Differential Mechanisms Involved in the Effect of Nicotinic Agonists DMPP and Lobeline to Release [ 3 H]5-HT from Rat Hippocampal Slices

Lendvai, Balázs; Sershen, Henry; Lajtha, Ábel; Sántha, Ernö; Baranyi, Mária; Vizi, E.S.

doi:10.1016/s0028-3908(96)00115-3

Cited by 50 publications

(17 citation statements)

References 27 publications

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“…The method of drug delivery seems appropriate for nicotine as it is widely accepted that nAChRs are involved in nonsynaptic transmission (Umbriaco et al, 1995;Vizi and Lendvai, 1999;Vizi, 2000;Vizi et al, 2004). Pressure application of drugs produce rapid, temporally limited responses, but the concentration set for the pipette internal solution is substantially higher than at the target sites where the receptors are located (Lendvai et al, 1996). We assume that during the short period of drug diffusion, nicotine or choline could only reach presynaptic targets in low concentrations.…”

Section: Discussionmentioning

confidence: 99%

The effect of nicotine on spiking activity and Ca²⁺ dynamics of dendritic spines in rat CA1 pyramidal neurons

et al. 2008

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Nicotinic acetylcholine receptors (nAChRs) of the hippocampus have been thought to contribute to cognitive enhancement by cigarette smoking. Although positive modulation on cognitive functions is linked to the smoked, low-dose nicotine, the cellular correlate behind this modulation is unknown. It has been accepted that cellular mechanisms underlying plastic effects on memory involve the association of backpropagating action potentials (bAPs) with synaptic activity in the hippocampus. Here, we show the effects of low-dose (1 microM) nicotine on bAP-evoked Ca2+ transients in basal dendrites and spines of pyramidal neurons in rat hippocampal slices. Although nicotine application failed to have any direct effect in low concentration, it could significantly enhance bAP-evoked Ca2+ transients through presynaptic nAChRs located on axon terminals innervating pyramidal cells. The activation of these receptors is known to release neurotransmitters and induce postsynaptic currents. High-dose (250-500 microM) nicotine could induce firing and Ca2+ accumulation in spines. Large amplitude currents were observed occasionally (8 out of 18 cells) in voltage clamp recordings in response to pressure application of high-dose nicotine. This may explain the relatively low incidence of nicotine-induced firing (7 out of 27 cells) under current clamp. These data indicate that (i) activation of presynaptic nAChRs can modulate backreporting in dendrites of pyramidal neurons and (ii) there is a group of pyramidal neurons with higher nicotine-sensitivity, producing firing at strong stimulations. Our data revealed a subcellular effect of nicotine through regulation of Ca2+ levels in the computational units of pyramidal neurons.

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Section: Discussionmentioning

confidence: 99%

The effect of nicotine on spiking activity and Ca²⁺ dynamics of dendritic spines in rat CA1 pyramidal neurons

et al. 2008

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“…The release of 5-HT into striatal slices due to nicotine exposure showed an increase over a number of days; for example a signifi cant enhancement after 10 days of nicotine treatment has been described [ 82 ]. Acute and chronic nicotine administration increased striatal 5-HT release in freely moving rats only when they were exposed to stress, likely by stimulating presynaptic nicotinic receptors in the striatum [ 83 ]. Nicotinic receptor agonists such as 1,1-dimethyl-4-phenylpiperazinium (DMPP), lobeline and nicotine have been shown to increase [ 3 H]5-HT release in hippocampal slices in the rat; however cytisine, epibatidine and nicotine had no effect in others [ 84 , 85 ].…”

Section: Serotonergic Involvement In the Cns Effects Of Nicotinementioning

confidence: 99%

Role of Central Serotonin Receptors in Nicotine Addiction

et al. 2014

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Regulation of normal or abnormal behaviour is critically controlled by the central serotonergic systems. Recent evidence has suggested that serotonin (5-HT) neurotransmission dysfunction contributes to a variety of pathological conditions, including depression, anxiety, schizophrenia and Parkinson's disorders. There is also a great amount of evidence indicating that 5-HT signalling may affect the reinforcing properties of drugs of abuse by the interaction and modulation of dopamine (DA) function. This chapter is focused on one of the more addictive drugs, nicotine. It is widely recognised that the effects of nicotine are strongly associated with the stimulatory action it exhibits on mesolimbic DAergic function. We outline the role of 5-HT and its plethora of receptors, focusing on 5-HT 2 subtypes with relation to their involvement in the neurobiology of nicotine addiction. We also explore the novel pharmacological approaches using 5-HT agents for the treatment of nicotine dependence. Compelling evidence shows that 5-HT 2C receptor agonists may be possible therapeutic targets for smoking cessation, although further investigation is required.

