Indirect Modulation by α7 Nicotinic Acetylcholine Receptors of Noradrenaline Release in Rat Hippocampal Slices: Interaction with Glutamate and GABA Systems and Effect of Nicotine Withdrawal

Barik, Jacques; Wonnacott, Susan

doi:10.1124/mol.105.018184

Cited by 123 publications

(100 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the hippocampus as elsewhere (Albuquerque et al, 2009), a7nAChRs are prominently associated with nerve terminals, where they can be targeted to modulate glutamate release (Fabian-Fine et al, 2001;Gray et al, 1996;Lagostena et al, 2008). a7nAChR agonists enhance, whereas a7nAChR antagonists reduce, the release of glutamate into the extracellular compartment (Barik and Wonnacott, 2006). Therefore, although a primary effect of KYNA on NMDARs cannot be ruled out based on our present results, we propose that the reductions and elevations of extracellular glutamate described here are caused by fluctuations of endogenously produced KYNA acting through a7nAChRs.…”

Section: Discussioncontrasting

confidence: 37%

Fluctuations in Endogenous Kynurenic Acid Control Hippocampal Glutamate and Memory

Pocivavsek

Potter

et al. 2011

Neuropsychopharmacol

146

158

View full text Add to dashboard Cite

Kynurenic acid (KYNA), an astrocyte-derived metabolite, antagonizes the a7 nicotinic acetylcholine receptor (a7nAChR) and, possibly, the glycine co-agonist site of the NMDA receptor at endogenous brain concentrations. As both receptors are involved in cognitive processes, KYNA elevations may aggravate, whereas reductions may improve, cognitive functions. We tested this hypothesis in rats by examining the effects of acute up-or downregulation of endogenous KYNA on extracellular glutamate in the hippocampus and on performance in the Morris water maze (MWM). Applied directly by reverse dialysis, KYNA (30-300 nM) reduced, whereas the specific kynurenine aminotransferase-II inhibitor (S)-4-(ethylsulfonyl)benzoylalanine (ESBA; 0.3-3 mM) raised, extracellular glutamate levels in the hippocampus. Co-application of KYNA (100 nM) with ESBA (1 mM) prevented the ESBA-induced glutamate increase. Comparable effects on hippocampal glutamate levels were seen after intra-cerebroventricular (i.c.v.) application of the KYNA precursor kynurenine (1 mM, 10 ml) or ESBA (10 mM, 10 ml), respectively. In separate animals, i.c.v. treatment with kynurenine impaired, whereas i.c.v. ESBA improved, performance in the MWM. I.c.v. co-application of KYNA (10 mM) eliminated the pro-cognitive effects of ESBA. Collectively, these studies show that KYNA serves as an endogenous modulator of extracellular glutamate in the hippocampus and regulates hippocampus-related cognitive function. Our results suggest that pharmacological interventions leading to acute reductions in hippocampal KYNA constitute an effective strategy for cognitive improvement. This approach might be especially useful in the treatment of cognitive deficits in neurological and psychiatric diseases that are associated with increased brain KYNA levels.

show abstract

Section: Discussioncontrasting

confidence: 37%

Fluctuations in Endogenous Kynurenic Acid Control Hippocampal Glutamate and Memory

Pocivavsek

Potter

et al. 2011

Neuropsychopharmacol

146

158

View full text Add to dashboard Cite

show abstract

“…We cannot exclude this possibility with the current extracellular recording approach; yet, the fact that corticosterone by itself did not change the basal synaptic response in any respect seems to argue against it. Similarly, it is unlikely that bicuculline-induced enhancement of endogenous noradrenaline release (Barik and Wonnacott 2006) can explain the findings, in view of the continuous perfusion prior to …”

Section: Effect Of Corticosterone On Ltp In the Dgmentioning

confidence: 80%

Corticosterone time-dependently modulates β-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

Pu¹,

Krugers²,

Joëls³

2007

Learn. Mem.

View full text Add to dashboard Cite

Previous experiments in the hippocampal CA1 area have shown that corticosterone can facilitate long-term potentiation (LTP) in a rapid non-genomic fashion, while the same hormone suppresses LTP that is induced several hours after hormone application. Here, we elaborated on this finding by examining whether corticosterone exerts opposite effects on LTP depending on the timing of hormone application in the dentate gyrus as well. Moreover, we tested rapid and delayed actions by corticosterone on ␤-adrenergic-dependent changes in LTP. Unlike the CA1 region, our in vitro field potential recordings show that rapid effects of corticosterone do not influence LTP induced by mild tetanization in the hippocampal dentate gyrus, unless GABA A receptors are blocked. In contrast, the ␤-adrenergic agonist isoproterenol does initiate a slow-onset, limited amount of potentiation. When corticosterone was applied concurrently with isoproterenol, a further enhancement of synaptic strength was identified, especially during the early stage of potentiation. Yet, treatment with corticosterone several hours in advance of isoproterenol fully prevented any effect of isoproterenol on LTP. This emphasizes that corticosterone can regulate ␤-adrenergic modulation of synaptic plasticity in opposite directions, depending on the timing of hormone application.

show abstract

“…1C). Release was insensitive to the heteromeric b2-subunitpreferring nAChR antagonist DHbE, 18 partially blocked by the homomeric a7 nAChR antagonist methyllycaconitine (MLA), 19 and partially blocked by the selective voltage-gated Na þ channel blocker TTX (Fig. 1C).…”

Section: Resultsmentioning

confidence: 99%

Nicotinic receptor-evoked hippocampal norepinephrine release is highly sensitive to inhibition by isoflurane

Westphalen

Gomez²,

Hemmings

2009

British Journal of Anaesthesia

View full text Add to dashboard Cite

Background. Inhaled anaesthetics (IAs) produce multiple dose-dependent behavioural effects including amnesia, hypnosis, and immobility in response to painful stimuli that are mediated by distinct anatomical, cellular, and molecular mechanisms. Amnesia is produced at lower anaesthetic concentrations compared with hypnosis or immobility. Nicotinic acetylcholine receptors (nAChRs) modulate hippocampal neural network correlates of memory and are highly sensitive to IAs. Activation of hippocampal nAChRs stimulates the release of norepinephrine (NE), a neurotransmitter implicated in modulating hippocampal synaptic plasticity. We tested the hypothesis that IAs disrupt hippocampal synaptic mechanisms critical to memory by determining the effects of isoflurane on NE release from hippocampal nerve terminals.

show abstract

Indirect Modulation by α7 Nicotinic Acetylcholine Receptors of Noradrenaline Release in Rat Hippocampal Slices: Interaction with Glutamate and GABA Systems and Effect of Nicotine Withdrawal

Cited by 123 publications

References 43 publications

Fluctuations in Endogenous Kynurenic Acid Control Hippocampal Glutamate and Memory

Fluctuations in Endogenous Kynurenic Acid Control Hippocampal Glutamate and Memory

Corticosterone time-dependently modulates β-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

Nicotinic receptor-evoked hippocampal norepinephrine release is highly sensitive to inhibition by isoflurane

Contact Info

Product

Resources

About