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Amino acid transmitters in the mammalian central nervous system

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<strong>Am<strong>in</strong>o</strong> Acid Transmitters <strong>in</strong> <strong>the</strong> Mammalian Central Nervous System<br />

149<br />

Table 9. Enzyme levels <strong>in</strong> extracts of cat sp<strong>in</strong>al cord and roots (~tmole/hr/g wet tissue)<br />

Enzyme Dorsal Dorsal Dorsal Ventral Ventral Ventral Reference<br />

roots white grey grey white roots<br />

Aspartate 545 2 454 5 412 5 418 2 480 537 GRAHAM and APRISON<br />

transam<strong>in</strong>ase (1969)<br />

Glutamate 17 149 446 448 139 16 GRAHAM and APRISON<br />

dehydrogenase (1969)<br />

Glutam<strong>in</strong>e 7 20 67 67 19 4 GRAHAM and APRISON<br />

syn<strong>the</strong>tase (I 969)<br />

Glutam<strong>in</strong>ase 12 67 397 331 66 13 GRAHAM and APRISON<br />

(1969)<br />

Glutamate 4 0 13 a 7 0 3 GRAHAM and APR1SON<br />

decarboxylase (1969)<br />

GABA 1 3 14 13 3 1 GRAHAM and APRISON<br />

transam<strong>in</strong>ase (1969)<br />

D-<strong>Am<strong>in</strong>o</strong> <strong>acid</strong> 0.8 2.2 2.1 0.4 DE MARCHI and<br />

oxidase JOHNSTON (1969)<br />

Glyc<strong>in</strong>e 6.6 9.9 9.6 7 JOHNSTON, VITALI<br />

transam<strong>in</strong>ase and ALEXANDER (1970)<br />

Ser<strong>in</strong>e hydroxy- 2.5 4.3 a 5 2.5 DAVIES and<br />

methyltransferase JOHNSTON (1973)<br />

a Levels <strong>in</strong> dorsal grey significantly different from those <strong>in</strong> ventral grey.<br />

(DAvIDOFF et al., 1967). In <strong>the</strong>se animals, which showed no response to nociceptive<br />

cutaneous stimulation <strong>in</strong> <strong>the</strong> affected segments, sp<strong>in</strong>al monosynaptic reflexes<br />

were enhanced, polysynaptic reflexes were reduced, and although some evidence<br />

has been obta<strong>in</strong>ed for antidromic <strong>in</strong>hibition mediated by Renshaw cells, details<br />

have not been published regard<strong>in</strong>g o<strong>the</strong>r types of sp<strong>in</strong>al <strong>in</strong>hibition (MuRAYAMA<br />

and SMITH, 1965). In <strong>the</strong> rat; however, h<strong>in</strong>dlimb rigidity produced <strong>in</strong> <strong>the</strong> same<br />

fashion is accompanied by reduced responses to pa<strong>in</strong>ful cutaneous stimulation,<br />

enhanced monosynaptic and reduced polysynaptic reflexes, and reduction of<br />

two types of <strong>in</strong>hibition of ankle extensor motoneurones: short latency ("postsynaptic")<br />

<strong>in</strong>hibition by impulses <strong>in</strong> <strong>the</strong> deep peroneal nerve and prolonged<br />

(" presynaptic ") <strong>in</strong>hibition by repetitive impulses <strong>in</strong> <strong>the</strong> posterior biceps nerve<br />

(MATSUSHITA and SMITH, 1970). There is thus evidence <strong>in</strong> <strong>the</strong>se studies of a loss<br />

of both excitatory and <strong>in</strong>hibitory sp<strong>in</strong>al mechanisms associated with <strong>in</strong>terneurones.<br />

Useful <strong>in</strong>formation might also. be provided by transection of dorsal roots,<br />

although subsequent alterations <strong>in</strong> am<strong>in</strong>o <strong>acid</strong> levels and associated enzymes<br />

may be complicated by disturbances of <strong>the</strong> blood supply (Rat: SUGAR and GER-<br />

ARD, 1940. Cat: CHAMBERS, ELDRED, and EGGETT, 1972) <strong>in</strong> addition to loss of<br />

primary afferent fibres. With both aortic occlusion and de-afferentation, histological<br />

control and unchanged levels of some metabolites are required to exclude<br />

"non-specific" loses of am<strong>in</strong>o <strong>acid</strong>s produced by <strong>in</strong>farction, oedema, gliosis or<br />

cavity formation (see DAVIDOEE et al., 1967).

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