Effects of Amphetamine and Phenylethylamine on Catecholamine Release in the Glomerular Layer of the Rat Olfactory Bulb

Abstract

In the present work, we have shown electrochemically that in the rat olfactory bulb (OB), extracellular dopamine (DA) was highest in the glomerular layer (GL), whereas extracellular noradrenaline (NA) appeared to be more uniformly distributed across layers. The GL catecholamine (CA) responses to amphetamine (AMPH) and phenylethylamine (PEA) were also characterized electrochemically using an in vivo model. Results of this investigation show that at a lower dose (1 mg/kg), PEA had no effect on CA release. In contrast, at a higher dose (10 mg/kg), it produced similar increases in either extracellular DA (17.5 ± 7%) or extracellular NA (14 ± 3%), and DA exhibited dose-independent increases to AMPH (93 ± 8%: 1 mg/kg vs. 97 ± 6%: 10 mg/kg) whereas NA exhibited dose-dependent increases to AMPH (24.5 ± 6%: 1 mg/kg vs. 39 ± 7%: 10 mg/kg). These data indicate that (i) PEA may increase CA release but less efficiently than AMPH. (ii) AMPH is more efficient on the DAergic than on the NAergic system since AMPH-induced DA release exceeded 2–4 times the AMPH-induced NA release.

Combined treatment with MAO-A inhibitor and MAO-B inhibitor increases extracellular noradrenaline levels more than MAO-A inhibitor alone through increases in β-phenylethylamine

“…It is well known that β-phenylethylamine is related to catecholamine release (Mesfioui et al, 1998;Nakamura et al, 1998;Burchett and Hicks, 2006). Recently, Xie and Miller (2004) reported that β-phenylethylamine inhibited noradrenaline uptake and induced efflux of noradrenaline through trace amine-associated receptor 1, which exists in the brainstem and other brain regions, including the prefrontal cortex (Bunzow et al, 2001).…”

“…A main substance of MAO-B, β-phenylethylamine, exists in the brain; it is related to catecholamine release (Mesfioui et al, 1998;Nakamura et al, 1998;Burchett and Hicks, 2006). Accordingly, we also measured extracellular noradrenaline and serotonin levels after local infusion of β-phenylethylamine to the mPFC of rats.…”

Down-Regulated GABAergic Expression in the Olfactory Bulb Layers of the Mouse Deficient in Monoamine Oxidase B and Administered With Amphetamine

“…This down-regulated GAD 67 expression likewise could be compensation to presumably altered levels of GABA induced by Amph, as it was shown that the level of GABA release was increased or decreased in the nucleus accumbens and striatum of the rat after receiving acute or repeated Amph administration (Lindefors et al, 1992; Del Arco et al, 1998; Bartolletti et al, 2004). Moreover, Amph may induce alterations in dopamine, and/or other monoamine content in the layers to affect the GABA level and GAD 67 expression (Mesfiou et al, 1998; Deng et al, 2007). By contrast, our previous study found up-regulation of GAD 67 after repeated Amph treatment in the rat neocortical areas, nucleus accumbens and hippocampus (Yin et al, 2004).…”

“…Amph is known to be an indirect catecholamine agonist, and Amph-administered animals are utilized as models for examining addiction and Amph psychosis. The Amph-induced abnormal behavior is associated with the release of dopamine and/or other monoamines in distinct brain areas, including OlfB (Seiden et al, 1993; Karler et al, 1997; Featherstone et al, 2007; Mesfiou et al, 1998; Deng et al, 2007). There was also greater down-regulation of the OlfB pCREB in KO mice produced by the Amph exposure than that of the WT mice.…”

Activation of β-noradrenergic receptors enhances rhythmic bursting in mouse olfactory bulb external tufted cells

“…Although NE fibers are sparse in the glomeruli, the fibers are concentrated in the deep portion of the glomeruli where ET somata are located (McLean et al 1989). Additionally, neurochemical studies indicate that the NE concentration in the glomerular layer is similar to that in the deeper layers (Mesfioui et al 1998;Nadi et al 1981).…”