Nicotinic acetylcholine receptors of the dorsal hippocampus and the basolateral amygdala are involved in ethanol-induced conditioned place preference

Neuroscience ◽  
2010 ◽  
Vol 168 (2) ◽  
pp. 505-513 ◽  
Author(s):  
M.R. Zarrindast ◽  
J. Meshkani ◽  
A. Rezayof ◽  
R. Beigzadeh ◽  
P. Rostami
Keyword(s):  
Conditioned Place Preference ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Basolateral Amygdala ◽  
Dorsal Hippocampus ◽  
Place Preference ◽  
Nicotinic Acetylcholine

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.

Acquisition and reinstatement of ethanol-induced conditioned place preference in rats: Effects of the cholinesterase inhibitors donepezil and rivastigmine

2016 ◽  
Vol 30 (7) ◽  
pp. 676-687 ◽  
Author(s):  
Kinga Gawel ◽  
Krzysztof Labuz ◽  
Ewa Gibula-Bruzda ◽  
Malgorzata Jenda ◽  
Marta Marszalek-Grabska ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Acetylcholine Receptor ◽  
Conditioned Place Preference ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Cholinesterase Inhibitors ◽  
Muscarinic Acetylcholine Receptor ◽  
Similar Efficacy ◽  
Place Preference ◽  
Nicotinic Acetylcholine

The present study examined the influence of the cholinesterase inhibitors donepezil (a selective inhibitor of acetylcholinesterase) and rivastigmine (also an inhibitor of butyrylcholinesterase) on the acquisition and reinstatement of ethanol-induced conditioned place preference (CPP) in rats. Before the CPP procedure, animals received a single injection of ethanol (0.5 g/kg, 10% w/v, intraperitoneally [i.p.]) for 15 days. The ethanol-induced CPP (biased method) was developed by four injections of ethanol (0.5 g/kg, 10% w/v, i.p.) every second day. Control rats received saline instead of ethanol. Donepezil (0.5, 1 or 3 mg/kg, i.p.) or rivastigmine (0.03, 0.5 or 1 mg/kg, i.p.) were administered before ethanol during conditioning or before the reinstatement of ethanol-induced CPP. The cholinesterase inhibitors were equally effective in increasing (dose dependently) the acquisition of ethanol-induced CPP. Furthermore, priming injections of both inhibitors reinstated (cross-reinstatement) the ethanol-induced CPP with similar efficacy. These effects of both cholinesterase inhibitors were reversed by mecamylamine (3 mg/kg, i.p.), a nicotinic acetylcholine receptor antagonist, but not by scopolamine (0.5 mg/kg, i.p.), a muscarinic acetylcholine receptor antagonist. Thus, our results show that the cholinergic system is involved in the reinforcing properties of ethanol, and nicotinic acetylcholine receptors play an important role in the relapse to ethanol-seeking behaviour.

scholarly journals Contrasting effects of the α7 nicotinic receptor antagonist methyllycaconitine in different rat models of heroin reinstatement

2021 ◽  
pp. 026988112199157
Author(s):  
Josephine Palandri ◽  
Sharon L Smith ◽  
David J Heal ◽  
Sue Wonnacott ◽  
Chris P Bailey
Keyword(s):  
Acetylcholine Receptor ◽  
Conditioned Place Preference ◽  
Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Place Preference ◽  
Self Administration ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine ◽  
Α7 Nicotinic Acetylcholine Receptors

