N-Methyl-Glutamate Carrier Protein Analysis

AD is a progressive age-related neurodegenerative disorder that poses increasing challenges to the global healthcare system and economic development. AD is characterized by extracellular neurotic plaques composed of Aβ deposits and intracellular neurofibrillary tangles composed of hyperphosphorylated tau with progressive loss of synapses in the brain [1]. Evidence demonstrates a potential link between oxidative stress, mitochondrial dysfunction and AD development [2]. Oxidative damage has been known to occur at a very early stage of AD even prior to Aβ plaque formation and the onset of symptoms [3, 4, 5]. Several cellular changes by oxidative stresses have been related with Aβ plaques formation and pathophysiological events of AD [6].

NMDA Receptor is one of the crucial glutamate receptors present in the nerve cell. It gets activated when glutamate or Glycine binds to it. NMDA receptor is known for its role in synaptic plasticity and membrane function (learning and memory). Its activity is highly dependent on calcium influx. It is a tri heteromeric receptor with three different subunits NR1, NR2 and NR3. Each subunit has several other subunits, each of them having a unique function: NR1 has 8, NR2 has 4 (NR2A, NR2B, NR2C, NR2D), NR3 has 2 (NR3A, NR3B). Out of all the subunits, NR2A and NR2B have been extensively studied. NR2A, also known as GluN2A is believed to be involved in cell death pathways whereas NR2B, also known as GluN2B is believed to be involved in cell survival cascades (Bayer et al., 2006). Interestingly, GluN2B and GluN2A have differing roles, and both can affect either long-term potentiation (LTP) or long-term differentiation (LTD)

The amount of aspartic acid from aspartame is less than would be expected from other dietary sources. Aspartame gives only between 1% and 2% of the daily intake of aspartic acid. According to some researches, it may lead to excitotoxicity when aspartame is combined with other amino acids such as glutamate. However, clinical studies have not shown any sign of neurotoxic effects, and suggest it is not possible to ingest enough aspartic acid and glutamate through food and drink to amounts that can cause

At the molecular level of explanation these processes are dependent on the interplay between glutamate receptors, Ca2+ channels, the increase of intracellular Ca2+ levels, Ca2+-dependent proteins like Akt, ERK, mTOR and neurotrophins such as brain derived neurotrophic factor (BDNF) (24, 25).

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

Introduction. Dysregulation of β-cat causes abnormal brain development (121-123) and defective dendritic morphogenesis (124, 125). By interacting with N-cadherin, β-cat shapes synaptic structure (83, 84) and regulates excitatory postsynaptic strength (126, 127). In addition, the axonal localization and translation of β-cat modulate presynaptic vesicle release (128-130). As a consequence, abnormal levels of β-cat in different brain regions or circuits lead to impaired memory (12, 131, 132), and a depression-like phenotype (91). However, the circuitry mechanisms for how β-cat dysfunction leads to the pathogenesis of ASDs are largely unknown. An imbalance of excitatory and inhibitory signals has been implicated in the pathophysiology of

The majority of neurons, at least within the central nervous system, contain both AMPA and NMDA receptors. Under normal conditions, the NMDA receptor is blocked by a magnesium ion,

Attempts to cure or slow down the progression of Parkinson’s disease have largely failed; researchers in this paper maintain this is obviously a direct result of the lack of insight into the pathogenesis of the disease. Parkinson’s disease is the product of the deaths of a number of dopaminergic (dopamine-secreting) neurons in the substantia nigra pars compacta region (SNc) of the brain. But what causes these deaths? In the paper “‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease,” Chen and researchers find that older neurons in the SNc are unusually reliant on calcium channels and that after blocking these channels, the cells are “rejuvenated” and begin acting like their juvenile counterparts; as a

