Tonic facilitation of glutamate release by glycine binding sites on presynaptic NR2B-containing NMDA autoreceptors in the rat visual cortex

Li, Yanhai; Han, Tao; Meng, Kai

doi:10.1016/j.neulet.2007.12.023

Cited by 24 publications

(23 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A small but significant increase of the PPR occurred in the presence AP5 (control: 0.98 Ϯ 0.04, n ϭ 46, vs. AP5: 1.17 Ϯ 0.07, n ϭ 20, t-test ϭ 2.35; P Ͻ 0.05), which suggests a decrease in the presynaptic release probability (Zucker and Regehr 2002) due to inhibition of NMDARs. This is in agreement with previous studies, which showed that there is a tonic activity of presynaptic NMDARs that facilitates spontaneous and evoked neurotransmitter release (Bender et al 2006;Berretta and Jones 1996;Brasier and Feldman 2008;Corlew et al 2007;Li and Han 2007;Li et al 2008;Sjostrom et al 2003).…”

Section: Pharmacology Of Synaptic Plasticity Induced In Pfc By Stdp Asupporting

confidence: 94%

Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex

Zaitsev

Anwyl

2012

Journal of Neurophysiology

View full text Add to dashboard Cite

Zaitsev AV, Anwyl R. Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex. J Neurophysiol 107: 205-215, 2012. First published October 5, 2011 doi:10.1152/jn.00452.2011.-The induction of long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic currents was investigated in proximal synapses of layer 2/3 pyramidal cells of the rat medial prefrontal cortex. The spike timing-dependent plasticity (STDP) induction protocol of negative timing, with postsynaptic leading presynaptic stimulation of action potentials (APs), induced LTD as expected from the classical STDP rule. However, the positive STDP protocol of presynaptic leading postsynaptic stimulation of APs predominantly induced a presynaptically expressed LTD rather than the expected postsynaptically expressed LTP. Thus the induction of plasticity in layer 2/3 pyramidal cells does not obey the classical STDP rule for positive timing. This unusual STDP switched to a classical timing rule if the slow Ca 2ϩ -dependent, K ϩ -mediated afterhyperpolarization (sAHP) was inhibited by the selective blocker N-trityl-3-pyridinemethanamine (UCL2077), by the ␤-adrenergic receptor agonist isoproterenol, or by the cholinergic agonist carbachol. Thus we demonstrate that neuromodulators can affect synaptic plasticity by inhibition of the sAHP. These findings shed light on a fundamental question in the field of memory research regarding how environmental and behavioral stimuli influence LTP, thereby contributing to the modulation of memory.␤-adrenergic receptor; cannabinoid receptor type 1; excitatory postsynaptic currents; long-term depression; long-term potentiation VARIOUS METHODS HAVE BEEN demonstrated for inducing longterm potentiation (LTP) and long-term depression (LTD) in the neocortex. LTP and LTD are induced by classical high-frequency stimulation (HFS) and low-frequency stimulation, respectively (Kirkwood et al. 1993). In addition, long-term plasticity in the neocortex has recently been found to be evoked by spike timing-dependent plasticity (STDP), which appears to be closer to natural physiological conditions. A pairing of presynaptic action potentials (APs) leading postsynaptic APs (pre-leading-post; positive timing) induced spike timing-dependent LTP (tLTP), whereas postsynaptic APs leading presynaptic APs (post-leading-pre; negative timing) induced spike timing-dependent LTD (tLTD). Both occurred within narrow timing windows: ϳ15 ms for the induction of tLTP and up to 100 ms for the induction of tLTD (Markram et al. 1997b;Sjostrom et al. 2001 Sjostrom et al. , reviewed in 2008.

show abstract

Section: Pharmacology Of Synaptic Plasticity Induced In Pfc By Stdp Asupporting

confidence: 94%

Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex

Zaitsev

Anwyl

2012

Journal of Neurophysiology

View full text Add to dashboard Cite

show abstract

“…It has been shown that the release of many neurotransmitters is regulated by specific presynaptic receptors in several brain areas. Recently, it has been demonstrated the existence of NMDA presynaptic receptors in glutamatergic terminals in different areas of central nervous system [31][32][33][34]. We are tempted to speculate about the possibility of this kind of receptors existing in MBH and POA, being eventually responsible for the neurosteroid modulation shown in this article.…”

