Role of α7-nicotinic acetylcholine receptors in tetanic stimulation-induced γ oscillations in rat hippocampal slices

Song, Chuanzhe; Murray, Teresa A.; Kimura, Ryuji; Wakui, Makoto; Ellsworth, Kevin; Javedan, Sam; Marxer-Miller, Syndia; Lukas, Ronald J.; Wu, Jie

doi:10.1016/j.neuropharm.2005.01.003

Cited by 86 publications

(62 citation statements)

References 53 publications

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“…Through these synergistic actions, nicotine can enhance the excitation of interneurons and thereby enhance inhibitory output. Consistent with this, nicotine increases the gamma oscillations that are dependent on interneuron function [127].…”

Section: The Cholinergic System: Reversing Disinhibition and Cognitivmentioning

confidence: 56%

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Lisman

Coyle

Green

et al. 2008

Trends in Neurosciences

922

824

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Many risk genes interact synergistically to produce schizophrenia and many neurotransmitter interactions have been implicated. We have developed a circuit-based framework for understanding gene and neurotransmitter interactions. NMDAR hypofunction has been implicated in schizophrenia because NMDAR antagonists reproduce symptoms of the disease. One action of antagonists is to reduce the excitation of fast-spiking interneurons, resulting in disinhibition of pyramidal cells. Overactive pyramidal cells, notably those in the hippocampus, can drive a hyperdopaminergic state that produces psychosis. Additional aspects of interneuron function can be understood in this framework, as follows. (i) In animal models, NMDAR antagonists reduce parvalbumin and GAD67, as found in schizophrenia. These changes produce further disinhibition and can be viewed as the aberrant response of a homeostatic system having a faulty activity sensor (the NMDAR). (ii) Disinhibition decreases the power of gamma oscillation and might thereby produce negative and cognitive symptoms. (iii) Nicotine enhances the output of interneurons, and might thereby contribute to its therapeutic effect in schizophrenia.

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Section: The Cholinergic System: Reversing Disinhibition and Cognitivmentioning

confidence: 56%

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Lisman

Coyle

Green

et al. 2008

Trends in Neurosciences

922

824

View full text Add to dashboard Cite

show abstract

“…In the adult rat, choline activates α7 receptors with a potency that is 10-fold lower than observed for ACh without any detectable effect at α4, α 2, β2, or β4 ACh receptor subtypes (Papke et al, 1996). In the mammalian brain, α7-nAChRs constitute one of the predominant nAChR subtypes and nicotine application to the ventral tegmental area, paired with postsynaptic stimulation, contributes to a form of long-term potentiation, an effect attributed to presynaptic α7-nAChRs on glutamatergic afferents (Jones and Wonnacott, 2004;Mansvelder and McGehee, 2000;Rousseau et al, 2005;Song et al, 2005). Of relevancy to the present study is the observation that prenatal choline supplementation increases the sensitivity of adult rats to the clock-speed enhancing effect of nicotine (Meck and Williams, 1997a), thus suggesting the possibility that prenatal choline supplementation can alter α7-nAChR function in adulthood (e.g., Cheng et al, 2006;Fayuk and Yakel, 2004;Gueseva et al, 2006;Morley et al, 1977;Stevens et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Prenatal choline supplementation increases sensitivity to time by reducing non-scalar sources of variance in adult temporal processing

Cheng

Meck

2007

Brain Research

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Choline supplementation of the maternal diet has a long-term facilitative effect on timing and temporal memory of the offspring. To further delineate the impact of early nutritional status on interval timing, we examined effects of prenatal-choline supplementation on the temporal sensitivity of adult (6 mo) male rats. Rats that were given sufficient choline in their chow (CON: 1.1 g/kg) or supplemental choline added to their drinking water (SUP: 3.5 g/kg) during embryonic days (ED) 12-17 were trained with a peak-interval procedure that was shifted among 75%, 50%, and 25% probabilities of reinforcement with transitions from 18s -> 36s ->72s temporal criteria. Prenatalcholine supplementation systematically sharpened interval-timing functions by reducing the associative/non-temporal response enhancing effects of reinforcement probability on the Start response threshold, thereby reducing non-scalar sources of variance in the left-hand portion of the Gaussian-shaped response functions. No effect was observed for the Stop response threshold as a function of any of these manipulations. In addition, independence of peak time and peak rate was demonstrated as a function of reinforcement probability for both prenatal-choline supplemented and control rats. Overall, these results suggest that prenatal-choline supplementation facilitates timing by reducing impulsive responding early in the interval, thereby improving the superimposition of peak functions for different temporal criteria.

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“…There is very limited information regarding the effects of nicotine on gamma oscillations in normal or disordered populations. A study in rat hippocampul slices reported that the infusion of highly concentrated nicotine (100 μg) promoted hippocampul gamma activity (Song et al, 2005). Although there are no studies of the direct effects of nicotine on gamma activity in humans, a study in smokers found that chronic smokers exhibited larger gamma band oscillations than never smokers (Crawford et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Phillips¹,

Ehrlichman²,

Siegel³

2007

Neuroscience

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Cigarette smoking is significantly more prevalent in individuals with schizophrenia than in nonaffected populations. Certain neurocognitive deficits and disruptions common in schizophrenia may be altered by smoking, leading to the hypothesis that schizophrenics engage in smoking behavior to alleviate specific neurocognitive symptoms of the disorder. Additionally, research suggests that individuals with schizophrenia have altered auditory event related potentials (ERPs) and abnormalities in evoked gamma oscillations which are both indices of sensory information processing. This study was conducted to examine the effect of acute administration of nicotine and the non-specific nicotinic antagonist mecamylamine on the P20 and N40 components of the auditory event related potential (ERP) and evoked gamma oscillations in mice. Acute nicotine (1 mg/kg) significantly increased P20 amplitude, an effect that was blocked by pretreatment with mecamylamine (2 mg/kg). Additionally, acute nicotine increased the normal burst of evoked gamma following an auditory stimulus. The increase in evoked gamma was also blocked by mecamylamine pretreatment. Although acute nicotine decreased amplitude of the N40 component, this decrease was not attenuated by mecamylamine. These results replicate findings that nicotine may enhance early sensory information processing through the nicotinic acetylcholinergic receptor system in an established model (ERPs) and extend these findings in an emerging, novel model (evoked gamma oscillations) of sensory information processing. The results also support the hypothesis that nicotine may be beneficial to individuals with deficits in neurocognitive functions, such as those suffering from schizophrenia.

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Role of α7-nicotinic acetylcholine receptors in tetanic stimulation-induced γ oscillations in rat hippocampal slices

Cited by 86 publications

References 53 publications

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia

Prenatal choline supplementation increases sensitivity to time by reducing non-scalar sources of variance in adult temporal processing

Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

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