Rabbit polyclonal antiserum to L-glutamate may be used in immunohistochemical techniques on formalin- or glutaraldehyde-fixed, vibratome or frozen sections of human or animal tissues. Immunohistochemical methods provide increased anatomical resolution over conventional biochemical methods.
The amino acids L-glutamate (Glu) and L-aspartate (Asp) are considered the major excitatory neurotransmitters in the central nervous system (CNS) and represent the most abundant mammalian neurotransmitter class. Both L-glutamate and L-aspartate are present in the brain at high concentrations and are distributed in most excitatory pathways in the CNS. Glu- and Asp-immunoreactivities are localized in high concentrations in synaptic terminals. In nerve terminals, L-glutamate is formed by deamidation of its major precursor, L-glutamine, by the enzyme glutaminase.
The actions of the excitatory amino acids on neurons are mediated by different receptor subtypes. These receptors are coupled to integral ion channels or to a second messenger system which utilizes inositol triphosphate (IP3). L-glutamate and L-aspartate may play an important role in the pathogenesis of certain neurological disorders such as Huntington′s disease, Alzheimer′s disease, epilepsy and brain ischemia. The excitoxic and neurotoxic effects of L-glutamate, leading to extensive neuronal damage, appear to be mediated by the N-methyl-D-aspartate (NMDA) receptor subtype.
Glutamate is an amino acid that acts as a excitatory neurotransmitter in the vertebrate brain and functions in all brain processes. It is released from one end of the neuron and it binds to receptors on the surface of adjacent neurons. Glutamate is released in a calcium-dependent manner in response to depolarizing stimuli. It serves as a substrate in certain metabolic pathways, such as, synthesis of glutamine and γ-aminobutyric acid (GABA) Excessive release of glutamate or aspartate have been observed in the pathogenesis of certain neurodegenerative diseases, such as, Huntington′s disease, Alzheimer′s disease. The same is also observed in selective neuronal degenerations involved in epilepsy, ischemia, and hypoglycemia.
