China
Africa
Explore chapters and articles related to this topic
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
A false neurotransmitter is a chemical that is not one of the normal NEUROTRANSMITTERS but which can be taken up by a TERMINAL, packaged into SYNAPTIC VESICLES, and released in response to normal stimulation. PHENYLETHYLAMINE is an example of a false neurotransmitter.
Advances in prodrug design for Parkinson’s disease
Published in Expert Opinion on Drug Discovery, 2018
Ivana Cacciatore, Michele Ciulla, Lisa Marinelli, Piera Eusepi, Antonio Di Stefano
Parkinsonism is one of the major neurodegenerative and progressive diseases of the central nervous system (CNS) and is characterized by the loss of dopaminergic neurons and their connections, predominantly in two brain areas: the Substantia Nigra pars compacta (SNpc), which is responsible for motor control, and the locus coeruleus, responsible for psychic control [1]. In addition to this effect, there is also a massive reduction in dopamine (DA) concentration, which is the neurotransmitter that regulates the transmission of central dopaminergic neurons and numerous hypothalamic–pituitary functions. Furthermore, the presence of Lewy bodies has been identified as a marker of Parkinson’s disease (PD) [2]. Lewy bodies consist of protein agglomerations (α-synuclein, parkin, and other proteins) embedded in the cytoplasm of dead neurons, indicating that the degenerative process has already occurred [3]. However, cholinergic and serotonergic dysfunctions were also observed in PD patients. Notably, cholinergic and muscarinic receptors were observed to be decreased in PD patients, causing cholinergic system degeneration that is responsible for cognitive and motor impairments [4]. Moreover, recent studies suggested that dysfunction of the serotonergic system is directly correlated to nonmotor symptoms (such as depression, fatigue, and hallucinations) observed in PD patients. Striatal levels of 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindolacetic acid were reduced in PD brains. It has been observed that serotonin neurons innervating the striatum (caudate and putamen) may improve the antiparkinsonian action of L-Dopa (LD), by converting LD into DA and then releasing DA from the serotonin neurons as a false neurotransmitter [5].