Modulation of AMPA receptor mediated current by nicotinic acetylcholine receptor in layer I neurons of rat prefrontal cortex

Tang, Bo; Luo, Dong; Yang, Jie; Xu, Xiaoyan; Zhu, Binglin; Wang, Xuefeng; Yan, Zhen; Chen, Guojun

doi:10.1038/srep14099

Cited by 24 publications

(26 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, Coogan et al [79] demonstrated that in addition to the high-frequency stimulation-induced LTP, ERK1/2 inhibitor PD98059 prevented LTP induced by the application of the metabotropic glutamate receptor (mGluR) agonist (S)-dihydrophenylglycine (S-DHPG) and the K+ channel blocker tetraethylammonium chloride (TEA-LTP). Moreover, there is evidence showing that LTP-induction through high frequency stimulation in CA1 region of the hippocampus activates ERK in an NMDA receptor activation-dependent manner [81]. These results draw a clear link between ERK1/2 activation and hippocampal LTP, demonstrating a critical regulatory role for ERK1/2 in hippocampal plasticity.…”

Section: Effects Of Nicotine On Hippocampal Kinases and Transcriptionmentioning

confidence: 69%

“…In addition, nicotine increased AMPA/NMDA receptor ratio in the ventral tegmental area dopaminergic neurons [80]. Also, recently, Tang et al [81] found that nicotine increased AMPAR-mediated current amplitude in the prefrontal cortex and this effect was reversed by an α7-nAChR antagonist methyllycaconitine (MLA). This is similar to results from Mitsushima et al [82]that found that α7-nAChR antagonism blocked learning-related CA1 synaptic plasticity.…”

Section: Effects Of Nicotine On Hippocampus-dependent Learning and Mementioning

confidence: 99%

“…ERK1/2 is activated by several different factors such as growth factors, G protein-coupled receptors, and other MAPK kinases [152, 153] and it contributes to the activation of transcription factors such as CREB [154, 155]. Given its role in the Ca2+ mediated cell signaling cascades, ERK1/2 plays modulatory roles in LTP [79–81, 113, 155]. For example, Kandel and his colleagues [80] found that ERK has a critical role in the theta frequent stimulation-induced LTP, which requires PKA, by modulating excitability of hippocampal neurons.…”

Section: Effects Of Nicotine On Hippocampal Kinases and Transcriptionmentioning

confidence: 99%

See 2 more Smart Citations

Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory

Kutlu

Gould

2016

Physiology & Behavior

View full text Add to dashboard Cite

The hippocampus is a key brain structure involved in synaptic plasticity associated with long-term declarative memory formation. Importantly, nicotine and activation of nicotinic acetylcholine receptors (nAChRs) can alter hippocampal plasticity and these changes may occur through modulation of hippocampal kinases and transcription factors. Hippocampal kinases such as cAMP-dependent protein kinase (PKA), calcium/calmodulin-dependent protein kinases (CAMKs), extracellular signal-regulated kinases 1 and 2 (ERK1/2), and c-jun N-terminal kinase 1 (JNK1), and the transcription factor cAMP-response element-binding protein (CREB) that are activated either directly or indirectly by nicotine may modulate hippocampal plasticity and in parallel hippocampus-dependent learning and memory. Evidence suggests that nicotine may alter hippocampus-dependent learning by changing the time and magnitude of activation of kinases and transcription factors normally involved in learning and by recruiting additional cell signaling molecules. Understanding how nicotine alters learning and memory will advance basic understanding of the neural substrates of learning and aid in understanding mental disorders that involve cognitive and learning deficits.

show abstract

Section: Effects Of Nicotine On Hippocampal Kinases and Transcriptionmentioning

confidence: 69%

Section: Effects Of Nicotine On Hippocampus-dependent Learning and Mementioning

confidence: 99%

Section: Effects Of Nicotine On Hippocampal Kinases and Transcriptionmentioning

confidence: 99%

See 1 more Smart Citation

Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory

Kutlu

Gould

2016

Physiology & Behavior

View full text Add to dashboard Cite

show abstract

“…; Tang et al . ). Both of these processes are dependent on Ca 2+ influx and involve interaction with several other postsynaptic proteins.…”

Section: Discussionmentioning

confidence: 97%

Perinatal nicotine exposure impairs the maturation of glutamatergic inputs in the auditory brainstem

