Phenylketonuria has been around for a long time but only recently has it been realized that the problem is not so much poisoning with abnormal ketones produced as a result of the absence of tyrosine hydroxylase, but the fact that these patients have very low levels of catecholamines in their brains. In fact the SN is devoid of neuromelanin, an end product of catecholamine metabolism. Studies of emotional functions in these patients should prove interesting. Transmitter systems involved in neural plasticity underlying increased anxiety and defense-implications for understanding anxiety following traumatic stress. Basolateral amygdala stimulation evokes glutamate receptor-dependent dopamine efflux in the nucleus accumbens of the anesthetized rat.
Phencyclidine interferes with the hippocampal gating of nucleus accumbens neuronal activity in vivo.
Neuroscience 87, 823-830. Monoamines and nitric oxide are employed by afferents in midline thalamic regulation. Neurotransmitter positron emission tomographic-studies in adults with phenylketonuria, a pilot study. Nitric oxide production in rat thalamus changes with behavioral state, local depolarization and brainstem stimulation.