory GABAA receptor-mediated postsynaptic currents. This effect was partly presynaptic and demonstrates that TRP channels play a role in regulating synaptic transmission in the MPN. The results imply that such mechanisms may possibly contribute to the thermoregulation by MPN neurons.

Brain function implies complex information processing in neuronal circuits, critically dependent on the molecular machinery that enables signal transmission across synaptic contacts between neurons. The types of ion channels and receptors in the neuronal membranes vary with neuron types and brain regions and determine whether neuronal responses will be excitatory or inhibitory and often allow for functional synaptic plasticity which is thought to be the basis for much of the adaptability of the nervous system and for our ability to learn and store memories. The present thesis is a study of synaptic transmission in the medial preoptic nucleus (MPN), a regulatory center for several homeostatic functions but with most clearly established roles in reproductive behaviour. The latter behaviour typically shows several distinct phases with dramatically varying neuronal impulse activity and is also subject to experience-dependent modifications. It seems likely that the synapses in the MPN contribute to the behaviour by means of activity-dependent functional plasticity. Synaptic transmission in the MPN, however, has not been extensively studied and is not well understood. The present work was initiated to clarify the synaptic properties in the MPN. The aim was to achieve a better understanding of the functional properties of the MPN, but also to obtain information on the functional roles of ion channel types for neurotransmission and its plastic properties in general. The studies were carried out using a brain slice preparation from rat as well as acutely isolated neurons with adhering nerve terminals. Presynaptic nerve fibres were stimulated electrically or, in a few cases, by raised external K+ concentration, and postsynaptic responses were recorded by tight-seal perforated-patch techniques, often combined with voltage-clamp control of the post-synaptic membrane potential. Glutamate receptors of α-amino-3-hydroxy-5-methyl-4-izoxazole propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) types were identified as mediating the main excitatory synaptic signals and γ-aminobutyric acid (GABA)A receptors as mediating the main inhibitory signals. Both types of signals were suppressed by serotonin. The efficacy of AMPA-receptor-mediated transmission displayed several types of short-term plasticity, including paired-pulse potentiation and paired-pulse depression, depending on the stimulus rate and pattern. The observed plasticity was attributed to mainly presynaptic mechanisms. To clarify some of the presynaptic factors controlling synaptic efficacy, the role of presynaptic L-type Ca2+ channels, usually assumed not to directly control transmitter release, was investigated. The analysis showed that (i) L-type channels are present in GABA-containing presynaptic terminals on MPN neurons, (ii) that these channels provide a means for differential control of spontaneous and impulse-evoked GABA release and (iii) that this differential control is prominent during short-term synaptic plasticity. A model where Ca2+ influx through L-type channels may lead to reduced GABA release via effects on Ca2+-activated K+ channels, membrane potential and other Ca2+-channel types explains the observed findings. In addition, massive Ca2+ influx through L-type channels during high-frequency stimulation may contribute to increased GABA release during post-tetanic potentiation. In conclusion, the findings obtained in the present study indicate that complex neurotransmission mechanisms and different forms of synaptic plasticity contribute to the specific functional properties of the MPN.

Consolidation of associative memories may depend on communication between the lateral entorhinal cortex (LEC) and hippocampus (HPC) for recently learned memories and the LEC and medial prefrontal cortex (mPFC) for remote memories. To determine whether direct connections between these regions are necessary for the retrieval of a recently or remotely learned memory, rats acquired an associative memory through trace eyeblink conditioning and were tested for memory retention after inactivating the regions of interest with the GABAA agonist, muscimol. Inactivating the LEC-HPC connection did not impair memory retrieval. However, inactivating the LEC-mPFC connection impaired remote, but not recent, memory retrieval. Thus, the LEC and mPFC connection is necessary for the retrieval of a remotely, but not recently learned associative memory. Increased reliance on the entorhinal-prefrontal connection indicates the strengthening of functional connectivity between the two regions, which may be a biological correlate for the proposed reorganization during systems consolidation.