GABA receptors and benzodiazepine binding sites modulate hippocampal acetylcholine release in vivo

Moor, E; Deboer, P; Westerink, Ben H.C.

doi:10.1016/s0014-2999(98)00642-6

Cited by 56 publications

(31 citation statements)

References 56 publications

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“…Thus, inhibition of ␣7 receptors would decrease the liberation of GABA. C, GABA decreases acetylcholine (ACh) release in the hippocampus (Moor et al, 1998). Thus, if there are ␣7 receptors on the GABAergic terminals that modulate the release of ACh, then ␣7 inhibition should increase the liberation of ACh.…”

Section: Discussionmentioning

confidence: 99%

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Ferchmin

Pérez²,

Eterović³

et al. 2003

J Pharmacol Exp Ther

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Although in neuronal cultures nicotine was reported to prevent early and delayed excitotoxic death, no studies with nicotinic drugs have been done with acute hippocampal slices. We investigated the effect of nicotine and methyllycaconitine (MLA) on the toxicity of N-methyl-D-aspartate (NMDA) in the CA1 area of hippocampal slices. The excitotoxic effect of NMDA was assessed as decreased recovery of the capability to produce synaptically evoked population spikes (PSs). Application of nicotine or MLA before NMDA application increased the recovery of PSs. This electrophysiological recovery was used as a measure of the early neuroprotective events. The neuroprotection conferred by both nicotine and MLA was inhibited by dihydro-␤-erythroidine, showing mediation of neuroprotection by ␣4␤2 neuronal nicotinic receptors (nAChRs). Because nicotine activates ␣4␤2 and other nAChR subtypes, whereas 10 nM MLA inhibits the ␣7 subtype, we propose the involvement of a neuronal circuitry-dependent mechanism for nicotinic neuroprotection. The effect of nicotine downstream from the receptors was investigated using inhibitors of cell signaling. The results suggest that the effect of nicotine is mediated by tyrosine receptor kinases, 1,2-phosphatidylinositol-3 kinase, and the mitogen-activated extracellular signal-regulated kinases. Although nicotine neuroprotection is Ca 2ϩ -dependent, neither L-type Ca 2ϩ channels nor calmodulin-dependent protein kinase is involved in the effect of nicotine. In summary, these results suggest that in acute slices nicotinic protection is initiated either by direct activation of ␣4␤2 or indirectly by inhibition of ␣7 followed by signal transduction involving tyrosine kinases, phospholipid-dependent kinases, and mitogen-activated kinases.

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Section: Discussionmentioning

confidence: 99%

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Ferchmin

Pérez²,

Eterović³

et al. 2003

J Pharmacol Exp Ther

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“…On the other hand, a wealth of evidence indicates that septal GABA receptor activation does likely impair memory through a process that involves, at least in part, inhibition of hippocampal ACh. Septal infusions of muscimol decrease a variety of measures of hippocampal ACh (Blaker et al 1983;Costa et al 1983;Brioni et al 1990;Gorman et al 1994;Moor et al 1998a), prevent training-or handling-induced increases in hippocampal ACh (Durkin 1992;Moor et al 1998b), and modulate the dose-response properties of hippocampal infusions of cholinergic agonists on memory (Farr et al 1999). Also, only those doses of muscimol that impair memory affect hippocampal ACh (Brioni et al 1990).…”

Section: Upregulation Of Hippocampal Ach Reverses Septal Memory Deficitsmentioning

confidence: 99%

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

Parent¹,

Baxter²

2004

Learn. Mem.

