Nicotinic acetylcholine receptor mediated modulation of evoked excitatory amino acid release in the nucleus tractus solitarius of the rat: evidence from in vivo microdialysis

Ashworth-Preece, Mark A; Jarrott, Bevyn; Lawrence, Andrew J

doi:10.1016/s0006-8993(98)00773-2

Cited by 12 publications

(7 citation statements)

References 14 publications

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“…However, nicotine's site and mechanism of inducing NE release in PVN and AMYG are unknown. Since glutamatergic afferents to NTS are known to be activated by nicotine (Ashworth-Preece et al, 1998b;Ferreira et al, 2002), the present studies focused on the role of glutamate and NO within the NTS to determine whether they mediate nicotine-induced NE release in PVN and AMYG. A direct microinjection of nicotine into NTS-A2 stimulated NE release in both the PVN and AMYG within 15 min.…”

Section: Discussionmentioning

confidence: 99%

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Nicotine-Induced Norepinephrine Release in Hypothalamic Paraventricular Nucleus and Amygdala Is Mediated by N-Methyl-d-aspartate Receptors and Nitric Oxide in the Nucleus Tractus Solitarius

Zhao¹,

Chen²,

Sharp³

2006

J Pharmacol Exp Ther

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The noradrenergic projections from brainstem nucleus tractus solitarius (NTS) to hypothalamic paraventricular nucleus (PVN) and amygdala (AMYG) are involved in nicotine-related stress responses and drug craving. Previous studies demonstrated that i.v. nicotine-induced norepinephrine (NE) release in the PVN and AMYG depends on nicotinic cholinergic receptors in the brainstem. However, the direct site and mechanism of nicotine's action in brainstem are unknown. The present study determined the roles of NTS ionotropic glutamate receptors and nitric oxide (NO) in the effects of both local and systemic nicotine on NE release in PVN and AMYG. In male rats, an intra-NTS microinjection of nicotine (1.2 g free base) or i.v. nicotine infusion (0.065 or 0.09 mg/kg) significantly increased NE levels in PVN and AMYG microdialysates. Prior microinjection of the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonopentanoic acid (0.75 or 1.5 g), but not an ␣-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonist, dose dependently nearly abolished both PVN and AMYG NE responses to nicotine administered into NTS or systemically. NO involvement was assessed with intra-NTS microinjections of the nonselective nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester hydrochloride (10 -30 nmol), or the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (0.1-0.2 nmol); both agents dose dependently inhibited i.v. nicotine-induced NE release. These results indicate that nicotine-induced NE release in PVN and AMYG is mediated entirely through the local effects of nicotine on NTS glutamate afferents and NMDA receptors that, in part, stimulate NO production, resulting in activation of noradrenergic neurons. Therefore, nicotine acts indirectly on noradrenergic NTS neurons to elicit NE release in forebrain structures.

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Section: Discussionmentioning

confidence: 99%

“…nAChRs expressed in NTS (Ashworth-Preece et al, 1998a) have been shown to be involved in the modulation of evoked release of excitatory amino acids in NTS (Ashworth-Preece et al, 1998b). Moreover, nicotine elicited glutamate release in NTS and other regions such as prefrontal cortex and nucleus accumbens (Reid et al, 2000;Lambe et al, 2003).…”

mentioning

confidence: 99%

Nicotine-Induced Norepinephrine Release in Hypothalamic Paraventricular Nucleus and Amygdala Is Mediated by N-Methyl-d-aspartate Receptors and Nitric Oxide in the Nucleus Tractus Solitarius

Zhao¹,

Chen²,

Sharp³

2006

J Pharmacol Exp Ther

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“…Focal administration of nicotine to the NTS causes robust endocrine and cardiovascular responses by activation of functional nicotinic acetylcholine receptors (nAChRs) and stimulation of important presympathetic and preparasympathetic signaling pathways (Kubo and Misu, ; Robertson et al, ; Nagata and Osumi, ; Matta et al, ; Tseng et al, ; Valentine et al, ; Fu et al, ; Ashworth‐Preece et al, ; Dhar et al, ; Ferreira et al, ; de Oliveira et al, ; Sun et al, ; Chen et al, ; Smith and Uteshev, ; Kalappa et al, ). These pathways originate in the NTS and extend to the key autonomic nuclei of the hypothalamus and the brainstem (Dampney, ; Guyenet, ; Ulrich‐Lai and Herman, ).…”

mentioning

confidence: 99%

“…Within the NTS, functional nAChRs (predominantly α3β4‐containing subtypes) are expressed both presynaptically and somatodendritically (Smith and Uteshev, ; Kalappa et al, ; Feng et al, ). Activation of NTS nAChRs by nicotinic agents modulates release of neurotransmitters and neuroendocrine substances within and outside of the NTS (Matta et al, ; Valentine et al, ; Fu et al, ; Ashworth‐Preece et al, ; Sun et al, ; Chen et al, ; Smith and Uteshev, ; Cheng et al, ; Kalappa et al, ). Moreover, activation of NTS nAChRs causes bradycardic and depressor responses (Kubo and Misu, ; Robertson et al, ; Tseng et al, ; Dhar et al, ; Ferreira et al, ) and modulates gastric tone and emptying (Ferreira et al, ).…”

