scholarly journals Noradrenaline Modulates the Membrane Potential and Holding Current of Medial Prefrontal Cortex Pyramidal Neurons via β1-Adrenergic Receptors and HCN Channels

2017 ◽  
Vol 11 ◽  
Author(s):  
Katarzyna Grzelka ◽  
Przemysław Kurowski ◽  
Maciej Gawlak ◽  
Paweł Szulczyk
Keyword(s):  
Prefrontal Cortex ◽  
Membrane Potential ◽  
Medial Prefrontal Cortex ◽  
Adrenergic Receptors ◽  
Pyramidal Neurons ◽  
Hcn Channels

scholarly journals α2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex

2008 ◽  
Vol 99 (1) ◽  
pp. 394-401 ◽  
Author(s):  
Albert M. I. Barth ◽  
E. Sylvester Vizi ◽  
Tibor Zelles ◽  
Balazs Lendvai
Keyword(s):  
Prefrontal Cortex ◽  
Adrenergic Receptors ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Hcn Channels ◽  
Transient Activation ◽  
Dendritic Spikes ◽  
Dendritic Spike ◽  
Frequency Threshold

Although dendritic spikes are generally thought to be restricted to the distal apical dendrite, we know very little about the possible modulatory mechanisms that set the spatial limits of dendritic spikes. Our experiments demonstrated that high-frequency trains of backpropagating action potentials avoided filtering in the apical dendrite and initiated all-or-none dendritic Ca2+ transients associated with dendritic spikes in layer 5 pyramidal neurons of the prefrontal cortex. The block of hyperpolarization-activated currents ( Ih) by ZD7288 could shift the frequency threshold and decreased the number of action potentials required to produce the all-or-none Ca2+ transient. Activation of α2-adrenergic receptors could also shift the frequency domain of spike induction to lower frequencies. Our data suggest that noradrenergic activity in the prefrontal cortex influences dendritic Ih and extends the zone of dendritic spikes in the apical dendrite via α2-adrenergic receptors. This mechanism might be one cellular correlate of the α2-receptor–mediated actions on working memory.

scholarly journals Development of inhibitory synaptic inputs on layer 2/3 pyramidal neurons in the rat medial prefrontal cortex

2018 ◽  
Author(s):  
Mari A. Virtanen ◽  
Claudia Marvine Lacoh ◽  
Hubert Fiumelli ◽  
Markus Kosel ◽  
Shiva Tyagarajan ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Neurons ◽  
Synaptic Inputs ◽  
Layer 2

scholarly journals Constitutive Genetic Deletion of Hcn1 Increases Alcohol Preference during Adolescence

2020 ◽  
Vol 10 (11) ◽  
pp. 763
Author(s):  
Michael C. Salling ◽  
Neil L. Harrison
Keyword(s):  
Prefrontal Cortex ◽  
Alcohol Consumption ◽  
Medial Prefrontal Cortex ◽  
Neuronal Excitability ◽  
Cell Types ◽  
Brain Regions ◽  
Alcohol Preference ◽  
Hcn Channels ◽  
Direct Role ◽  
Genetic Deletion

The hyperpolarization-activated cyclic nucleotide-gated channel (HCN), which underlies the hyperpolarization-activated cation current (Ih), has diverse roles in regulating neuronal excitability across cell types and brain regions. Recently, HCN channels have been implicated in preclinical models of substance abuse including alcohol. In the prefrontal cortex of rodents, HCN expression and Ih magnitude are developmentally regulated during adolescence and may be vulnerable to alcohol’s effects. In mice, binge alcohol consumption during the adolescent period results in a sustained reduction in Ih that coincides with increased alcohol consumption in adulthood, yet the direct role HCN channels have on alcohol consumption are unknown. Here, we show that the genetic deletion of Hcn1 causes an increase in alcohol preference on intermittent 2-bottle choice task in homozygous null (HCN1−/−) male mice compared to wild-type littermates without affecting saccharine or quinine preference. The targeted viral deletion of HCN1 in pyramidal neurons of the medial prefrontal cortex resulted in a gradual loss of Hcn1 expression and a reduction in Ih magnitude during adolescence, however, this did not significantly affect alcohol consumption or preference. We conclude that while HCN1 regulates alcohol preference, the genetic deletion of Hcn1 in the medial prefrontal cortex does not appear to be the locus for this effect.

scholarly journals Noradrenaline enhances the excitatory effects of dopamine on medial prefrontal cortex pyramidal neurons in rats

2020 ◽  
Vol 40 (4) ◽  
pp. 348-354 ◽  
Author(s):  
Fumiya Shinohara ◽  
Saya Arakaki ◽  
Taiju Amano ◽  
Masabumi Minami ◽  
Katsuyuki Kaneda
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Neurons
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