.BETA.-Phenylethylamine Stimulates Striatal Acetylcholine Release through Activation of the AMPA Glutamatergic Pathway

Ishida, Katsuhiro; Murata, Mikio; Kato, Masaaki; Utsunomiya, Iku; Hoshi, Keiko; Taguchi, Kyoji

doi:10.1248/bpb.28.1626

Cited by 13 publications

(6 citation statements)

References 32 publications

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“…The ACh concentrations increase exponentially with the dose of neostigmine. Basal value (Ichikawa et al,2002b,c); NEO 0.02 μM (Ishida et al,2005); NEO 0.1 μM (Acquas and Di Chiara,1999a,b; Kato et al,2001); NEO 0.3 μM (Parada et al,1997); NEO 1 μM (Buchholzer et al,2002; Hernandez et al,2003,2006,2008); NEO 10 μM (Taguchi et al,1998); PHYS 10 μM (Antoniou et al,1997; Ikarashi and Yuzurihara,2002; Kikuchi et al,1998); PHYS 100 μM (Hasegawa et al,1996); PHYSS 7 μM (Giovannini et al,1994a,1995; Rakovska et al,2002).…”

Section: Resultsmentioning

confidence: 99%

The impact of acetylcholinesterase inhibitors on the extracellular acetylcholine concentrations in the adult rat brain: A meta‐analysis

Noori

Fliegel

Brand

et al. 2012

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In vivo microdialysis has become a key method in investigating the dynamics of different neurotransmitter systems such as acetylcholine in the extracellular fluid. Depending on the sensitivity of the analytical method applied for measuring acetylcholine levels in brain dialysates, acetylcholinesterase (AChE) inhibitors are often used to increase the basal acetylcholine level up to a detectable magnitude. This artificial manipulation of the system questions the outcome of pharmacological studies and has led to a large number of experiments pursuing the appropriate physiological and pharmacological concentration of the AChE inhibitors in a range between 0.01 and 100 μM. However, the complexity of the action of these substances, particularly through the involvement of muscarinic autoreceptors and the induction of an autoinhibitory effect on acetylcholine release, did not allow this quest to be resolved completely and suggests the application of advanced mathematical methods for the evaluation of acetylcholine baseline levels. Here we performed a meta-analysis on published datasets of in vivo microdialysis measurements to assess the concentration-dependent effects of various AChE inhibitors on acetylcholine levels within the prefrontal cortex, nucleus accumbens, caudate putamen, and hippocampus in adult rats. In total 3255 rats were analyzed and we found that when compared with the minority of studies (14%) that did not use AChE inhibitors (these studies yielded basal levels between 0.55 and 2.71 nM depending on the brain site) an up to 350-fold increase in baseline values after the application of an inhibitor could be detected. Especially, the derivates neostigmine bromide and physostigmine sulfate seem to produce dramatic effects. Furthermore, concentration-dependent effects after the application of AChE inhibitors could not be established. In the case of neostigmine bromide an inverted concentration (0.1-10 μM)-response relationship was even detected. We conclude that although the presynaptic action of AChE inhibitors is well understood the nonphysiological and concentration-independent augmentation of the acetylcholine system requires the use of a standard protocol in order to produce replicable and comparable results. Our meta-analysis suggests the use of 0.1 μM neostigmine which produces an approximately 10-fold boost of brain baseline levels.

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Section: Resultsmentioning

confidence: 99%

The impact of acetylcholinesterase inhibitors on the extracellular acetylcholine concentrations in the adult rat brain: A meta‐analysis

Noori

Fliegel

Brand

et al. 2012

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“…The ability of PEA to modulate DA neurotransmission in the nigrostriatal pathway was reported by Barroso & Rodriguez (1996). Ishida et al (2005) found that PEA stimulates acetylcholine release by activating glutamatergic signaling pathways. More recently Geracitano et al (2004), Federici et al (2005), and Berretta et al (2005) demonstrated that the TAs depress GABA B responses in dopaminergic neurons by inhibiting G-βγ-gated inwardly rectifying potassium channels.…”

Section: 42mentioning

confidence: 87%

Trace amine-associated receptor 1—Family archetype or iconoclast?

