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Neurotransmitters gaba and glutamate,what to eat when you have cancer,zone diet basics,paleo healthy desserts - PDF Review

Dopamine is the neurotransmitter used by the reward pathway (also called the mesolimbic pathway, which is closely linked with the mesocortical pathway).
Dopamine and another neurotransmitter called serotonin are released by just a small number of neurons in the brain.
Serotonin is another neurotransmitter affected by many drugs of abuse, including cocaine, amphetamines, LSD, and alcohol. Serotonin plays a role in many brain processes, including body temperature regulation, sleep, mood, appetite, and pain. Glutamate and GABA (gamma-aminobutyric acid) are the brain's most plentiful neurotransmitters.
Since GABA is inhibitory and glutamate is excitatory, both neurotransmitters work together to control many processes, including the brain's overall level of excitation. Amino acid transmitters provide the majority of excitatory and inhibitory neurotransmission in the nervous system.
Neurons receive many thousands of synaptic inputs some excitatory, some inhibitory, and some modulatory. Inhibitory synapses (like those utilizing glycine and GABA) tend to be localized near the neuronal soma and are referred to as Type II (Figure 13.2, box labeled Axosomatic synapse). Initially, amino acids were not considered viable candidates for neurotransmitters since they are ubiquitous cellular constituents and are required for protein synthesis. Amino acid neurotransmitters are all products of intermediary metabolism with the exception of GABA. Glutamate and aspartate are products of the Kreb's cycle, and both have excitatory effects in the CNS.
The actions of glutamate are terminated by high-affinity uptake systems in neurons and glia (represented by red cylinders in the neuron and glia membranes). Glycine is the main neurotransmitter that mediates the inhibitory actions of spinal cord interneurons.
All of these amino acid neurotransmitters are released by Ca2+-dependent exocytosis at presynaptic specializations as discussed in Chapter 8, Part 7 and Chapter 10, Part 4.
Receptors for each of the amino acid neurotransmitters can either directly open an ion channel (ionotropic) or couple to a G-protein (G-protein coupled receptor; GPCR) except for glycine.
Ionotropic glutamate receptors open channels that cause the cell to depolarize and are therefore excitatory (driving the membrane potential towards firing an action potential). GABA and glycine ionotropic receptors are selectively permeable to Cl- (reversal potential near -70 mV). The ionotropic and G-protein coupled GABA receptors are referred to as GABAA and GABAB, respectively.
The GABAA receptor is composed of five subunits that each contain four membrane spanning domains. The glycine receptor, like the GABAA receptor also permits the influx of Cl- into neurons and displays a reversal potential near -70 mV. Glutamate GPCRs are members of a large family of receptors that couple with G proteins to produce their effects. The glutamate GPCR's best known effects are the activation of phospholipase C which generates inositol-trisphosphate (IP3) and diacylglycerol (DAG) from the precursor lipid phosphatidylinositol bisphosphate (See Figure 13.8). The GABAB receptor, like the glutamate GPCR, produces its effects not by directly opening ion channels, but by coupling to G-proteins and enzymes that influence metabolites within the neuron.
Two basic mechanisms, diffusion and high affinity uptake, terminate the response to amino acid transmitters. The neurotransmitter glutamate is highly toxic to neurons when present for extended periods. Because glutamate is the major excitatory transmitter in the human brain, derangements in glutamate metabolism or receptor activation have been implicated in a wide variety of pathologic conditions.
One explanation for the establishment of focal epilepsy is decreased local GABA-mediated inhibition. Mood disorders (generalized anxiety disorder) can also be controlled by drugs which potentiate GABA's inhibitory activity.
Glutamate is recovered into a usable pool for neurons through it's metabolism in glial cells.
Glutamate is removed from the extracellular space by high-affinity up-take transporters in the plasma membranes of neurons and glia.
A critical feature of the NMDA receptor is that at the resting potential of the neuronal membrane it is inactive even if glutamate is bound. Opening of K+-channels will produce inhibition by hyperpolarizing the membrane potential, but GABA and glycine do not open ion channels permeable to K+. Donations to Neuroscience Online will help continue development of new features and content. Since GABA is inhibitory and Glutamate is excitatory, both neurotransmitters work together to control many processes, including the brain’s overall level of excitation.
Benzodiazepines (benzos) effect GABA, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties. When you go off Lamictal it’s like you’re pushing down the gas pedal on the Glutamate system.
Brain pathways are made up of interconnected neurons, and signals travel along them from one brain region to another. But there are two other important pathways in the brain that use dopamine: the nigrostriatal pathway and the tuberoinfundibular pathway. Problems with the serotonin pathway are linked to obsessive-compulsive disorder, anxiety disorders, and depression.
Many of the drugs of abuse change the balance of glutamate or GABA, exerting tranquilizing or stimulating effects on the brain. Excitatory synaptic connections are typically found on the major receiving area of the neuron, the dendrite, and most often on spines that project from the dendrite (Figure 13.2). Morphologically, the synapses again have specializations for release of vesicles and for anchoring receptors.

Also, unlike the specific enzymes in neurons that synthesize ACh and catecholamines, enzymes that synthesize glutamate, aspartate and glycine are not unique to neurons.