175

132

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The neurotransmitter acetylcholine (ACh) has been accorded an important role in supporting learning and memory processes in the hippocampus. Cholinergic activity in the hippocampus is correlated with memory, and restoration of ACh in the hippocampus after disruption of the septohippocampal pathway is sufficient to rescue memory. However, selective ablation of cholinergic septohippocampal projections is largely without effect on hippocampal-dependent learning and memory processes. We consider the evidence underlying each of these statements, and the contradictions they pose for understanding the functional role of hippocampal ACh in memory. We suggest that although hippocampal ACh is involved in memory in the intact brain, it is not necessary for many aspects of hippocampal memory function.The goal of this review is to consider the role of septohippocampal acetylcholine (ACh) in learning and memory processes. The evidence in this regard falls broadly into two different classes. On the one hand, considerable data implicate septohippocampal ACh in memory function. This system is engaged during memory processing, indexed by ACh release or by modification of cholinergic markers, and manipulations that affect memory produce parallel changes in hippocampal cholinergic activity. Furthermore, agents that increase hippocampal cholinergic function are sufficient to reverse memory impairments caused by disruption of the septohippocampal system. However, data from studies of selective lesions of septohippocampal cholinergic neurons with the immunotoxin 192 IgG-saporin call into question the essential role of this system in learning and memory, because these studies generally failed to find severe impairments in memory function. Our goal in this article is to review the data underlying each of these lines of evidence, and to attempt to reconcile these apparently disparate observations.The discrepancy between these lines of evidence might imply that septohippocampal ACh is involved in memory processing, but is not necessary for it to occur. This viewpoint would allow for correlated changes in ACh release and memory, and for the ability of cholinergic agents to reverse memory impairments caused by disruption of septohippocampal function. However, it also would permit memory to proceed relatively normally in the absence of septohippocampal cholinergic input. By describing this viewpoint and its implications for the functional role of hippocampal ACh in memory, we seek to promote the idea that data from lesions are compatible with data from other experimental approaches. Furthermore, we suggest that a convergent approach that incorporates observations from different experimental methods will reveal functional characteristics of hippocampal ACh that would not be apparent from studies using a single strategy.Before discussing the role of this system in cognition, a brief review of its anatomical and neurochemical organization is warranted. The septum is connected to the hippocampus via the fimbria-fornix, which carries projections ...

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“…A crucial prerequisite for the indirect modulation of the release of a neurotransmitter via an inhibitory GABAergic interneuron has to be taken into account: the nerves from which this neurotransmitter is released must be endowed with GABA receptors. In fact, evidence has been presented that inhibitory GABA A and/or GABA B receptors are operative on cholinergic (Supavilai and Karobath, 1985;Moor et al, 1998;Ikarashi et al, (5-methyl-1-(3-pyridylcarbamoyl) -1,2,3,5-tetrahydropyrrolo[2,3-f]indole) hydrochloride (5-HT 2B/2C antagonist/inverse agonist); SB 204741, N- urea (5-HT 2B antagonist); VTA, ventral tegmental area; BW 723C86, ␣-methyl-5-(2-thienylmethoxy)-1H-indole-3-ethanamine hydrochloride (5-HT 2B agonist); SB 243213, 5-methyl-1-[[2-[(2-methyl-3-pyridyl)oxyl]-5-pyridyl]carbamoyl]-6-trifluoromethyl-indone (5-HT 2C antagonist); SR 46349B, (trans-4-(3Z)3-[(2-dimethylaminoethyl)oxyimino]-3-(2-fluorophenyl)propen-1-yl)-phenol hemifumarate (5-HT 2A antagonist); DRN, dorsal raphe nucleus; DAU 6285, endo-6-methoxy-8-methyl-8-azabicyclo [3.2.1]oct-3-yl-2,3-dihydro-2-oxo-1H-benzimidazole-1-carboxylate hydrochloride (5-HT 3/4 antagonist); SB 207710, (1-n-butyl-4-piperidinyl)methyl-8-amino-7-iodo-1,4-benzodioxane-5-carboxylate (5-HT 4 antagonist); MDL 73005EF, 8-[2- (1,4-benzodioxan-2-ylmethylamino)ethyl]-8-azaspiro [4.5]decane-7,9-dione (5-HT 1A agonist); amino]propoxy]-1,3-benzodioxole HCl (5-HT 1A agonist); ICI 170,809, 2,2[dimethylamino-2-methylpropylthio]-3-phenylquinoline hydrochloride (5-HT 2 antagonist); DOM, R(Ϫ) -1-(2,5-dimethoxy-4-methylphenyl)-2 aminopropane (5-HT 2 agonist); IPSC, inhibitory postsynaptic current; mIPSC, miniature inhibitory postsynaptic current; IPSP, inhibitory postsynaptic potential; SCN, suprachiasmatic nucleus; 4-DAMP, 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (M 3 antagonist); …”

Section: Introduction: Background Definitions and Scopementioning

confidence: 99%

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

325

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GABA receptors and benzodiazepine binding sites modulate hippocampal acetylcholine release in vivo

Cited by 56 publications

References 56 publications

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

5-HT Receptor Regulation of Neurotransmitter Release

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