Amino acid neurotransmitters
Unlike for the ‘‘classical’’ neurotransmitters such as acetylcholine and noradrenaline, it has not been possible to map the distribution of the amino acid transmitters in the mammalian brain. The reason for this is that these transmitters are present in numerous metabolic pools in the brain and are not restricted to one particular type of neuron as occurs with the ‘‘classical’’ transmitters. As an example, glutamate is involved in peptide and protein synthesis, in the detoxification of ammonia in the brain (by forming glutamine), in intermediary metabolism, as a precursor of the inhibitory transmitter GABA and as an important excitatory transmitter in its own right With regard to the possible role of these neurotransmitters in psychiatric and neurological diseases, there is growing evidence thatglutamate is causally involved in the brain damage that results from cerebral anoxia, for example following stroke, and possibly in epilepsy. Conversely, GABA deficiency has been implicated in anxiety states, epilepsy, Huntington’s chorea and possibly parkinsonism. The roles of the excitatory amino acid aspartate and the inhibitory transmitter glycine in disease are unknown.
Unlike for the ‘‘classical’’ neurotransmitters such as acetylcholine and noradrenaline, it has not been possible to map the distribution of the amino acid transmitters in the mammalian brain. The reason for this is that these transmitters are present in numerous metabolic pools in the brain and are not restricted to one particular type of neuron as occurs with the ‘‘classical’’ transmitters. As an example, glutamate is involved in peptide and protein synthesis, in the detoxification of ammonia in the brain (by forming glutamine), in intermediary metabolism, as a precursor of the inhibitory transmitter GABA and as an important excitatory transmitter in its own right With regard to the possible role of these neurotransmitters in psychiatric and neurological diseases, there is growing evidence thatglutamate is causally involved in the brain damage that results from cerebral anoxia, for example following stroke, and possibly in epilepsy. Conversely, GABA deficiency has been implicated in anxiety states, epilepsy, Huntington’s chorea and possibly parkinsonism. The roles of the excitatory amino acid aspartate and the inhibitory transmitter glycine in disease are unknown.
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