Chemical Evaluation Of Zinc Effects At 5 Ht1ar And Serotonin Neurotransmission

However, invasive methods and stress causing techniques are still used in animal research today as evident in a study by Meaney et al. (2011) which involved both socially raising rats and isolating others. Further, the investigation involved the killing of the rats in order to obtain brain tissue for the study of differences in the development of the glucocorticoid receptor (GR) systems in various parts of the brain. The study found the GR was enhanced due to prolonged single stress exposure in the prefrontal cortex and the hippocampus. Early handling of the rats protected them against ongoing stress-induced of GR expression of the prefrontal cortex, but not in the hippocampus. The study highlights the importance that the early life upbringing

These adaptive mechanisms can become maladaptive if unresolved after precipitating events have passed, leading to interferences in emotional regulation (Liston, McEwen, & Casey, 2009; Juster et al., 2011). Imaging studies show alterations in the brain structures that assist in regulation of the stress response—the amygdala, hippocampus, and prefrontal cortex—due to prolonged exposure to stress (Carrion et al. 2010; Rao et al. 2010). The over activation of this fear circuitry in the brain can lead to distorted processing, contributing to depression (Thienkrua et al., 2006; Neria, Besser, Kiper, & Westphal, 2010; Rao et al., 2010), anxiety (Derryberry and Reed, 2002; Goldin et al., 2009; Graham and Milad, 2014), and mood impairments (Kobasa, 1979; Linehan, 1993; Haller and Miles, 2004). These cognitive changes can also contribute to insomnia, chronic pain, addictive disorders, impairment of immunity, and development of coping mechanisms such as smoking, use of alcohol or drugs, overeating, and other survival mechanisms (Raja, 2012). The allostatic load of a chronically over-activated hypothalamus-pituitary-adrenal system can lead to development of comorbid health conditions such as cardiovascular disease,

showed that prenatal stress decreases cell turnover and proliferation in the hypothalamus of adult rats, which reduces structural plasticity and reduces the response to stress in adulthood. This study also showed that when prenatally stressed rats were stressed in adulthood the females showed an increase in corticotropin-releasing hormone suggesting it to be an up-regulation in the hypothalamic-pituitary adrenal axis. Males showed no elevation of corticosterone levels. Increase in adrenocorticotropic hormone with no effect of adult stress and a decrease in the corticotropin-releasing hormone mRNA in the hypothalamus showed a down-regulation. The author concludes that this makes prenatally stressed females less reactive to later life stressors than

The PVT has shown to have implications in stress processing due to its diverse population of neurons, holding a variety of functions. People are still discovering more about the PVT and its roles, but it is important to be able to categorize the neurons directly involved in stress. To discover more, I worked with c-fos, a protein which is a promoter for previous neuronal activity for the two restraint-stress experiments. For the first experiment, I used immunohistochemistry to label neurons expressing c-fos in both control and restraint mice. The raw data shows that with restraint there is an increase of c-fos expression in the PVT. In addition, the stainings show that there are two groups of neurons activated during times

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

What is more, several metabolomic studies to investigate drug response on patients with a chronic mild stress (CMS) model of depression were performed. One of these, conducted by Zhao and colleges, identified biochemical changes induced by two widely used anti-depressants: fluoxetine and imipramine [83]. Metabolic profiling of hippocampus of C57BL/6J mouse by gas chromatography-mass spectrometry

Further concerns arise from the authors’ conclusion that EA benefits are specific to St36 stimulation. Eshkevari et al. cite elevated ACTH and CORT levels in sham-EA rats as evidence that the suppression of the stress hormones is specific to EA at St36. The results section, however, reveals

The hypothalamo-pituitary-adrenocortical (HPA) axis is a critical adaptive system that maximizes survival potential in the face of physical or psychological challenge. The principal end-products of the HPA axis, glucocorticoid hormones, act on multiple organ systems, including the brain, to maintain homeostatic balance. Ryan Jankord and James P. Herman LIMBIC REGULATION OF HYPOTHALAMO-PITUITARY-ADRENOCORTICAL FUNCTION DURING ACUTE AND CHRONIC STRESS

notably altering behaviour and cognition, as well as disease susceptibility in adulthood (6). Stress hormones like glucocorticoids and CRH could interact with their receptors in the foetal brain, which have an influence on neuronal differentiation and function at different stages of development (9). During pregnancy, maternal psychosocial stress threatens the CNS and shortens the length of gestation (8). Low birth weight can also alter brain development and is associated with behavioural and cognitive disorders in adulthood (1, 4, 5, 6, 7, 8, 9). The offspring of stressed mothers are more likely to have reduced head circumferences (7), show emotional problems (7, 9), impaired memory (4, 5, 7) as well as supress cognitive performances including schizophrenia (5, 6, 9), attention deficit (5, 6, 9), antisocial behaviour (2, 6, 7), increased vulnerability to post-traumatic stress disorder (PTSD), learning difficulties (6, 9), anxiety disorders and depression (4, 6, 8, 9), impaired intelligence and thus lower school grades (7,

