The Depletion Of The Rat Model Of Monoamine

Major depressive disorder is one of the most common mental disorders, with a 12-month prevalence of 6.7% of adults in the United States (NIMH). There is no definite etiology of depression, but several risk factors have been identified. Functional and structural changes in the brain have also been explored. The most common treatment for depression is the use of drugs that act on monoamine transmitters, including norepinephrine, dopamine, and serotonin. Decreases in these transmitters, especially serotonin, were hypothesized to play an important role in the cause of depression (Breedlove & Watson, 2013). The serotonin hypothesis led to the development of selective-serotonin reuptake inhibitors (SSRIs), which increase the amount of serotonin in the brain. Further research suggests that the serotonin hypothesis is not entirely accurate and the neurobiology of depression is much more complex. The “chemical imbalance” explanation of depression may not reflect the full range of causes and may be given greater credibility by patients and doctors than is supported by evidence based research.

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

A cohort of mice underwent a second mTBI after 24 hours. Mice from both WT and Tg groups were assessed 2 days, 9 weeks, and 16 weeks after mTBI treatment. Primarily, H&E stain was employed along with Gomori’s iron stain to localize site and severity of mTBI injury. The degree of A deposition in the somatosensory cortex (SSC), the perihippocampal cortex (PHC), and the hippocampus (HP) of both hemispheres was determined by 4G8 immunostaining. In addition, GFAP staining was used to quantify the population of astrocytes at the site of the injury. Furthermore, Sandwich ELISA was utilized in mice groups 16 weeks after injury to measure A40 and A42 peptide levels in various brain regions, including the cerebral cortex, the hippocampus, and the cerebellum. Such tissues were also analyzed for isoprostane levels that are produced by lipid peroxidation. Isoprostanes were also detected in urine samples at various survival periods. Moreover, mice underwent Morison water maze (MWM) and composite neuroscore (NS) tests at 16 weeks’ post-injury to examine cognitive and motor functions respectively. Uryu and collegues found a significant increase in iron deposits and reactive astrocytes in the repetitive mTBI postmortem sections of Tg mice, when compared to other groups at 16 weeks after the injury. This was not the case in WT mice. Similarly, there was a significant increase in the A burden within select brain regions (i.e. SSC, PHC, HP) of single and

Although many studies have shown that impaired neurotransmission of serotonergic and dopaminergic pathways are related to depression [2], the pathophysiology of depression is yet to be fully elucidated [3]. Several studies are being conducted to unravel the underlying mechanism in evaluating the therapeutic efficacy of antidepressants [4,5]. More so, chronic stress exposure has been found to cause atrophy of neurons in rodent hippocampus. [6,7] As such, decreased hippocampal plasticity might be closely connected to depression. Recent studies have found that administration of antidepressant agents to either stress-induced models or patients could heighten developed neurons in the hippocampus, which in turn attenuates the depression symptoms [8,9]. Researches have demonstrated that the expression of SYP is reduced in brain of depressed patients, suggesting a correlation to the pathophysiology of depression [10,11]. Brain magnetic resonance imaging shows that hippocampal volume is significantly smaller in patients with depression compared with normal control [12]. In vitro experiments have also established that depression ensues along with high levels of cell apoptosis as well as increased protein level of Beclin 1 and LC3 [13, 14]. Thus, apoptosis and autophagy

Neurorestorative events include neurogenesis, gliogenesis, angiogenesis, synaptic plasticity and axonal sprouting. neuroprotection mentions to the relative preservation of neuronal structure or function. Numerous mechanisms behind neurodegeneration are the same. General mechanisms consist of increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory alters, iron accumulation, and aggregation of protein. Some of neuroprotective treatments including Glutamate antagonists, Caspase inhibitors, Trophic factors, Anti protein aggregation agents, Therapeutic hypothermia, Erythropoietin has been reported to protect nerve cells from hypoxia-induced glutamate

