β-Phenylethylamine modulates acetylcholine release in the rat striatum: involvement of a dopamine D2 receptor mechanism

Kato, Masaaki; Ishida, Katsuhiro; Chuma, Toichiro; Abe, Kenji; Shigenaga, Toshiro; Taguchi, Kyoji; Miyatake, Tadashi

doi:10.1016/s0014-2999(01)00914-1

Cited by 8 publications

(3 citation statements)

References 29 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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“…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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“…In biochemical studies, systemic application of ␤-PEA stimulates the release of DA in the striatum (Dyck et al, 1983;Philips, 1986;Bailey et al, 1987) and postsynaptic DA receptors (Antelman et al, 1977). Because ␤-PEA alters several neurotransmitter systems (Sloviter et al, 1980;Kato et al, 2001) and stimulates the release of DA, dopaminergic neurons could be involved in ␤-PEA-induced behaviors (Barroso and Rodriguez, 1996). An in vivo microdialysis study indicated that locally applied ␤-PEA directly produced a dose-dependent increase in extracellular DA release in the nucleus accumbens (Nakamura et al, 1998).…”

mentioning

confidence: 99%

Effects of β-Phenylethylamine on Dopaminergic Neurons of the Ventral Tegmental Area in the Rat: A Combined Electrophysiological and Microdialysis Study

Ishida

Murata²,

Katagiri³

et al. 2005

J Pharmacol Exp Ther

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The effects of systemic administration of ␤-phenylethylamine (␤-PEA) and microiontophoretically applied ␤-PEA on the spontaneous discharge of dopamine (DA) neurons in the ventral tegmental area (VTA) of the anesthetized rat were examined. Intravenous administration of ␤-PEA (1.0, 2.5, and 5.0 mg/kg) and microiontophoretic applications of ␤-PEA caused inhibitory responses in DA neurons. Systemic administration and microiontophoretic applications of ␤-PEA induced dose-or currentdependent responses. The systemic ␤-PEA-induced inhibitory responses were reversed by pretreatment with the DA D 2 receptor antagonists haloperidol (0.5 mg/kg i.p.) and sulpiride (10 mg/kg i.p). Pretreatment with reserpine (5 mg/kg i.p. 24 h earlier) did not completely block the systemic administration of ␤-PEA (2.5 mg/kg) inhibition. A microdialysis study of freely moving rats demonstrated that the extracellular DA level increased significantly in response to local application of ␤-PEA (100 M) in the VTA via a microdialysis probe, and local application of ␤-PEA-stimulated somatodendritic DA release in the VTA. The ␤-PEA-induced release of DA was calcium ion-independent and was enhanced by pretreatment with pertussis toxin. These findings indicate that ␤-phenylethylamine inhibits DA neuron activity via DA D 2 autoreceptors in the rat VTA and that this inhibitory effect is mediated by the somatodendritic DA release.

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β-Phenylethylamine modulates acetylcholine release in the rat striatum: involvement of a dopamine D2 receptor mechanism

Cited by 8 publications

References 29 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 Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications

Effects of β-Phenylethylamine on Dopaminergic Neurons of the Ventral Tegmental Area in the Rat: A Combined Electrophysiological and Microdialysis Study

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