Presynaptic terminals

Parkinson's disease (PD), characterized by the absence of dopamine in the striatum[1], is caused by the death of the substantia nigra pars compacta dopamine (SNcDA) neurons in the midbrain. The loss of these autonomously pacemaking[2] neurons is attributed to irreparable damage due to a dysregulation cascade starting from excess cytosolic dopamine and its decomposition into its aldehyde[3]. However, it is unresolved if dopamine dysregulation in SNcDA neurons themselves is the cause of PD or if it is a mere symptom. Here, we applied a recent theory of metabolic spikes[4] to SNcDA neurons, to

Schizophrenia (SCZ) is characterized by the aberrant development of the central nervous system and thereby results in impairments of multiple aspects of synaptic transmission, neuronal connectivity, and activity patterns. Dysfunctions of the dopaminergic circuitry were already postulated several decades ago. Patients with SCZ suffer from disturbances in the reward system, as well as in executive and cognitive functions. The two dopaminergic pathways, mesolimbic and mesocortical, have been implicated in neuropsychiatric disorders. Both originate from the ventral tegmental area and project to th

…and off-target effects when applied to presynaptic terminals. In my talk, I will present a new so

…that both postsynaptic spines and presynaptic terminals exhibit rapid translation, which exhibits differential sensitivity to different neurotransmitters and neuromodulators. In addition, we have explored the unique mechanisms neurons use to meet protein demands at synapses, identifying the transcriptome and transla