Background: α7 Nicotinic acetylcholine receptors are implicated in the reinstatement of drug-seeking, an important component of relapse. We showed previously that the α7 nicotinic acetylcholine receptor antagonist, methyllycaconitine, specifically attenuated morphine-primed reinstatement of conditioned place preference in rodents and this effect was mediated in the ventral hippocampus. Aims: The purpose of this study was to evaluate α7 nicotinic acetylcholine receptor antagonism in reinstatement of the conditioned place preference for the more widely abused opioid, heroin, and to compare the effect of α7 nicotinic acetylcholine receptor blockade on reinstatement of heroin-seeking and heroin self-administration in an intravenous self-administration model of addictive behaviour. Methods: Rats were trained to acquire heroin conditioned place preference or heroin self-administration; both followed by extinction of responding. Methyllycaconitine or saline was given prior to reinstatement of drug-primed conditioned place preference, or drug-prime plus cue-induced reinstatement of intravenous self-administration, using two protocols: without delivery of heroin in response to lever pressing to model heroin-seeking, or with heroin self-administration, using fixed and progressive ratio reward schedules, to model relapse. Results: Methyllycaconitine had no effect on acquisition of heroin conditioned place preference or lever-pressing for food rewards. Methyllycaconitine blocked reinstatement of heroin-primed conditioned place preference. Methyllycaconitine did not prevent drug-prime plus cue-induced reinstatement of heroin-seeking, reinstatement of heroin self-administration, or diminish the reinforcing effect of heroin. Conclusions: The α7 nicotinic acetylcholine receptor antagonist, methyllycaconitine, prevented reinstatement of the opioid conditioned place preference, consistent with a role for α7 nicotinic acetylcholine receptors in the retrieval of associative memories of drug liking. The lack of effect of methyllycaconitine in heroin-dependent rats in two intravenous self-administration models suggests that α7 nicotinic acetylcholine receptors do not play a role in later stages of heroin abuse.

scholarly journals α-Conotoxin TxIB Inhibits Development of Morphine-Induced Conditioned Place Preference in Mice via Blocking α6β2* Nicotinic Acetylcholine Receptors

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaodan Li ◽  
Jian Xiong ◽  
Baojian Zhang ◽  
Dongting Zhangsun ◽  
Sulan Luo
Keyword(s):  
Conditioned Place Preference ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Place Preference ◽  
Rewarding Effect ◽  
Nicotinic Acetylcholine ◽  
Selective Ligand ◽  
Morphine Addiction ◽  
Abused Drugs ◽  
Main Component

Morphine, the main component of opium, is a commonly used analgesic in clinical practice, but its abuse potential limits its clinical application. Nicotinic acetylcholine receptors (nAChRs) in the mesolimbic circuitry play an important role in the rewarding effects of abused drugs. Previous studies have showed that α6β2* (* designated other subunits) nAChRs are mainly distributed in dopaminergic neurons in the midbrain area, which regulates the release of dopamine. So α6β2* nAChRs are regarded as a new target to treat drug abuse. α-Conotoxin TxIB was discovered in our lab, which is the most selective ligand to inhibit α6β2* nAChRs only. Antagonists of α6β2* nAChRs decreased nicotine, cocaine, and ethanol rewarding effects previously. However, their role in morphine addiction has not been reported so far. Thus, it is worth evaluating the effect of α-conotoxin TxIB on the morphine-induced conditioned place preference (CPP) and its behavioral changes in mice. Our results showed that TxIB inhibited expression and acquisition of morphine-induced CPP and did not produce a rewarding effect by itself. Moreover, repeated injections of TxIB have no effect on learning, memory, locomotor activity, and anxiety-like behavior. Therefore, blocking α6/α3β2β3 nAChRs inhibits the development of morphine-induced CPP. α-Conotoxin TxIB may be a potentially useful compound to mitigate the acquisition and/or retention of drug-context associations.

scholarly journals Activation of Nicotinic Acetylcholine Receptors Increases the Frequency of Spontaneous GABAergic IPSCs in Rat Basolateral Amygdala Neurons

2005 ◽  
Vol 94 (5) ◽  
pp. 3081-3091 ◽  
Author(s):  
Ping Jun Zhu ◽  
Randall R. Stewart ◽  
J. Michael McIntosh ◽  
Forrest F. Weight
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Basolateral Amygdala ◽  
Bathing Solution ◽  
Patch Clamp Recording ◽  
Nicotinic Acetylcholine ◽  
Whole Cell Patch Clamp ◽  
Agonist And Antagonist ◽  
Subunit Combination ◽  
Conditioned Responses

