Dopaminergic antagonists prevent long-term maintenance of posttetanic LTP in the CA1 region of rat hippocampal slices

Frey, Uwe; Schroeder, Helmut; Matthies, H

doi:10.1016/0006-8993(90)91578-5

Cited by 305 publications

(211 citation statements)

References 35 publications

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“…Monoaminergic involvement of LTP induction and maintenance is also supported by reports that have measured the concentrations and temporal dynamics of such neuromodulators during LTP (Frey et al, 1990;Harley, 1991;Bronzino et al, 2001). These reports showed that local NA and DA concentrations could rise to several times the basal value upon tetanus stimulation during induction of LTP.…”

Section: Discussionmentioning

confidence: 59%

Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

Mishima

Fujiwara²,

Kofuji³

et al. 2012

J. Neurosci.

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The membrane protein HPC-1/syntaxin 1A is believed to play a key role in synaptic vesicle exocytosis, and it was recently suggested to be required for synaptic plasticity. Despite evidence for the function of HPC-1/syntaxin 1A in synaptic plasticity, the underlying cellular mechanism is unclear. We found that although fast synaptic transmission and long-term depression were unaffected, HPC-1/syntaxin 1A knock-out (STX1A Ϫ/Ϫ ) mice showed impaired long-term potentiation (LTP) in response to theta-burst stimulation in CA1 hippocampal slices. The impairment in LTP was rescued by the application of forskolin, an adenylyl cyclase activator, or more robust stimulation, suggesting that cAMP/protein kinase A signaling was suppressed in these mice. In addition, catecholamine release from the hippocampus was significantly reduced in STX1A Ϫ/Ϫ mice. Because HPC-1/syntaxin 1A regulates exocytosis of dense-core synaptic vesicles, which contain neuromodulatory transmitters such as noradrenaline, dopamine and 5-HT, we examined the effect of neuromodulatory transmitters on LTP induction. Noradrenaline and dopamine enhanced LTP induction in STX1A Ϫ/Ϫ mice, whereas catecholamine depletion reduced LTP induction in wild-type mice. Theses results suggest that HPC-1/syntaxin 1A regulates catecholaminergic systems via exocytosis of dense-core synaptic vesicles, and that deletion of HPC-1/syntaxin 1A causes impairment of LTP induction.

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Section: Discussionmentioning

confidence: 59%

Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

Mishima

Fujiwara²,

Kofuji³

et al. 2012

J. Neurosci.

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“…A role of the hippocampus in episodic memory, reward learning, and the generation of contextually appropriate reward seeking has been indicated, though (McDonald and White, 1993;Eichenbaum, 2013;Dickerson and Eichenbaum, 2009). Several studies have demonstrated that DA transmission facilitates hippocampal synaptic long-term potentiation (Jay, 2003;Li et al, 2003) and likely has an important role in the formation and reactivation of rewardrelated memories (Shohamy and Adcock, 2010;Frey et al, 1990;Otmakhova and Lisman, 1998). In humans, neuroimaging studies have provided evidence of hippocampal activation following exposure to drug cues (Grant et al, 1996;Kilts et al, 2001;Wexler et al, 2001;Chase et al, 2011;Tang et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Cocaine Cue-Induced Dopamine Release in Amygdala and Hippocampus: A High-Resolution PET [18F]Fallypride Study in Cocaine Dependent Participants

Fotros

Casey

Larcher

et al. 2013

Neuropsychopharmacol

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Drug-related cues are potent triggers for relapse in people with cocaine dependence. Dopamine (DA) release within a limbic network of striatum, amygdala and hippocampus has been implicated in animal studies, but in humans it has only been possible to measure effects in the striatum. The objective here was to measure drug cue-induced DA release in the amygdala and hippocampus using high-resolution PET with [ 18 F]fallypride. Twelve cocaine-dependent volunteers (mean age: 39.6 ± 8.0 years; years of cocaine use: 15.9 ± 7.4) underwent two [ 18 F]fallypride high-resolution research tomography-PET scans, one with exposure to neutral cues and one with cocaine cues. To our knowledge this study provides the first evidence of drug cue-induced DA release in the amygdala and hippocampus in humans. The preferential induction of DA release among high-craving responders suggests that these aspects of the limbic reward network might contribute to drug-seeking behavior.

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“…DA prolongs long-term potentiation (LTP; Frey et al, 1990Frey et al, , 1993Huang and Kandel, 1995), a cellular mechanism necessary for successful memory formation and consolidation (for review, see Cooke and Bliss, 2006). In humans, molecular imaging studies have related higher D2 receptor binding in hippocampus to better recall of verbal (Takahashi et al, 2007) and pictorial (Takahashi et al, 2008) memory.…”

Section: Dopaminergic Modulation Of Episodic Memorymentioning

confidence: 99%

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Papenberg¹,

Li²,

Nagel³

et al. 2014

Neurobiology of Aging

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a b s t r a c tBoth the dopaminergic and glutamatergic systems modulate episodic memory consolidation. Evidence from animal studies suggests that these two neurotransmitters may interact in influencing memory performance. Given that individual differences in episodic memory are heritable, we investigated whether variations of the dopamine D2 receptor gene (rs6277, C957T) and the N-methyl-D-aspartate 3A (NR3A) gene, coding for the N-methyl-D-aspartate 3A subunit of the glutamate N-methyl-D-aspartate receptor (rs10989591, Val362Met), interactively modulate episodic memory in large samples of younger (20e31 years; n ¼ 670) and older (59e71 years; n ¼ 832) adults. We found a reliable gene-gene interaction, which was observed in older adults only: older individuals carrying genotypes associated with greater D2 and N-methyl-D-aspartate receptor efficacy showed better episodic performance. These results are in line with findings showing magnification of genetic effects on memory in old age, presumably as a consequence of reduced brain resources. Our findings underscore the need for investigating interactive effects of multiple genes to understand individual difference in episodic memory.

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Dopaminergic antagonists prevent long-term maintenance of posttetanic LTP in the CA1 region of rat hippocampal slices

Cited by 305 publications

References 35 publications

Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

Cocaine Cue-Induced Dopamine Release in Amygdala and Hippocampus: A High-Resolution PET [18F]Fallypride Study in Cocaine Dependent Participants

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

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