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Indicators
A tricyclic compound chemically related to tricyclic antidepressants (TCA) with anticonvulsant and analgesic properties. Carbamazepine exerts its anticonvulsant activity by reducing polysynaptic responses and blocking post-tetanic potentiation. Its analgesic activity is not understood; however, carbamazepine is commonly used to treat pain associated with trigeminal neuralgia.
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Complement C2 (752 aa, ~83 kDa) is encoded by the human C2 gene. This protein is involved in post-translational protein processing and complement activity.
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Cystatin-C (146 aa, ~16 kDa) is encoded by the human CST3 gene. This protein is involved in the inhibition of cysteine proteinases.
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A non-essential, non-polar, non-optical, glucogenic amino acid. Glycine, an inhibitory neurotransmitter in the CNS, triggers chloride ion influx via ionotropic receptors, thereby creating an inhibitory post-synaptic potential. In contrast, this agent also acts as a co-agonist, along with glutamate, facilitating an excitatory potential at the glutaminergic N-methyl-D-aspartic acid (NMDA) receptors. Glycine is an important component and precursor for many macromolecules in the cells.
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A nonessential amino acid derivative formed during post-translational protein modification through hydroxylation of the amino acid proline by the enzyme prolyl hydroxylase which requires vitamin C as a co-factor. Hydroxyproline is a major component of the protein collagen and plays a key role in the stability of the collagen triple helix. It can be used as an indicator to determine the amount of collagen. Increased hydroxyproline levels in the urine and/or serum are normally associated with degradation of connective tissue. Vitamin C deficiency decreases the conversion of proline to hydroxyproline, which leads to reduced collagen stability.
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A hydantoin derivative and a non-sedative antiepileptic agent with anticonvulsant activity. Phenytoin potentially acts by promoting sodium efflux from neurons located in the motor cortex reducing post-tetanic potentiation at synapses. The reduction of potentiation prevents cortical seizure foci spreading to adjacent areas, stabilizing the threshold against hyperexcitability. In addition, this agent appears to reduce sensitivity of muscle spindles to stretch causing muscle relaxation.
