Downregulation of muscarinic- and 5-HT1B-mediated modulation of [3H]acetylcholine release in hippocampal slices of rats with fimbria-fornix lesions and intrahippocampal grafts of septal origin

Cassel, J.C.; Jeltsch, Hélène; Neufang, B.; Lauth, Dorothee; Szabó, Béla; Jackisch, Rolf

doi:10.1016/0006-8993(95)01092-0

Cited by 51 publications

(21 citation statements)

References 48 publications

(95 reference statements)

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“…The excessive increases in ACh levels in PF rats following the hippocampal infusion of physostigmine could impede further ACh release by over activation of such receptors. This receptor driven feed back mechanism has been shown to desensitized in rats with lesions of the fimbra-fornix (Cassel et al, 1995; Levey et al, 1995). Thus, in rats with damage to the septo-hippocampal pathway increases in hippocampal ACh levels, via direct physostigmine, are less likely to impact autoregulation of ACh release.…”

Section: Discussionmentioning

confidence: 99%

Increasing hippocampal acetylcholine levels enhance behavioral performance in an animal model of diencephalic amnesia

et al. 2008

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Pyrithiamine-induced thiamine deficiency (PTD) was used to produce a rodent model of WernickeKorsakoff syndrome that results in acute neurological disturbances, thalamic lesions, and learning and memory impairments. There is also cholinergic septo-hippocampal dysfunction in the PTD model. Systemic (Experiment 1) and intrahippocampal (Experiment 2) injections of the acetylcholinesterase inhibitor physostigmine were administered to determine if increasing acetylcholine levels would eliminate the behavioral impairment produced by PTD. Prior to spontaneous alternation testing, rats received injections of either physostigmine (systemic = 0.075 mg/kg; intrahippocampal = 20, 40 ng/µl) or saline. In Experiment 2, intrahippocampal injections of physostigmine significantly enhanced alternation rates in the PTD-treated rats. In addition, although intrahippocampal infusions of 40 ng of physostigmine increased the available amount of ACh in both Pair-fed (PF) and PTD rats, it did so to a greater extent in PF rats. The increase in ACh levels induced by the direct hippocampal application of physostigmine in the PTD model likely increased activation of the extended limbic system, which was dysfunctional, and therefore led to recovery of function on the spontaneous alternation task. In contrast, the lack of behavioral improvement by intrahippocampal physostigmine infusion in the PF rats, despite a greater rise in hippocampal ACh levels, supports the theory that there is a optimal range of cholinergic tone for optimal behavioral and hippocampal function.

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Section: Discussionmentioning

confidence: 99%

Increasing hippocampal acetylcholine levels enhance behavioral performance in an animal model of diencephalic amnesia

et al. 2008

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“…Interestingly, it was reported that the difference between WT and HTR1B KO mice is more evident when animals are challenged with difficult tasks that require higher cognitive flexibility [181,182]. This can be related to the fact that HTR1B activity results in a down-regulation of the cholinergic tone in the hippocampus and in enhanced cholinergic tone in the frontal cortex [31,40]. Moreover, HTR1B are expressed on terminals of retinal ganglion cells in the superior colliculus [22] where they control visual attentional processes with an inhibitory role [21]; uninhibited visual activity may be intuitively related to enhanced ability in spatial tests.…”

Section: Htr1b and Memorymentioning

confidence: 99%

HTR1B as a risk profile maker in psychiatric disorders: a review through motivation and memory

Drago

Alboni

Brunello

et al. 2009

Eur J Clin Pharmacol

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Purpose Serotonin receptor 1B (HTR1B) is involved in the regulation of the serotonin system, playing different roles in specific areas of the brain. We review the characteristics of the gene coding for HTR1B, its product and the functional role of HTR1B in the neural networks involved in motivation and memory; the central role played by HTR1B in these functions is thoroughly depicted and show HTR1B to be a candidate modulator of the mnemonic and motivationally related symptoms in psychiatric illnesses. Methods In order to challenge this assessment, we analyze how and how much the genetic variations located in the gene that codes for HTR1B impacts on the psychiatric phenotypes by reviewing the literature on this topic. Results We gathered partial evidence arising from genetic association studies, which suggests that HTR1B plays a relevant role in substance-related and obsessive compulsive disorders. On the other hand, no solid evidence for other psychiatric disorders was found. This finding is quite striking because of the heavy impairment of motivation and of mnemonic-related functions (for example, recall bias) that characterize major psychiatric disorders. Conclusions The possible reasons for the contrast between the prime relevance of HTR1B in regulating memory and motivation and the limited evidence brought by genetic association studies in humans are discussed, and some suggestions for possible future directions are provided.

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“…It has been suggested that many of the serotonin actions could be mediated by a modulation of the cholinergic system [29,31]. Biochemical and anatomical studies have shown a functional interaction between serotonergic and cholinergic systems [82,83] and therefore, serotonergic receptors could modulate the activity of the cholinergic system to cooperate in the regulation of cognitive processes [84,83]. In keeping with this idea, in a recent work, we analyzed the ratio between cholinergic/serotonergic levels, e.g.…”

Section: Interactions Between the Cholinergic And Serotonergic Systemmentioning

confidence: 82%

Involvement of the Serotonergic System in Cognitive and Behavioral Symptoms of Alzheimers Disease

Ramı́rez¹,

Aisa²,

Gil-Bea³

et al. 2005

CPSR

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Alzheimer's disease (AD) is a chronic progressive disorder characterized by dementia, but often featuring behavioral and psychological syndromes (BPSD), such as depression, overactivity, psychosis or aggressive behavior. Traditional treatments for BPSD are neuroleptics and sedatives, which are not devoid of serious adverse effects. Neurochemically, the classical hallmark of AD is the disruption of basal forebrain cholinergic pathways and consequent cortical cholinergic denervation of the neocortex and hippocampus. However, it is conceivable that, according to the complexity and diversity of BPSD, more than one transmitter system may contribute to a particular behavioral syndrome.The serotonergic system has been implicated not only in cognitive processes, but also in depression, psychosis or aggression. In AD, extensive serotonergic denervation has been reported. In particular, there is growing interest in the pathological functions and implication in BPSD of 5-HT6 receptors, due to its high affinity for antipsychotic drugs and its distribution in the brain. In this study we will review the present knowledge of the involvement of the serotonergic system and its receptors in cognitive deficits and BPSD. From the currently available data, it is possible to conclude that pharmacological manipulation of serotonergic system may improve not only cognitive function but behavioral disturbances in dementia.

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Downregulation of muscarinic- and 5-HT1B-mediated modulation of [3H]acetylcholine release in hippocampal slices of rats with fimbria-fornix lesions and intrahippocampal grafts of septal origin

Cited by 51 publications

References 48 publications

Increasing hippocampal acetylcholine levels enhance behavioral performance in an animal model of diencephalic amnesia

Increasing hippocampal acetylcholine levels enhance behavioral performance in an animal model of diencephalic amnesia

HTR1B as a risk profile maker in psychiatric disorders: a review through motivation and memory

Involvement of the Serotonergic System in Cognitive and Behavioral Symptoms of Alzheimers Disease

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