Nicotinic receptors on hippocampal cultures can increase synaptic glutamate currents while decreasing the NMDA-receptor component

  title={Nicotinic receptors on hippocampal cultures can increase synaptic glutamate currents while decreasing the NMDA-receptor component},
  author={Janet L. Fisher and John A. Dani},
Nicotinic and muscarinic reduction of unitary excitatory postsynaptic potentials in sensory cortex; dual intracellular recording in vitro.
Both carbachol and nicotine reduced short-term depression of EPSPs evoked by 10 Hz stimulation, indicating that EPSP reduction happens via reduction of presynaptic glutamate release.
Nicotine recruits glutamate receptors to postsynaptic sites
Muscarinic and nicotinic presynaptic modulation of EPSCs in the nucleus accumbens during postnatal development.
The results suggest that ACh can decrease or increase glutamatergic neurotransmission in the nAcb by acting on muscarinic and nicotinic receptors located on excitatory terminals, and that cholinergic modulation of AMPA/KA and NMDA receptor-mediated neurotransmission during postnatal development could play an important role in activity-dependent developmental processes.
Cholinergic Axons Modulate GABAergic Signaling among Hippocampal Interneurons via Postsynaptic α7 Nicotinic Receptors
It is shown that agonists of α7 receptors profoundly depress GABAergic IPSCs recorded in stratum radiatum interneurons in the CA1 region of the hippocampus, revealing a novel mechanism by which cholinergic neurons modulate information processing in the hippocampus.
Persistent decrease in synaptic efficacy induced by nicotine at Schaffer collateral–CA1 synapses in the immature rat hippocampus
It is shown that, at high P synapses, nicotine induces long‐term depression of AMPA‐ and NMDA‐mediated synaptic currents and a bi‐directional control of synaptic plasticity by nicotine would considerably enhance the computational properties of the network during a critical period of postnatal development thus contributing to sculpt the neuronal circuit.
Functional Modulation of the Mouse Prefrontal Cortex by Nicotinic Acetylcholine Receptors
Results confirmed the existence of a feedforward inhibitory loop between layer V pyramidal cells in the mouse similar to that found in the rat and ferret, and demonstrated that activation of nAChRs on the interceding interneuron can alter the strength of this feedforward loop.
Short- and long-term enhancement of excitatory transmission in the spinal cord dorsal horn by nicotinic acetylcholine receptors
  • J. Genzen, D. McGehee
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 2003
It is demonstrated that α7 nAChRs can contribute to both short- and long-term enhancement of glutamatergic synaptic transmission in the spinal cord dorsal horn and provide a possible mechanism for nicotinic hyperalgesia.
Effects of α7 Nicotinic Receptor Activation on Cell Survival in Rat Organotypic Hippocampal Slice Cultures
The results show that α7 nAChR stimulation did not significantly influence NMDA-induced excitotoxic cell damage as measured by propidium iodide uptake, and treatment of OHSCs with the α7NAChRs agonist choline alone induced an increase in the propidium iodine signal.


Neuronal nicotinic acetylcholine receptor activation modulates gamma-aminobutyric acid release from CA1 neurons of rat hippocampal slices.
It is suggested that activation of nAChRs present in GABAergic interneurons can evoke inhibitory activity in CA1 pyramidal neurons, thereby modulating processing of information in the hippocampus.
Choline and Selective Antagonists Identify Two Subtypes of Nicotinic Acetylcholine Receptors that Modulate GABA Release from CA1 Interneurons in Rat Hippocampal Slices
It is demonstrated that CA1 interneurons, in addition to expressing functional α7 nA ChRs, also express functional α4β2-like nAChRs and that activation of both receptors facilitates an action potential-dependent release of GABA.
Nicotine Selectively Enhances NMDA Receptor-Mediated Synaptic Transmission during Postnatal Development in Sensory Neocortex
The data suggest that nicotine acts at rapidly desensitizing, presynaptic α7 nAChRs to increase glutamate release onto postsynaptic NMDA receptors to contribute to experience-dependent synaptic plasticity in sensory neocortex during early postnatal life.
Synaptic Potentials Mediated via α-Bungarotoxin-Sensitive Nicotinic Acetylcholine Receptors in Rat Hippocampal Interneurons
These studies provide the first demonstration of a functional cholinergic synapse in the mammalian brain, in which the primary postsynaptic receptors are α-bungarotoxin-sensitive nicotinic acetylcholine receptors.
Role of Ca2+ Ions in Nicotinic Facilitation of GABA Release in Mouse Thalamus
It is proposed that the nicotinic facilitation of GABAergic transmission may contribute to the increase of signal-to-noise ratio observed in the thalamus in vivo during arousal.
Acetylcholine Activates an α-Bungarotoxin-Sensitive Nicotinic Current in Rat Hippocampal Interneurons, But Not Pyramidal Cells
Results suggest that α7-containing nAChRs also may play a postsynaptic role in the excitation of hippocampal interneurons by desensitizing these receptors, and nicotine may disrupt this action and indirectly excite pyramidal neurons by reducing GABAergic inhibition.
Glutamate and GABA Release Are Enhanced by Different Subtypes of Presynaptic Nicotinic Receptors in the Lateral Geniculate Nucleus
The results demonstrate that the LGNv neurons receive both glutamatergic and GABAergic inputs and that the release of these transmitters can be modulated by different presynaptic nAChRs, demonstrating the regulation of synaptic efficacy in the brain by presycholine receptors can be complex.
Modulation of excitatory synaptic transmission by low concentrations of glutamate in cultured rat hippocampal neurons.
Results suggest that the ambient glutamate level is an important determinant of synaptic efficacy, and relatively small changes in extracellular glutamate can alter fast excitatory synaptic transmission by both presynaptic and postsynaptic mechanisms.
Nicotinic Stimulation Produces Multiple Forms of Increased Glutamatergic Synaptic Transmission
The results with evoked synaptic currents showed that nAChR activity can alter the relationship between the incoming presynaptic activity and outgoing postsynaptic signaling along glutamatergic fibers, which suggests that the same information arriving along the same glutamatorgic afferents will be processed differently when properly timed nicotinic activity converges onto the glutamaterspine terminals.
Diversity of nicotinic acetylcholine receptors in rat brain. V. alpha-Bungarotoxin-sensitive nicotinic receptors in olfactory bulb neurons and presynaptic modulation of glutamate release.
The present results suggest that nicotinic synaptic transmission could play an important role in modulating the bulbar output at the glomerular level, and a presynaptic modulatory effect is one of the functions for the alpha-bungarotoxin-sensitive nAChRs in the mammalian central nervous system.