Abstract
Discussion and Conclusion
In the chicken, parenteral administration of GABA causes an inhibition of the photically evoked response recorded from the tectum. It does not have any marked effect on spontaneous potentials recorded from the same structure (4, 6). These results, considered with other data, lead to the conclusion that GABA acts primarily as an inhibitor upon axosoomatic synapses (6, 10). LSD decreases the amplitude of spontaneous activity, enhances the evoked response and uncovers a prolonged series of potentials (afterpotentials) following the evoked response (7, 11). At the synaptic level, these results suggest an inhibitory effect upon axodendritic (depression of spontaneous activity) and an excitatory effect upon axosomatic connections (evoked response plus afterpotentials) (12, 13).
The interaction of LSD and GABA is not surprising. It now appears possible to state more precisely the site and mechanism of LSD action in the avian brain.
It has long been known that lowered brain GABA levels are associated with increased CNS excitability. The motor component of this excitation, however, is not easily correlated with GABA levels. Convulsions induced by the thiosemicarbazides and pyridoxine antagonists are accompanied by a decrease in brain GABA levels (14). But other experiments have shown that under the appropriate conditions thiosemicarbazide-induced motor convulsions can be terminated even though brain GABA levels remain low (9). Moreover, in the opposite situation, seizures can be induced with thiosemicarbazides even in the presence of raised GABA levels (8).
Since there have been no previous studies concerned with brain GABA levels and sensory excitability, we feel that the current results support a view that GABA and CNS excitability studies could best be restricted to sensory mechanisms.
The action of LSD on the electrophysiology of the tectum is predominantly excitatory, but there appears to be no concomitant motor effect as observed in the intact animal (personal observation) that cannot be attributed to sensory stimulation.
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