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confidence: 99%

Projection target‐specific action of nicotine in the caudal nucleus of the solitary tract

Feng

Uteshev

2014

J of Neuroscience Research

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The brainstem nucleus of the solitary tract (NTS) is the key integrating relay in the central processing of sensory information from the thoracic and from most subdiaphragmatic viscera. Modulation of neuronal excitability and synaptic activity in the NTS by nicotinic agents can have potent effects on vital physiological functions, such as feeding, digestion, respiration, and blood circulation. Caudal NTS neurons demonstrate considerable heterogeneity in projection targets, synaptic properties, and expression of nicotinic acetylcholine receptors (nAChRs). However, despite its heterogeneity, the caudal NTS may contain discrete subsets of neurons with unique projection target-specific properties. To test this hypothesis, we used in vivo fluorescent tracing and ex vivo patch-clamp electrophysiology to evaluate responsiveness to nicotine of anatomically identified caudal NTS neurons that project to the hypothalamic paraventricular nucleus (PVN) and the brainstem caudal ventrolateral medulla (CVLM). The results of this study demonstrate that responsiveness to nicotine correlates with where the neurons project. Specifically, PVN-projecting caudal NTS neurons respond to nicotine only presynaptically (i.e., via activation of presynaptic nAChRs and potentiation of synaptic release of glutamate), suggesting indirect, glutamate-dependent effects of nicotine on the PVN-projecting NTS circuitry. By contrast, CVLM-projecting caudal NTS neurons exhibit only limited presynaptic, but dominant somatodendritic, responsiveness to nicotine, suggesting that the effects of nicotine on the CVLM-projecting NTS circuitry are direct and largely glutamate independent. Understanding the relationships among function-specific brainstem/hypothalamic neuronal networks, nuclei, and individual neurons could help develop therapies targeting identifiable neuronal circuits to offset impaired autonomic homeostasis.

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“…Therefore, the attenuated effects of puerarin on PCAand MK-801-induced impairment might be related to modulating the central serotonergic activity. On the other hand, the serotonergic system mainly inhibits acetylcholine release in hippocampal slices [7] and nicotinic acetylcholine receptor mediated modulation of evoked excitatory amino acid release in rat [19]. Therefore, the relationship among excitatory amino acids, serotonin and nicotinic receptors on the reversal caused by puerarin from the impairment shall be further investigated and demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Effects of Puerarin on Scopolamine-, Mecamylamine-,p-Chloroamphetamine- and Dizocilpine-Induced Inhibitory Avoidance Performance Impairment in Rats

Hsieh¹,

Kuo²,

Tsai³

et al. 2002

Planta med

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Puerarin at 10-50 mg/kg attenuated the mecamylamine- but not scopolamine-induced acquisition impairment of inhibitory avoidance performance in an inverse U-shape manner. p-Chloroamphetamine- and dizocilpine-induced acquisition impairment were reversed by puerarin at 25-50 mg/kg. Both piracetam, and tacrine attenuated impairment of inhibitory avoidance performance induced by all used drugs. Furthermore, puerarin, piracetam and tacrine alone did not alter step-through latency in the training trail but puerarin at 50 mg/kg and tacrine plus mecamylamine prolonged it in comparison with mecamylamine alone. From these results, we suggest that puerarin attenuated the deficits of inhibitory avoidance performance induced by mecamylamine, p-chloroamphetamine, and dizocilpine, the effects were related to increasing cholinergic activity via nicotinic but not muscarinic receptors, activating NMDA receptors, and decreasing serotonergic neuronal activity.

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Nicotinic acetylcholine receptor mediated modulation of evoked excitatory amino acid release in the nucleus tractus solitarius of the rat: evidence from in vivo microdialysis

Cited by 12 publications

References 14 publications

Nicotine-Induced Norepinephrine Release in Hypothalamic Paraventricular Nucleus and Amygdala Is Mediated by N-Methyl-d-aspartate Receptors and Nitric Oxide in the Nucleus Tractus Solitarius

Nicotine-Induced Norepinephrine Release in Hypothalamic Paraventricular Nucleus and Amygdala Is Mediated by N-Methyl-d-aspartate Receptors and Nitric Oxide in the Nucleus Tractus Solitarius

Projection target‐specific action of nicotine in the caudal nucleus of the solitary tract

Effects of Puerarin on Scopolamine-, Mecamylamine-,p-Chloroamphetamine- and Dizocilpine-Induced Inhibitory Avoidance Performance Impairment in Rats

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