In the cord preparations with TTX treatment, 5-HT application reintroduced the negative slope conductance in the I-V curve of healthy motoneurons failing to show the negative slope conductance in the presence of NMDA alone (Schmidt and Jordan, 2000). Moreover, in other motoneurons showing the negative slope conductance in the presence of NMDA alone, 5-HT caused the negative slope conductance to shift toward the hyperpolarizing direction, which could be reversed by 5-HT antagonist mianserin (Schmidt and Jordan, 2000). Reducing the bath concentration of Mg2+ also mimicked the hyperpolarizing shift of the negative slope conductance by 5-HT (Schmidt and Jordan, 2000). Via 5-HT2 receptor activation, protein kinase C (PKC) can enhance the hyperpolarizing shift of the negative slope conductance in the I-V curve of NMDA receptors and also reduce Mg2+ blockade of the receptor channels (Blank et al., 1996; Chen and Huang, 1992). Therefore, the effect of 5-HT on the negative slope conductance of NMDA receptors may result from reduction of Mg2+ blockade of the receptor channels. Even more interestingly, Li and Zhuo (1998) discovered that 5-HT can induce the transformation of silent glutamatergic synapses into functional ones in some rat superficial dorsal horn neurons (Li and Zhuo, 1998). They detected silent synapses, which are excitatory postsynaptic currents mediated by NMDA receptors, by depolarizing the cells from -70 mV to +40 mV (Li and Zhuo, 1998). However, 5-HT

The central objective of this thesis is the complete In-Vitro and preliminary In-Vivo development of biosensor devices suitable to measure the excitatory neurotransmitters, Aspartate and Glutamate, within the ECF of the brain, and for the subsequent characterisation of these devices. Owing to the circumstance that both Aspartate and Glutamate are actually electro-inactive compounds, their direct electrochemical detection is not possible. As such, another means of detection was required to overcome this situation and is provided for by way of an “indirect” measuring system. The enzymes, aspartate oxidase, (L-AOx), and glutamate oxidase, (GluOx), react selectively towards aspartate and glutamate respectively. During each of these reactions, hydrogen peroxide, (H2O2), is produced, which is readily electrochemically detected. Consequently, the production of this particular molecule made these enzyme/substrate pairs choice candidates for our purpose.

rubbing, chewing generalized seizures involve all areas of the brain absence: occur in clusters; blank staring and subtle movement e.g. blinking tonic: muscles stiffen atonic or “drop: sudden loss of muscle control clonic: rhythmic jerking of neck, face, arms myoclonic: sudden brief jerking of limbs tonic-clonic: loss of consciousness, whole body stiffening or jerking CORRECT MECHANISM glutamate ionotropic receptors: all permeable to Na and K ions alpha-amino-2,3-dihydro-5-methyl-3-oxo-4-isoxazolepropanoic acid (AMPA kainate N-methyl-D-aspartate (NMDA) has Ca channel blocked by Mg ions in membrane depolarization, Mg is displaced and Ca floods cell glutamate metabotropic receptor

The major effect of acidosis is depression of the central nervous system. When the pH of the blood falls below 7.35, the central nervous system malfunctions, and the individual becomes disoriented and possibly comatose as the condition worsens. Causes for acidosis include things such as; obesity, disease of the airway and diseases involving the chest. (Hadjiliadis, 2014)

The present findings showed the development of hyperexcitability in the cerebellum of rat model of PD induced by intrastriatal injection of rotenone. This was indicated from the significant increase in the excitatory amino acid neurotransmitters; glutamate and aspartate and the significant decrease in the inhibitory amino acids; GABA, glycine and taurine. These neurotransmitters are involved in many functions such as motor behavior, cognition, and emotion (Ottersen and Storm-Mathisen, 1986, Schmidt et al., 1992)1,2. The balance between excitatory and inhibitory neurotransmission is important for brain to sustain proper neuronal function (Mel et al., 2004)[1]. Perturbation in glutamatergic and GABAergic neurotransmission is associated with several neurological and psychiatric disorders (Sanacora et al., 2004) (3) [glutamate gaba balance 1].

By 6-OHDA intrastriatal injection, progressive neuronal degeneration is caused in the substantia nigra and ventral tegmental complex (ST-VTA).

There are billions of nerve cells in a human brain. Neurodegenerative diseases, like Parkinson’s and Huntington’s disease cause the selective loss of approximately 500,000 cells in the brain which once performed critical functions. (Bachoud-Levi, 2000) The loss of these cells results in result in devastating, oftentimes fatal symptoms. The course of these disease is often gradual and occurs over many years, producing an overall deterioration of motor skills and brain function. While the cause of neurodegenerative diseases has been theorized, the specifics of the causes are unknown. (Ezzell, 1992) Less than five percent