Grandy

2007

Pharmacology & Therapeutics

176

211

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Interest has recently been rekindled in receptors that are activated by low molecular weight, noncatecholic, biogenic amines that are typically found as trace constituents of various vertebrate and invertebrate tissues and fluids. The timing of this resurgent focus on receptors activated by the 'trace amines' (TAs) β-phenylethylamine (PEA), tyramine (TYR), octopamine (OCT), synephrine (SYN), and tryptamine (TRYP) is the direct result of two publications that appeared in 2001 describing the cloning of a novel G protein-coupled receptor (GPCR) referred to by their discoverers as TA1 (Borowsky et al., 2001) and TAR1 (Bunzow et al., 2001). When heterologously expressed in Xenopus laevis oocytes and various eukaryotic cell lines recombinant rodent and human TA receptors dosedependently couple to the stimulation of cAMP production. Structure-activity profiling based on this functional response has revealed that in addition to the TAs, other biologically active compounds containing a 2 carbon aliphatic side chain linking an amino group to at least one benzene ring are potent and efficacious TA receptor agonists with amphetamine, methamphetamine, 3-iodothyronamine, thyronamine, and dopamine among the most notable. Almost 100 years after the search for TA receptors began numerous TA1/TAR1-related sequences, now called Trace AmineAssociated Receptors (TAARs), have been identified in the genome of every species of vertebrate examined to date. Consequently, even though heterologously expressed TAAR1 fits the pharmacological criteria established for a bona fide TA receptor a major challenge for those working in the field is to discern the in vivo pharmacology and physiology of each purported member of this extended family of GPCRs. Only then will it be possible to establish whether TAAR1 is the family archetype or an iconoclast.

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“…Second, TAs could bind to yet unidentified TA-sensitive signaling proteins located on pre- or post-synaptic neurons containing GPCRs for the classic monoamines, thereby modulating their corresponding intracellular second messenger pathways (Premont et al, 2001 ; Sotnikova et al, 2004 ; Burchett and Hicks, 2006 ). Moreover, in addition to altering the major aminergic pathways, TAs have been shown to modulate neuronal signaling mediated by other important neurotransmitters, such as gamma-aminobutyric acid (GABA; Berretta et al, 2005 ; Federici et al, 2005 ) and acetylcholine (Kato et al, 2001 ; Ishida et al, 2005 ), but the functional relevance of such interactions is not well-understood at present.…”

Section: Trace Aminesmentioning

confidence: 99%

Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications

2016

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Biogenic amines are a collection of endogenous molecules that play pivotal roles as neurotransmitters and hormones. In addition to the “classical” biogenic amines resulting from decarboxylation of aromatic acids, including dopamine (DA), norepinephrine, epinephrine, serotonin (5-HT), and histamine, other biogenic amines, present at much lower concentrations in the central nervous system (CNS), and hence referred to as “trace” amines (TAs), are now recognized to play significant neurophysiological and behavioral functions. At the turn of the century, the discovery of the trace amine-associated receptor 1 (TAAR1), a phylogenetically conserved G protein-coupled receptor that is responsive to both TAs, such as β-phenylethylamine, octopamine, and tyramine, and structurally-related amphetamines, unveiled mechanisms of action for TAs other than interference with aminergic pathways, laying the foundations for deciphering the functional significance of TAs and its mammalian CNS receptor, TAAR1. Although, its molecular interactions and downstream targets have not been fully elucidated, TAAR1 activation triggers accumulation of intracellular cAMP, modulates PKA and PKC signaling and interferes with the β-arrestin2-dependent pathway via G protein-independent mechanisms. TAAR1 is uniquely positioned to exert direct control over DA and 5-HT neuronal firing and release, which has profound implications for understanding the pathophysiology of, and therefore designing more efficacious therapeutic interventions for, a range of neuropsychiatric disorders that involve aminergic dysregulation, including Parkinson's disease, schizophrenia, mood disorders, and addiction. Indeed, the recent development of novel pharmacological tools targeting TAAR1 has uncovered the remarkable potential of TAAR1-based medications as new generation pharmacotherapies in neuropsychiatry. This review summarizes recent developments in the study of TAs and TAAR1, their intricate neurochemistry and pharmacology, and their relevance for neurodegenerative and neuropsychiatric disease.

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.BETA.-Phenylethylamine Stimulates Striatal Acetylcholine Release through Activation of the AMPA Glutamatergic Pathway

Cited by 13 publications

References 32 publications

The impact of acetylcholinesterase inhibitors on the extracellular acetylcholine concentrations in the adult rat brain: A meta‐analysis

The impact of acetylcholinesterase inhibitors on the extracellular acetylcholine concentrations in the adult rat brain: A meta‐analysis

Trace amine-associated receptor 1—Family archetype or iconoclast?

Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications

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