Comparing The Different Classes Of Glutamate Receptors Essay

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).

The main components of the synapses are as follows: The Axon terminal, found at the end of the Axon, passes neurotransmitters to other neurons via synaptic transmission. Synaptic Vesicles contain neurotransmitters within the Axon. Neurotransmitters themselves are chemical messengers that travel through the neurons and activate receptors on the receiving cell. The neurotransmitters are diffused through the synaptic cleft—a region between the two neurons and gap the neurotransmitter needs to cross to make it to the receiving cell. Said receiving cell is what receives the neurotransmitters and starts the process over again. The receptors on the cell are structures that receive the neurotransmitters and

Glutamate-receptor-interacting protein (GRIP) is the interacting protein which is associated with AMPAR protein receptor in the postsynaptic cell. Amount of GRIP is associated with AMPAR receptors can lead to the prediction of activity in the presynaptic cell. AMPAR receptor change shape to be ready to receive neurotransmitter when GRIP bind. The presynaptic cell contains vesicle which neurotransmitters are accommodated. When calcium enters the presynaptic cell by calcium channel, vesicles dock to the presynaptic cell to become ready to release neurotransmitters to the synaptic gap. Neurotransmitters are released in a packet called quanta. AMPAR receptor has to change its shape by GRIP to receive the release of quanta in the synaptic

Neurotransmitters are chemicals made by neurons and used by them to transmit signals to the other neurons or non-neuronal cells (e.g., skeletal muscle; myocardium, pineal glandular cells) that they innervate. The neurotransmitters produce their effects by being released into synapses when their neuron of origin fires (i.e., becomes depolarized) and then attaching to receptors in the membrane of the post-synaptic cells. This causes changes in the fluxes of particular ions across that membrane, making cells more likely to become depolarized, if the neurotransmitter happens to be excitatory, or less likely if it is inhibitory.

Once in the synapses, the impulses triggers the release of chemical messages called neurotransmitters; which then bind to receptors on the receiving cell as the transmission of the impulse repeated again. The message or impulse continues traveling from one neuron to the next throughout the body until it reaches its destination as it relays a signal. All of this activity happens in less than a split second and without conscious thought. At the end of this process, the brain has the task of interpreting the message and making the decision as to what to do with this new information. (Carlson, 2011.Pg.45-52)

Previous data proposes impairments in synaptic proteins of specific NMDA receptors (GluN2B, GluN2A, GluN1), AMPA receptors (GluR1, GluR2), Calcium Calmodulin Kinase, Protein Kinase A/C, CREB (cAMP response element binding protein), signalling molecules of MAPK (Mitogen-Activated Protein Kinase) – ERK (Extracellular Receptor Kinase), Akt (Protein Kinase B) etc (Minh Vu Chuong Nguyen et al., 2012).

Every day, your brain maintains a delicate balance between chemicals that push its cells to fire and opposing chemicals that pull its cells back toward inactivity. Two of the most common neurochemicals that play this tug of war are glutamate and GABA, both of which are classified as neurotransmitters, chemical messengers that communicate between neighboring brain cells. The purpose of glutamate is to elicit action, while the function of the GABA neurotransmitter is to restore calm.

Wang, et al, said that synaptic plasticity (the ability to strengthen or weaken synapses over time) was heavily influenced by astrocytes because of their role in glutamate production and uptake; specifically, LTP and LTD. The course and distribution of glutamate in and around the synapse is important for the coordination of intracellular messaging which directly affects synaptic strength. According to the multipartite synapse concept; glutamate regulation is dictated by astrocytes which can also release D-serine (glutamate co-agonist) to enhance NMDA receptor activity causing excitatory transmission which encourages synaptic plasticity (Panatier et al., 2006.) High K+ extracellular fluid (ECF) concentrations also encourage synaptic plasticity because it initiates glutamate release, this is also mediated by astrocytes since they buffer ECF K+ composition.

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,

In glutamatergic synapses the neurotransmitter glutamate transmits nerve impulses. Glutamate is the prevalent excitatory neurotransmitter in the central nervous system (CNS). It can act on two distinguished receptors: ligand gated ion channels (ionotropic receptors) and G-protein coupled receptors (metabotropic receptors). In addition, several drugs can interfere with glutamatergic such as: Riluzole, N-Acetylcysteine (NAC) and Tezampanel.

Schizophrenia research has examined many glutamatergic components, which has altered the Glutamate Hypothesis many times; nonetheless, the updated hypothesis explains Schizophrenic symptoms as the result of the malfunctioning of NMDA (n-methyl-d-aspartate) receptors, which are ionotropic glutamate receptors (Howes et al., 2015). For instance, a psychopharmacological study by Krystal et al. (1994) examined the effects of Ketamine, an NMDA non-competitive antagonist, on behavior. They observed the behavior of three groups of healthy adults that were administered a placebo or a high or low dose of Ketamine via an I.V. injection. Subsequently, those injected with Ketamine presented dose-dependent schizophrenia-like behaviors that were similar to positive and negative symptoms (Krystal et al., 1994). Similar studies have replicated these findings; however, to ensure that these behaviors are not only related to acute treatment, other studies have looked at prolonged use. Stone et al. (2014) compared the mental states of a group of chronic Ketamine users with a group of poly-drug users, and found that six of the fifteen chronic Ketamine users were formally at-risk for a psychotic episode, while none of the poly-drug users fit such criteria. Secondly, they used proton magnetic resonance spectroscopy (H-MRS) to measure the activity of glutamatergic system proteins, such as glutamine, creatine, and N-acetyl aspartate (NAA), in

This synaptic specificity does not only take place in the cellular layers but also in the subcellular level. Therefore, the signal pathway that occurs in both the cellular and subcellular passes through the positive and the inhibitory cues. The positive cues allow the recognition of partner cells and chaining membranes, however, it can also miscommunicate the recognition to non-target cells. The inhibitory cues are on the non-target cells, and they are essential regulators for synapse specificity. Essentially, these cues function as passages that allow or prevent connections and recognitions of cells, and also help in the distribution of synapses alongside the

What happens during synaptic transmission ? Well what occurs during synaptic transmission is most communication between neurons occurs at a specialized structure called a synapse this is an area where two neurons come close enough to touch another. they are able to pass chemical signals from one cell to another.the neurons are not actually connected but they are separated by microscopical small space called the synaptic cleft. The neuron were the signal is initiated is called the presynaptic neuron. The neuron that receives the signal is called the postsynaptic neuron .the Chemical signals called neurotransmitters that are packaged into small sacs are called vesicles each vesicle can contain thousands of neurotransmitter molecules when the

Neurotransmission plays an essential role in communication between neurons. In such process, neurotransmitters are released by the axon terminal and those bind to a receptor on the dendrite of another neuron. Among all neurotransmitters, glutamate is the most significant one in vertebrates. It is used in a large percentage of circuits in the cerebral cortex that support learning and complex behaviors. Modifications to transmission of glutamate will affect the function of neural circuits on a large scale in the brain.[1] Glutamate transmission can be studied at the level of individual dendritic sites. In this case, recent studies

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].