Unlike all the other amino acid neurotransmitters, GABA is not used in protein synthesis and is produced by an enzyme (glutamic acid decarboxylase; GAD) uniquely located in neurons.
They are produced in the mitochondria, transported into the cytoplasm, and packaged into synaptic vesicles (Figure 13.4). Under normal circumstances most uptake is back into the neuron and this glutamate can immediately be pumped into vesicles for subsequent release. The block of inhibition leads to hyperexcitation and typically a patient with strychnine poisoning asphyxiates due to an inability to relax the diaphragm.
All vesicles (both small molecule and neuropeptide) also contain ATP that is co-released when these vesicles fuse with the membrane. There is no known GPCR for glycine and all of glycine's effects are mediated through an ion channel permeable to Cl-.
The reversal potential (near 0 mV) of the EPSP indicates that glutamate opens receptors selectively permeable to cations (Na+, K+, and Ca2+). First, they have a high permeability to Ca2+ (although they are also permeable to Na+ and K+), and when they open significant increases in the level of Ca2+ can be detected in the neuron (Figure 13.10).
When they open, they cause the neuron to hyperpolarize and therefore drive the membrane potential away from the threshold for firing an action potential.
When GABA is released into the synapse, it binds to a population of the available receptors, but typically not all of them (Figure 13.12). These receptors like those for serotonin, norepinephrine, epinephrine, muscarinic ACh, and dopamine, produce the large majority of their effects through alterations in the activity of metabolic enzymes and not by directly opening ion channels in the membranes. Reported effects include alterations (either increases or decreases) in cAMP levels, increases in K+-conductance, and decreases in Ca2+-conductance. One of the best understood clinical conditions involving glutamate is neuronal injury following stroke or trauma. Many facets of epilepsy can be elicited experimentally by blocking GABA receptors with the toxin picrotoxin previously described. Some of the most widely prescribed drugs-benzodiazepines (Librium and Valium)-produce their pharmacological effects by increasing GABA's ability to hyperpolarize neuronal membranes, thereby quieting the system. Results in its metabolism into GABA by glutamic acid decarboxylase This answer is INCORRECT. When glutamate is bound and the membrane potential moves towards positive the receptor becomes unblocked, permitting ion flow.
Require membrane depolarization to permit ion flow and are NOT permeable to Ca2+ This answer is INCORRECT. When activated Na+ and Ca2+ flow into the cell and K+ flows out of the cell through NMDA receptors (and additional types of channels as well). Glutamate binding to these receptors cause direct opening of the channel, thus producing rapid discrete responses.
Opening of ion channels permeable to Na+ depolarizes the membrane potential and GABA and glycine do not open ion channels permeable to Na+. While GABA can bind to both ionotropic and metabotropic (G-protein coupled) receptors, glycine only binds to an ionotropic type of receptor. Glumatergic (excitatory) synapses respond to the neurotransmitterВ  glutamate, and GABAergic (inhibitory) synapses respond to gamma-aminobutyric acid (GABA).В  GABA is formed by decarboxylating glutamate. Over half of all brain synapses release Glutamate, and 30-40% of all brain synapses release GABA. In order to post comments, please make sure JavaScript and Cookies are enabled, and reload the page. These neurons reach and dump serotonin onto almost the entire brain, as well as the spinal cord. Figure 13.1 shows a monosynaptic connection in the spinal cord between the sensory neuron (in green) and the motor neuron innervating the extensor muscle (in blue). These excitatory synapses have identifiable morphological characteristics and are referred to as Type I (Figure 13.2, box labeled Dendrites).
Therefore, for neurons lacking regenerative processes in their dendrites, EPSPs that are far from the point of action potential generation (the cell soma and axon hillock) attenuate to a greater degree than IPSPs which are generated closer to the neuron's soma.
Recognize that N-methyl-D-Aspartate is a synthetic compound not found in the brain and is technically not a neurotransmitter.
When neuronal activity is high, extracellular glutamate concentration exceeds the capacity of neuronal uptake. ATP and its degradation product adenosine are themselves neurotransmitter molecules (termed purinergic transmission) that can also modify the pre- or postsynaptic cell's response if the appropriate receptors are present.
In contrast, glutamate and GABA can produce fast responses by directly opening ion channels and can produce slow responses by activating receptors coupled to G-proteins. These three distinct types of glutamate receptors have been characterized by using agonists that specifically activate each type. Increased levels of Ca2+ activate a wide variety of enzyme systems that alter both the short- and long-term response of the neurons (recall that activation of this receptor is required for the induction of long-term potentiation).
If benzodiazepines are present, the effectiveness of GABA binding to its receptor is increased significantly (Figure 13.13).
The proteins involved in transmitter uptake are related and each contains 12 membrane-spanning domains.
Both events produce massive release of glutamate in the brain that over-stimulates glutamate receptors. The decrease in GABA inhibition permits cells to fire synchronously, thus producing massive local excitation and initiation of a seizure.