The basolateral amygdala (BLA) is a critical component of the amygdaloid circuit, which is thought to be involved in fear conditioned responses. Using whole cell patch-clamp recording, we found that activation of nicotinic acetylcholine receptors (nAChRs) leads to an action potential-dependent increase in the frequency of spontaneous GABAergic currents in principal neurons in the BLA. These spontaneous GABAergic currents were abolished by a low-Ca2+/high-Mg2+ bathing solution, suggesting that they are spontaneous inhibitory postsynaptic currents (sIPSCs). Blockade of ionotropic glutamate receptors did not prevent this increased frequency of sIPSCs nor did blockade of α7 nAChRs. Among the nAChR agonists tested, cystisine was more effective at increasing the frequency of the sIPSCs than nicotine or 1,1-dimethyl-4-phenyl piperazinium iodide, consistent with a major contribution of β4 nAChR subunits. The nicotinic antagonist, dihydro-β-erythroidine, was less effective than d-tubocurarine in blocking the increased sIPSC frequency induced by ACh, suggesting that α4-containing nAChR subunits do not play a major role in the ACh-induced increased sIPSC frequency. Although α2/3/4/7 and β2/4 nAChR subunits were found in the BLA by RT-PCR, the agonist and antagonist profiles suggest that the ACh-induced increase in sIPSC frequency involves predominantly α3β4-containing nAChR subunits. Consistent with this, α-conotoxin-AuIB, a nAChR antagonist selective for the α3β4 subunit combination, inhibited the ACh-induced increase in the frequency of sIPSCs. The observations suggest that nicotinic activation increases the frequency of sIPSCs in the BLA by acting mainly on α3β4-containing nicotinic receptors on GABAergic neurons and may play an important role in the modulation of synaptic transmission in the amygdala.

scholarly journals α7-Containing nicotinic acetylcholine receptors on interneurons of the basolateral amygdala and their role in the regulation of the network excitability

2013 ◽  
Vol 110 (10) ◽  
pp. 2358-2369 ◽  
Author(s):  
Volodymyr I. Pidoplichko ◽  
Eric M. Prager ◽  
Vassiliki Aroniadou-Anderjaska ◽  
Maria F. M. Braga
Keyword(s):  
Emotional Disorders ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Basolateral Amygdala ◽  
Emotional Behavior ◽  
Mental Illnesses ◽  
Nicotinic Acetylcholine ◽  
Normal Functions ◽  
Whole Cell Recordings

The basolateral amygdala (BLA) plays a key role in fear-related learning and memory, in the modulation of cognitive functions, and in the overall regulation of emotional behavior. Pathophysiological alterations involving hyperexcitability in this brain region underlie anxiety and other emotional disorders as well as some forms of epilepsy. GABAergic interneurons exert a tight inhibitory control over the BLA network; understanding the mechanisms that regulate their activity is necessary for understanding physiological and disordered BLA functions. The BLA receives dense cholinergic input from the basal forebrain, affecting both normal functions and dysfunctions of the amygdala, but the mechanisms involved in the cholinergic regulation of inhibitory activity in the BLA are unclear. Using whole cell recordings in rat amygdala slices, here we demonstrate that the α7-containing nicotinic acetylcholine receptors (α7-nAChRs) are present on somatic or somatodendritic regions of BLA interneurons. These receptors are active in the basal state enhancing GABAergic inhibition, and their further, exogenous activation produces a transient but dramatic increase of spontaneous inhibitory postsynaptic currents in principal BLA neurons. In the absence of AMPA/kainate receptor antagonists, activation of α7-nAChRs in the BLA network increases both GABAergic and glutamatergic spontaneous currents in BLA principal cells, but the inhibitory currents are enhanced significantly more than the excitatory currents, reducing overall excitability. The anxiolytic effects of nicotine as well as the role of the α7-nAChRs in seizure activity involving the amygdala and in mental illnesses, such as schizophrenia and Alzheimer's disease, may be better understood in light of the present findings.

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