Mo, C., Renoir, T., & Hannan, A. J. (2014). Ethological endophenotypes are altered by elevated stress hormone levels in both huntington's disease and wildtype mice. Behavioural Brain Research, 274, 118-127. doi:10.1016/j.bbr.2014.07.044

The triggering of the large doses of hormones then triggers the hypothalamic-pituitary adrenal, HPA, axis. An HPA axis that is continuously activated can have some serious damaging effects. Some downsides of having an activated HPA are: impaired memory, shrinking of the hippocampus, increased risk of depression, and a weakening of the immune system. Along with the HPA axis, whenever the flight- or- flight syndrome is activated, stress hormones, also known as glucocorticoids, are secreted. A person’s genetic pattern and genes result in vulnerability to illnesses. A persons whose parents were exposed to depression are 1.5 to 3 times more likely to develop the disorder to those whose parents did not suffer from depression. Also, if one identical twin develops depression approximately 76% of the time the other twin will also develop depression. Genetic influence does not necessarily guarantee a person to develop depression but highly increases their chances. Studies: A study investigating DNA in relation to depression was done on 971 sibling pairs who were affect by recurrent

Exposure to chronic stress acts as a risk factor as well as a precipitating agent for mood and anxiety disorders, and such stress in early life manifests itself in common mental disorders in adults [1, 2]. Majority of studies focus on the manifestation of stressful experiences in young, but there are less reports on the immediate consequences of early-life stress. Such stress activates neuroendocrine adaptive responses to cope with consequent crisis. However, due to prolonged or chronic stress, these neuroendocrine responses turn maladaptive and contribute to a phenomenon known as allostatic load [3]. These stressful events act as predisposing factors in the development of psychiatric disorders and anxiety- and depression-associated behavioural alterations in susceptible individuals [3, 4].

The effects of stress various during the aging process, young children and the elderly are more prone to be sensitive to stress during these age periods of development. Individuals that are exposing to stress earlier in life have an increase reactivity to stress and demonstrate cognitive deficits in adulthood (Lupien et al, 2009). Production of glucocorticoids increases when stress activates the hypothalamus pituitary adrenal axis (HPA) (Lupien et al, 2009). Thus the receptors are than expressed throughout the brain; duties are to act as transcription factor in order to regulate gene expression. Whereas, glucocorticoids will than have a long term effect on the functioning of the brain. There have also been research in regards of prenatal stress that have affected the hippocampal MRs and GRs which resulted in an increase of glucocorticoid secretion in the brain (Lupien et al, 2009). There have been cases that have demonstrated when prenatal exposure to glucocorticoids can lead to an increase in adult corticotropin –releasing hormone which is located in the central nucleus of the amygdala (Lupien et al, 2009). The amygdala is an important

The temporary inactivation of basolateral amygdala prevents the stress-induced microgliosis. NC = Normal control (n = 06), ST = Stress (n = 06), LI+ ST = Lidocaine + Stress (n = 06), VC (SAL) + ST = Vehicle + Stress (n = 06), SC (LI) = Sham control (n = 06), LI per se = Lidocaine per se (n = 06) and VC (SAL) per se = Vehicle per se (n = 06). (B) Representative pictures of normal control, stress and permanent inactivation of BLA stained with Iba-1. The permanent inactivation of basolateral amygdala prevents the stress-induced enhanced microglial expression. One-way ANOVA followed by Tukey’s test. Data expressed as Mean ± SEM.**p<0.001 vs. ST; NC = Normal control (n = 06), ST = Stress (n = 06), IBO + ST = ibotenic acid + stress (n = 06), VC (PBS) + ST = Vehicle + stress (n = 06), SC (IBO) = Sham control (n = 06), IBO per se = Ibotenate lesion per se (n = 06) and VC (PBS) per se = Vehicle per se (n =

Anti-depressants are neurotransmitters classified as serotonin biogenic amines that are mainly inhibitory and secreted in the central nervous system, especially in the midbrain (Marieb and Hoehn 2013). Most antidepressants are taken for depression, but they are also used for treating anxiety disorders. They work by increasing serotonin levels in the brain to decrease depression (Study Ties Antidepressant Use… 2014). The