This finding suggests that some initial imbalance in the GABAergic system may underlie aspects of this disorder. In relation to charge and membrane polarization you can think of Cl- entry as having a similar effect as K+ exit. A distinct zone frequently exists in the pre-synaptic terminal of Type I synapses responsible for the release of vesicles containing glutamate and a corresponding zone under the postsynaptic membrane that serves to anchor the receptors for glutamate (click on the box for details).

For unknown reasons, the vesicles containing glycine or GABA are often elliptical in shape. Due to this spatial arrangement and the relatively small size of each EPSP (1 mV), many distant EPSPs must summate to cause the initiation of an action potential. Nevertheless, it is now known that amino acids constitute the major group of substances used for generating excitatory and inhibitory synaptic potentials in the CNS. It is a highly useful agonist that can mimic the actions of glutamate on a particular subset of glutamate receptors.
Like the other amino acid transmitters, GABA's actions are terminated by high affinity uptake systems in neurons and glia. For example, adenosine is a potent inhibitor of neurotransmitter release from presynaptic terminals. The structure of non-NMDA receptors loosely resembles the nicotinic ACh receptor, although glutamate receptors have some unique features. Therefore, effective doses of benzodiazepines enhance the ability of GABA to hyperpolarize the neuron by increasing the number of GABA receptors that open at a fixed concentration of GABA. Transporters use energy derived either from the hydrolysis of ATP or electrochemical ion gradients established across the membrane to pump the transmitters into neurons and glia. At resting membrane potentials, extracellular Mg2+ sits in the channel plugging it and inhibiting ion flow.
Or negative outcomes like during a stroke where lack of blood flow produces hyper activation of NMDA receptors, excess Ca2+-influx and excess Ca2+-dependent enzyme stimulation. In addition, vesicles that contain glutamate are small (~50 nm in diameter) and tend to have a spherical appearance.
Like glutamate, high-affinity uptake systems remove glycine from the synaptic cleft, which can then be repackaged into vesicles. The different subunits of the GABAA receptor are responsible for the binding of different drugs. The energy-dependent nature of these receptors means that in times of metabolic stress, such as during an ischemic episode, the pumps fail and toxic levels of these transmitters build up. As a consequence, the uncontrolled opening of glutamate receptors causes a large influx of Na+ followed by water that produces swelling and a large and sustained influx of Ca2+ that leads to hyperactivation of many calcium-dependent enzymes.
High dose barbiturates presumably potentiate GABA's inhibitory effects, preventing local hyperexcitation by hyperpolarizing the cell membranes. The neurotransmitters and the receptors that mediate these and other excitatory and inhibitory responses are the focus of this section.
On a typical cortical neuron, one might find 10,000 axodendritic excitatory synapses and only 10-50 axosomatic inhibitory synapses.
For example, glutamate to be used as a neurotransmitter is compartmentalized from metabolic glutamate used for protein synthesis by packaging the transmitter into synaptic vesicles for subsequent Ca2+-dependent release.
To recycle the glutamate taken up into glial cells, an enzymatic reaction catalyzed by glutamine synthase produces glutamine from glutamate (Figure 13.4). Compared with glutamate, a more elaborate set of reactions is necessary to return GABA to the neuron when it is taken up by glial cells.
Many different subunit isoforms have been cloned and characterized and mixing different subunits can significantly alter the properties of the mature non-NMDA receptor.
Recognize that benzodiazepines themselves do not open the receptor but simply enhance GABA binding.
Again, both glutamate bound to the receptor and membrane depolarization is required for NMDA receptors to permit ion flow.
Excitatory transmission (the production of EPSPs) is mediated largely by the acidic amino acid glutamate.
Glutamine is freely permeable to the glial and neuronal plasma membranes and diffuses back into the neuron. Some of these enzymes are shared with those for returning released glutamate to neurons described in Figure 13.4.
Barbiturates also produce their sedative effects by increasing the effectiveness of GABA binding to its receptor. The key to minimizing damage following stroke is well-controlled reestablishment of blood flow so that ATP production is supported and homeostasis is reestablished. Inhibitory neurotransmission (IPSPs) is mediated primarily by glycine in the spinal cord, and a metabolite of glutamate called gamma-aminobutyric acid (GABA) in the brain.
The neuronal enzyme glutaminase then metabolizes glutamine into glutamate where it can then be packaged into synaptic vesicles for another round of release (Figure 13.4).
Although it is premature to dwell on these details, future development of drugs that bind to specific glutamate receptor subtypes will find important clinical applications. This unique property imparts to the receptor the capacity to sense the membrane potential and open only when the neuron is depolarized. The naturally occurring toxin called picrotoxin is a potent inhibitor of the GABAA receptor and works by preventing Cl- flow through the receptor (Figure 13.11). The ability to sense presynaptic activity (through the binding of released glutamate) and postsynaptic activity (through sensing membrane potential) means the NMDA receptor associates the two activities. The glutamate is then converted to glutamine by the enzyme glutamine synthase and glutamine diffuses back into the neuron.
Finally, glutaminase converts glutamine into glutamate, which can again serve as a substrate for GAD, completing the cycle. Apparently, Ca2+-influx through the NMDA receptor initiates a set of biochemical changes so that the neuron remembers the conjoint activity and responds differently when activated in the future.

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