scholarly journals Nicotinic Acetylcholine Receptors Control Encoding and Retrieval of Associative Recognition Memory through Plasticity in the Medial Prefrontal Cortex

Cell Reports ◽  
2018 ◽  
Vol 22 (13) ◽  
pp. 3409-3415 ◽  
Author(s):  
Marie H. Sabec ◽  
Susan Wonnacott ◽  
E. Clea Warburton ◽  
Zafar I. Bashir
Keyword(s):  
Prefrontal Cortex ◽  
Recognition Memory ◽  
Medial Prefrontal Cortex ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Associative Recognition ◽  
Nicotinic Acetylcholine ◽  
Encoding And Retrieval

Brain nicotinic acetylcholine receptors are involved in stress-induced potentiation of nicotine reward in rats

2017 ◽  
Vol 31 (7) ◽  
pp. 945-955 ◽  
Author(s):  
Parastoo Javadi ◽  
Ameneh Rezayof ◽  
Maryam Sardari ◽  
Zahra Ghasemzadeh
Keyword(s):  
Prefrontal Cortex ◽  
Conditioned Place Preference ◽  
Chronic Stress ◽  
Medial Prefrontal Cortex ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Basolateral Amygdala ◽  
Acute Stress ◽  
Place Preference ◽  
Nicotinic Acetylcholine

The aim of the present study was to examine the possible role of nicotinic acetylcholine receptors of the dorsal hippocampus (CA1 regions), the medial prefrontal cortex or the basolateral amygdala in the effect of acute or sub-chronic stress on nicotine-induced conditioned place preference. Our results indicated that subcutaneous administration of nicotine (0.2 mg/kg) induced significant conditioned place preference. Exposure to acute or sub-chronic elevated platform stress potentiated the response of an ineffective dose of nicotine. Pre-conditioning intra-CA1 (0.5–4 µg/rat) or intra-medial prefrontal cortex (0.2–0.3 µg/rat) microinjection of mecamylamine (a non-selective nicotinic acetylcholine receptor antagonist) reversed acute stress-induced potentiation of nicotine reward as measured in the conditioned place preference paradigm. By contrast, pre-conditioning intra-basolateral amygdala microinjection of mecamylamine (4 µg/rat) potentiated the effects of acute stress on nicotine reward. Our findings also showed that intra-CA1 or intra-medial prefrontal cortex, but not intra-basolateral amygdala, microinjection of mecamylamine (4 µg/rat) prevented the effect of sub-chronic stress on nicotine reward. These findings suggest that exposure to elevated platform stress potentiates the rewarding effect of nicotine which may be associated with the involvement of nicotinic acetylcholine receptors. It seems that there is a different contribution of the basolateral amygdala, the medial prefrontal cortex or the CA1 nicotinic acetylcholine receptors in stress-induced potentiation of nicotine-induced conditioned place preference.

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