The prolonged excitatory activation of ionotropic N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors as well as metabotropic glutamate receptor lead to neuronal cell death (Caccamo et al., 2004, Park et al., 2004). It is commonly accepted that ionotropic glutamate receptors are responsible for the harmful effect of excitotoxicity. The continued binding of excess glutamate to NMDA receptor induces the uncontrolled influx of calcium ions (Ca2+). This massive overload of intracellular Ca2+ leads to activation of calpain and mitochondrial oxidative phosphorylation which ultimately causes apoptosis (Caccamo et al., 2004, Choi, 1992, Lawson and Lowrie, 1998). The AMPA receptor is involved in regulating the influx of sodium ions (Na+). The continued activation of AMPA receptors, due to the unwarranted glutamate level, induces influx of Na+ which consequently leads to osmotic imbalance and swelling of the neurons (Caccamo et al., 2004). The excess swelling of neurons can leads to necrosis (Park et al., 2004). Consider as a therapeutic target, extracellular glutamate concentrations increase to neurotoxic levels within the first three hours after the injury (Liu et al., 1999, Liu and Bilkey, 1999, McAdoo et al., 1999), leaving a small time window for immediate treatment to prevent

Nervous based stimulants can increase depression, increase mental illness, cause psychosis, lower sensory perception, impair of memory performance, cause cardiovascular difficulties, and lower the brain’s ability to transport and receive dopamine. Amphetamine based nervous stimulants should be properly used as prescribed by one’s doctor to help avoid any harmful effects. Chronic use of the drugs may cause the need to have rehabilitation and follow psychotherapeutic measures. As more are prescribed with amphetamines, it increases the need to develop protective measures to prevent chronic

The analyses demonstrated extensive contrast in ChE and NOS activities in the different parts of rat brain. The most astounding action was distinguished in the brain stem and cerebellum, bring down in basal ganglia and the least in the frontal cortex. The high NOS activity in the cerebellum is in concurrence with the outcomes portrayed by other authors.(13,14,15,16) In the present work, the i.p infusion of various dosages of the carbamate sevin brought about the inhibition of both ChE and NOS. Moreover past reviews demonstrated that the organochlorine and organophosphorus mixes attributable to their lipophilic nature, tie to the hydrophobic area of CaM and in this way impede CaM subordinate NOS activities like Ca2+ATPase phosphodiestrase.(16)

Serotonin syndrome is a drug-induced syndrome that results in mental, autonomic and neuromuscular changes. A range of toxic symptoms including clonus, hyperreflexia, tremor, agitation, confusion and shivering are results of the increased serotonin concentrations in the central nervous system (Hall and Buckley, 2003). Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter produced from the decarboxylation and hydroxylation of tryptophan. Serotonin is stored within the vesicles and released into the synaptic cleft when stimulated (Volpi-Abadie et al., 2013). As serotonin influences on mood, sleep, vomiting and pain perception, the serotonin levels are tightly regulated by the reuptake mechanisms, degradation by monoamine oxidase type A and feedback loop (Thanacoody,

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).

The in vivo experimental model shows a progressive selective degeneration of nigrostriatal dopaminergic neurons and the formation of Lewy bodies as in PD. And these experiments show the relevance of the development of PD by the pesticide exposure and the defect of systemic complex I. but in MPTP, it produces inhibition of Complex I in the catecholaminergic neurons only.

Alzheimer’s disease (AD) is a debilitating illness of the nervous system, affecting millions of geriatric population worldwide. Numerous factors are involved in the disease etiology viz. tau phosphorylation, amyloid β protein (Aβ) accumulation, lipid dysregulation, oxidative stress and inflammation. Among all factors oxidative stress plays a central role in the pathogenesis of AD leading to neuronal dysfunction and cell death (1). Oxidative stress is caused due to the increased production of reactive oxygen species (ROS) which denatures biomolecules such as proteins, lipids and nucleic acids through pathological redox reactions(2). Increased oxidative stress also results in excessive lipid peroxidation, weakening the cell membranes, causing

According to energyfiend.com a study in Japan showed that caffeine increases memory and has been shown to decrease the rate of Alzheimer’s. This study also showed that caffeine can decrease depression by increasing Dopamine (A mood altering hormone) in the brain. With the increase in production of Dopamine, daily intake of caffeine has also been shown to decrease the rate of Parkinson’s disease.

The rat studies showed that TCE exposure inhibited mitochondrial function in the substantia nigra, an area in the brain that produces dopamine and whose

During ischemia, adenine nucleotide catabolism results in an increase the intracellular concentration of hypoxanthine, which is then converted into toxic reactive oxygen species (ROS) upon the reoxygenation of tissue(Collard et al.,2001).