Abstract

Dopamine (DA) hyperactivity in the mesolimbic system is a well-known pathophysiological theory of schizophrenia.
The scientist hoped to present a novel theory that would shed light on the molecular basis of schizophrenia’s mesolimbic
DA hyperactivity. The D-neuron (trace amine (TA) neuron) decrease in the nucleus accumbens (Acc) of ponies was
demonstrated using patent-required histochemical methods under the Patent Cooperation Treaty (PCT). In short, in
schizophrenia, a decline in striatal D-neuron activation and, as a result, a decrease in TAAR1 (TA-associated receptor,
type 1) stimulation into terminals of midbrain ventral tegmental region (VTA) DA neurons causes mesolimbic DA
hyperactivity. D-neuron loss in Acc is caused by dysfunction of subventricular neural stem cells (NSC), which are partly
overlapping Acc. Hyperactivity of the DA. The rationale that the “D-cell hypothesis (TA hypothesis) of schizophrenia” is
a critical idea in linking NSC pathology to the DA hypothesis is highlighted. (1) TAAR1 agonists, (2) DA D2 antagonists,
and (3) neurotropic agents have the ability to normalise mesolimbic DA hyperactivity from a therapeutic standpoint.
The synthesis of TAAR1ligands, as well as the pathophysiology of NSC- and D-neuron in neuropsychiatric disorders,
must be investigated further in order to improve new therapeutic techniques.

Keywords: Amine Hypothesis