Baumann

Koch

2017

The Journal of Physiology

View full text Add to dashboard Cite

Key pointsr Chronic perinatal nicotine exposure causes abnormal auditory brainstem responses and auditory processing deficits in children and animal models.r The effect of perinatal nicotine exposure on synaptic maturation in the auditory brainstem was investigated in granule cells in the ventral nucleus of the lateral lemniscus, which receive a single calyx-like input from the cochlear nucleus.r Perinatal nicotine exposure caused a massive reduction in the amplitude of the excitatory input current.r This caused a profound decrease in the number and temporal precision of spikes in these neurons.r Perinatal nicotine exposure delayed the developmental downregulation of functional nicotinic acetylcholine receptors on these neurons.Abstract Maternal smoking causes chronic nicotine exposure during early development and results in auditory processing deficits including delayed speech development and learning difficulties. Using a mouse model of chronic, perinatal nicotine exposure we explored to what extent synaptic inputs to granule cells in the ventral nucleus of the lateral lemniscus are affected by developmental nicotine treatment. These neurons receive one large calyx-like input from octopus cells in the cochlear nucleus and play a role in sound pattern analysis, including speech sounds. In addition, they exhibit high levels of α7 nicotinic acetylcholine receptors, especially during early development. Our whole-cell patch-clamp experiments show that perinatal nicotine exposure causes a profound reduction in synaptic input amplitude. In contrast, the number of inputs innervating each neuron and synaptic release properties of this calyx-like synapse remained unaltered. Spike number and spiking precision in response to synaptic stimulation were greatly diminished, especially for later stimuli during a stimulus train. Moreover, chronic nicotine exposure delayed the developmental downregulation of functional nicotinic acetylcholine receptors on these neurons, indicating a direct action of nicotine in this brain area. This presumably direct effect of perinatal nicotine exposure on synaptic maturation in the auditory brainstem might be one of the underlying causes for auditory processing difficulties in children of heavy smoking mothers.

show abstract

“…Slices were cut at 2°C in a solution containing the following: 26 mM NaHCO 3 , 22 mM sucrose, 11 mM glucose, 1 mM NaH 2 PO 4 , 3 mM KCl, 0.5 mM CaCl 2 , and 7 mM MgCl 2 saturated with 95% O 2 and 5% CO 2 . Slices recovered for 1 h at room temperature in artificial cerebral spinal fluid (ACSF) (pH 7.4): 1.25 mM NaH 2 PO 4 , 124 mM NaCl, 3 mM KCl, 26 mM NaHCO 3 , 2.5 mM CaCl 2 , 10 mM glucose, and 1.3 mM MgCl 2 , saturated with 95% O 2 and 5% CO 2 (Tang et al, 2015). …”

Section: Methodsmentioning

confidence: 99%

The Phosphodiesterase 10A Inhibitor PF-2545920 Enhances Hippocampal Excitability and Seizure Activity Involving the Upregulation of GluA1 and NR2A in Post-synaptic Densities

Zhang

Gao

Zheng

et al. 2017

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Phosphodiesterase regulates the homeostasis of cAMP and cGMP, which increase the strength of excitatory neural circuits and/or decrease inhibitory synaptic plasticity. Abnormally, synchronized synaptic transmission in the brain leads to seizures. A phosphodiesterase 10A (PDE10A) inhibitor PF-2545920 has recently attracted attention as a potential therapy for neurological and psychiatric disorders. We hypothesized that PF-2545920 plays an important role in status epilepticus (SE) and investigated the underlying mechanisms. PDE10A was primarily located in neurons, and PDE10A expression increased significantly in patients with temporal lobe epilepsy. PF-2545920 enhanced the hyperexcitability of pyramidal neurons in rat CA1, as measured by the frequency of action potentials and miniature excitatory post-synaptic current. GluA1 and NR2A expression also increased significantly in post-synaptic densities, with or without SE in rats treated with PF-2545920. The ratio of p-GluA1/GluA1 increased in the presence of PF-2545920 in groups with SE. Our results suggest that PF-2545920 facilitates seizure activity via the intracellular redistribution of GluA1 and NR2A in the hippocampus. The upregulation of p-GluA1 may play an important role in trafficking GluA1 to post-synaptic densities. The data suggest it would be detrimental to use the drug in seizure patients and might cause neuronal hyperexcitability in non-epileptic individuals.

show abstract

Modulation of AMPA receptor mediated current by nicotinic acetylcholine receptor in layer I neurons of rat prefrontal cortex

Cited by 24 publications

References 49 publications

Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory

Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory

Perinatal nicotine exposure impairs the maturation of glutamatergic inputs in the auditory brainstem

The Phosphodiesterase 10A Inhibitor PF-2545920 Enhances Hippocampal Excitability and Seizure Activity Involving the Upregulation of GluA1 and NR2A in Post-synaptic Densities

Contact Info

Product

Resources

About