Section: Discussionmentioning

confidence: 77%

Allopregnanolone induces LHRH and glutamate release through NMDA receptor modulation

et al. 2011

View full text Add to dashboard Cite

LHRH release from hypothalamus is influenced by the neurotransmitter glutamate that acts, among others, on NMDA receptors present in LHRH neurons. On the other hand, the neurosteroid allopregnanolone can modulate the activity of specific neurotransmitter receptors and affect neurotransmitter release. We examined the role of allopregnanolone on in vitro LHRH and glutamate release from mediobasal hypothalamus and anterior preoptic area of ovariectomized rats with estrogen and progesterone replacement. Moreover, we evaluated whether the neurosteroid might act through modulation of NMDA receptors. Allopregnanolone induced an increase in LHRH release. This effect was reversed when the NMDA receptors were blocked by the NMDA antagonist 2-amino-7-phosphonoheptanoic acid (AP-7) indicating that this neurosteroid would interact with NMDA receptors. Moreover allopregnanolone induced an augment in K(+) evoked [(3)H]-glutamate release from mediobasal hypothalamus-anterior preoptic area explants and this effect was also reversed when NMDA receptors were blocked with AP-7. These results suggest an important physiologic function of allopregnanolone on the regulation of neuroendocrine function in female adult rats. Not only appears to be involved in enhancing LHRH release through modulation of NMDA receptors but also in the release of glutamate which is critical in the control of LHRH release.

show abstract

“…There is evidence that presynaptic NMDARs are localized in GABAergic terminals of several brain areas including the VM (Paquet and Smith, 2000) and their role seems to modulate the strength of synaptic transmission by varying the likelihood of neurotransmitter release (Pinheiro and Mulle, 2008). In most brain areas, the presence of presynaptic NMDARs contribute to release of inhibitory neurotransmitter in the cerebral cortex (Mathew and Hablitz, 2011;Ren et al, 2007), lateral amygdala (Humeau et al, 2003), cerebellum (Bidoret et al, 2009), entorhinal cortex (Chamberlain et al, 2008), and visual cortex (Li et al, 2008). In general these studies demonstrate that inhibition can be potentiated by axoaxonic contacts without the need for somatic interneuron firing; such mechanism alters the weight between excitatory and inhibitory inputs and therefore alters the output of the neuronal circuit.…”

Section: Discussionmentioning

confidence: 99%

Reduction in Ventral Midbrain NMDA Receptors Reveals Two Opposite Modulatory Roles for Glutamate on Reward

Hernández

Khodami-Pour

Lévesque

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

Glutamate is a major component of the reward circuitry and recent clinical studies suggest that new molecules that would target glutamate neurotransmission are most likely to constitute more effective medications for mood disorders. It is well known that activation of N-methyl-D-aspartate glutamate receptors (NMDARs) initiates dopamine burst firing, a mode associated with reward signaling; but NMDARs also contribute to the maintenance of an inhibitory drive to dopamine neurons. Such opposite modulatory functions imply that different subtypes of NMDARs are expressed on different ventral midbrain (VM) neurons and/or afferent inputs to dopamine neurons. By using the small interfering RNA (siRNA) technique, we studied the effects of VM downregulation of NMDAR subunits GluN1, GluN2A, and GluN2D on reward induced by dorsal raphe electrical stimulation. Reward thresholds were measured before and 24 h after each of three consecutive daily bilateral microinjections of siRNA for the targeted receptor subunit(s) or non-active RNA sequence. After the last measurement, reward thresholds were reassessed following a bilateral microinjection of the preferred GluN2A-NMDA antagonist, (2R,4S)-4-(3-Phosphopropyl)-2-piperidinecarboxylic acid (PPPA). Western-blot analysis showed that siRNAs reduced GluN1-and GluN2A-containing receptors whereas behavioral tests showed that only a reduction in GluN1 produced reward attenuation. Despite NMDAR reduction, reward-enhancing effect of PPPA remained unchanged. We conclude that VM glutamate relays the reward signal initiated by dorsal raphe electrical stimulation by acting on NMDARs devoid of GluN2A/2D subunits and exerts an inhibition on this reward signal by acting on GluN2A-containing NMDARs most likely located on afferent terminals.

show abstract

Tonic facilitation of glutamate release by glycine binding sites on presynaptic NR2B-containing NMDA autoreceptors in the rat visual cortex

Cited by 24 publications

References 25 publications

Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex

Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex

Allopregnanolone induces LHRH and glutamate release through NMDA receptor modulation

Reduction in Ventral Midbrain NMDA Receptors Reveals Two Opposite Modulatory Roles for Glutamate on Reward

Contact Info

Product

Resources

About