Modulation of hippocampal acetylcholine release after fimbria-fornix lesions and septal transplantation in rats

Erb, Christina; Klein, Jochen; Köppen, Andrea; Löffelholz, K.; Jeltsch, Hélène; Cassel, Jean‐Christophe

doi:10.1016/s0304-3940(97)00504-1

Cited by 17 publications

(6 citation statements)

References 14 publications

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“…These results suggest that hippocampal ACh release is under regulatory control of 5-HT 1A and 5-HT 1B receptors. Recent microdialysis studies confirm the stimulatory role of 5-HT 1A receptors in the regulation of cholinergic neurotransmission since local or systemic administration of the 5-HT 1A agonist 8-OH-DPAT increased the hippocampal ACh level in normal (Fujii et al, 1997) and fimbria-fornix lesioned animals with intra-hippocampal grafts of fetal septal cell suspension (Erb et al, 1997).…”

Section: Effect Of Serotonin On Acetylcholine Releasementioning

confidence: 87%

Neurochemistry and pharmacology of the major hippocampal transmitter systems: Synaptic and nonsynaptic interactions

1998

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Hippocampus plays a crucial role in important brain functions (e.g. memory, learning) thus in the past two decades this brain region became a major objective of neuroscience research. During this period large number of anatomical, neurochemical and electrophysiological data have been accumulated. While excellent reviews have been published on the anatomy and electrophysiology of hippocampal formation, the neurochemistry of this area has not been thoroughly surveyed. Therefore the aim of this review is to summarize the neurochemical and pharmacological data on the release of the major neurotransmitters found in the hippocampal region: glutamate (GLU), γ‐amino butyric acid (GABA), acetylcholine (ACh), noradrenaline (NA) and serotonin (5‐HT). In addition, this review analyzes the synaptic and nonsynaptic interactions between hippocampal neuronal elements and overviews how auto‐ and heteroreceptors are involved in the presynaptic modulation of transmitter release. The presented data clearly show that transmitters released from axon terminals without synaptic contact play an important role in the fine tuning of communication between neurons within a neuronal circuit. Hippocampus 1998;8:566–607. © 1998 Wiley‐Liss, Inc.

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Section: Effect Of Serotonin On Acetylcholine Releasementioning

confidence: 87%

Neurochemistry and pharmacology of the major hippocampal transmitter systems: Synaptic and nonsynaptic interactions

1998

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“…Thus, one possibility is that glucose enhances CREB phosphorylation through activation of the cholinergic system. Related to this possibility is evidence that fimbria-fornix lesions, which disrupt cholinergic innervation to the hippocampus (Erb et al, 1997; Nilsson and Björklund, 1992), also disrupt hippocampal CREB activation and impair memory for inhibitory avoidance (Taubenfeld et al, 1999, 2001). Acetylcholine can result in phosphorylation of CREB through binding to muscarinic 3 (M 3 ) receptors (Greenwood and Dragunow, 2002, 2010) or nicotinic α7 receptors (Bitner et al, 2007, 2010; Gubbins and Gopalakrishnan, 2010; Tietje et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Epinephrine and glucose modulate training-related CREB phosphorylation in old rats: Relationships to age-related memory impairments

Morris

Gold

2013

Experimental Gerontology

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Epinephrine enhances memory in young adult rats, in part, by increasing blood glucose levels needed to modulate memory. In old rats, epinephrine is deficient at raising blood glucose levels and thus is only moderately effective at enhancing memory. In contrast, systemic glucose injections improve memory in old rats, with resulting memory performance equal to that of young rats. The diminished response of glucose to training in old rats may blunt downstream neurochemical and molecular mechanisms needed to upregulate memory processes. In the first experiment, young adult and old rats were trained on an inhibitory avoidance task with immediate post-training injections of aCSF or glucose into the dorsal hippocampus. Old rats had significant memory impairments compared to young rats 7 days after training. Intrahippocampal injections of glucose reversed age-related deficits, improving memory scores in old rats to values seen in young rats. A second experiment examined age-related changes in activation of the transcription factor CREB, which is widely implicated in memory formation and may act downstream of hormonal and metabolic signals. Activation was assessed in response to training with systemic injections of epinephrine and glucose at doses known to enhance memory. Young adult and old rats were trained on inhibitory avoidance with immediate post-training systemic injections of saline, epinephrine, or glucose. After training, old rats had significant impairments in CREB phosphorylation in area CA1 and the dentate gyrus region of the hippocampus, and in the basolateral and lateral amygdala. Epinephrine and glucose attenuated age-related deficits in CREB phosphorylation, but were more effective in the amygdala and hippocampus, respectively. Together, these results support the view that age-related changes in blood glucose responses to epinephrine contribute to memory impairments, which may be related to alterations in regional patterns of CREB phosphorylation.

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“…A variety of lesion and transplantation studies has particularly stressed the importance of the cholinergic septohippocampal pathway for learning and memory Erb et al 1997), and inhibition of this pathway has also been implicated in the cognitive effects of ethanol by recent behavioural and electrophysiological studies. In rats, acute ethanol administration preferentially disrupted memory formation at the level of the hippocampus (Melia et al 1996) and led to a reduction of hippocampal theta activity and a suppression of long-term potentiation in vivo (Givens 1995;Givens and McMahon 1995).…”

Section: Claudia Henn · Konrad Löffelholz · Jochen Kleinmentioning

confidence: 99%

Stimulatory and inhibitory effects of ethanol on hippocampal acetylcholine release

Henn¹,

Löffelholz²,

Klein³

1998

Naunyn-Schmiedeberg's Arch Pharmacol

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Using the microdialysis technique and sensitive HPLC procedures for the determination of acetylcholine (ACh) and ethanol, we investigated the release of ACh in rat hippocampus after acute ethanol administration. Systemic administration of ethanol (0.8 and 2.4 g/kg i.p.) led to peak ethanol concentrations of 21 and 42 mM in the hippocampus, respectively. The high dose caused a long-lasting inhibition of basal ACh release by up to 33%. Local infusion of scopolamine (1 microM) enhanced hippocampal ACh release up to eightfold in the presence of neostigmine (10 microM), and this stimulated release was also inhibited after systemic ethanol administration (by up to 45%). The low dose of ethanol (0.8 g/kg) led to a delayed stimulation of hippocampal ACh release. A stimulatory effect on ACh release was also observed when ethanol (50-100 mM) was infused directly into the hippocampus or into the septal area, i.e. to the origin of the cholinergic septohippocampal pathway; thus, the stimulatory effect may be mediated by a direct effect on cholinergic fibres. We conclude that ethanol exerts dual modulatory effects on the activity of the septohippocampal cholinergic fibres, depending on the dose and the site of administration. It is suggested that the inhibition of hippocampal ACh release by intoxicating doses of ethanol may contribute to the well-known cognitive and amnesic effects of ethanol intake.

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Modulation of hippocampal acetylcholine release after fimbria-fornix lesions and septal transplantation in rats

Cited by 17 publications

References 14 publications

Neurochemistry and pharmacology of the major hippocampal transmitter systems: Synaptic and nonsynaptic interactions

Neurochemistry and pharmacology of the major hippocampal transmitter systems: Synaptic and nonsynaptic interactions

Epinephrine and glucose modulate training-related CREB phosphorylation in old rats: Relationships to age-related memory impairments

Stimulatory and inhibitory effects of ethanol on hippocampal acetylcholine release

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