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“…Activation of nAChRs in the hippocampus leads to the release of NE (139,146,179), GABA (83,101), and serotonin (90,156). In the striatum, nicotinic stimulation evokes the release of ACh (140), glutamate (162), dopamine (DA) (20,24,30,50,105,153,165), and serotonin (132).…”

Section: Presynaptic And/or Preterminal Nicotinic Acetylcholine mentioning

confidence: 99%

“…Nicotinic agonists may combine their actions on presynaptic/preterminal nAChRs with an effect on transmitter uptake molecules resulting in compound release mechanisms (79,81,82,90,141,156). The relative proportions of receptorial and nonconventional effects of dimethylphenylpiperazinium (DMPP) are determined by the concentration of the agonist (156).…”

Section: B Subtypes Of Nachrs Involved In the Release Of Transmittersmentioning

confidence: 99%

Nonsynaptic Chemical Transmission Through Nicotinic Acetylcholine Receptors

Lendvai¹,

Vizi²

2008

Physiological Reviews

124

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This review attempts to organize the different aspects of nicotinic transmission in the context of nonsynaptic interactions. Nicotinic acetylcholine receptors (nAChRs) dominantly operate in the nonsynaptic mode in the central nervous system despite their ligand-gated ion-channel nature, which would otherwise be better suited for fast synaptic transmission. This fast form of nonsynaptic transmission, most likely unique to nAChRs, represents a new avenue in the communication platforms of the brain. Cholinergic messages received by nAChRs, arriving at a later phase following synaptic activation, can interfere with dendritic signal integration. Nicotinic transmission plays a role in both neural plasticity and cellular learning processes, as well as in long-term changes in basic activity through fast activation, desensitization of receptors, and fluctuations of the steady-state levels of ACh. ACh release can contribute to plastic changes via activation of nAChRs in neurons and therefore plays a role in learning and memory in different brain regions. Assuming that nAChRs in human subjects are ready to receive long-lasting messages from the extracellular space because of their predominantly nonsynaptic distribution, they offer an ideal target for drug therapy at low, nontoxic drug levels.

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Differential Mechanisms Involved in the Effect of Nicotinic Agonists DMPP and Lobeline to Release [ 3 H]5-HT from Rat Hippocampal Slices

Cited by 50 publications

References 27 publications

The effect of nicotine on spiking activity and Ca²⁺ dynamics of dendritic spines in rat CA1 pyramidal neurons

The effect of nicotine on spiking activity and Ca²⁺ dynamics of dendritic spines in rat CA1 pyramidal neurons

Role of Central Serotonin Receptors in Nicotine Addiction

Nonsynaptic Chemical Transmission Through Nicotinic Acetylcholine Receptors

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Differential Mechanisms Involved in the Effect of Nicotinic Agonists DMPP and Lobeline to Release [ 3 H]5-HT from Rat Hippocampal Slices

Cited by 50 publications

References 27 publications

The effect of nicotine on spiking activity and Ca2+ dynamics of dendritic spines in rat CA1 pyramidal neurons

The effect of nicotine on spiking activity and Ca2+ dynamics of dendritic spines in rat CA1 pyramidal neurons

Role of Central Serotonin Receptors in Nicotine Addiction

Nonsynaptic Chemical Transmission Through Nicotinic Acetylcholine Receptors

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The effect of nicotine on spiking activity and Ca²⁺ dynamics of dendritic spines in rat CA1 pyramidal neurons

The effect of nicotine on spiking activity and Ca²⁺ dynamics of dendritic spines in rat CA1 pyramidal neurons