Nicotine and endogenous opioids: Neurochemical and pharmacological evidence

  title={Nicotine and endogenous opioids: Neurochemical and pharmacological evidence},
  author={Maria Hadjiconstantinou and Norton H. Neff},
Nicotine-induced changes of brain β-endorphin
Dopaminergic and cholinergic learning mechanisms in nicotine addiction
This work focuses on the acquisition phase of smoking addiction and reviews animal model studies on how nicotine modifies dopaminergic and cholinergic signaling in key nodes of the reinforcement circuitry: ventral tegmental area, nucleus accumbens, amygdala, and hippocampus.
Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum*
Nicotine altered levels of nine non-opioid peptides derived from precursors, including somatostatin and cerebellin, which potentially modulate neurotransmitter release and energy metabolism and suggests that apart from the opioid peptides, several other peptidergic systems are involved in the preoccupation/craving phase of drug dependence.
On the Role of Cannabinoid CB1- and μ-Opioid Receptors in Motor Impulsivity
Investigation of whether cannabinoid CB1 and/or μ-opioid receptors are involved in nicotine-induced impulsivity showed that the cannabinoidCB1 receptor antagonist SR141716A, but not the opioid receptor antagonist naloxone, reduced Nicotine-induced premature responding, indicating that nicotine- induced motor impulsivity is cannabinoid, butNot opioid receptor-dependent.
Neurophysiology of Nicotine Addiction.
Two general neural systems are emerging as critical for the initiation and maintenance of tobacco use and particular nAChR subtypes have roles that contribute to the overall nicotine addiction process.


Endogenous opioid systems and alcohol addiction
  • A. Herz
  • Biology, Medicine
  • 1997
Results obtained in genetic models of high preference for alcohol support the view that alcohol intake depends on the activity of the endogenous opioid reward system and that alcohol consumption may serve to compensate for inherent deficits in this system.
Opposing tonically active endogenous opioid systems modulate the mesolimbic dopaminergic pathway
Data show that tonic activation of mu and kappa receptors is required for the maintenance of basal dopamine release in the nucleus accumbens, which may have implications for the treatment of opiate dependence and affective disorders.
Endogenous cannabinoid and opioid systems and their role in nicotine addiction.
A possible role for the endogenous cannabinoid and opioid systems in the rewarding properties of nicotine as well as in the development of nicotine physical dependence and relapse to nicotine-seeking behaviour will be examined.
κ and δ-opioid receptor agonists differentially inhibit striatal dopamine and acetylcholine release
Dynorphin and some benzomorphans potently and selectively inhibit the release of dopamine from slices of rat corpus striatum, by activating κ-opioid receptors.
Reward processing by the opioid system in the brain.
This review summarizes the present knowledge on brain sites where the endogenous opioid system controls hedonic responses and is modified in response to drugs of abuse in the rodent brain and outlines key molecular actors of the system and neural sites where opioid peptides and receptors contribute to the onset of addictive disorders.
Nicotine and Endogenous Opioids: Toward Specific Pharmacotherapy
The role of opioid antagonism on smoking behaviour is unclear, despite the publication of 5 trials on the subject, and psychiatrists can hope to have a more specific pharmacotherapy to address the cravings and short-term rewards of nicotine use.
Stimulation of Endorphin Neurotransmission in the Nucleus Accumbens by Ethanol, Cocaine, and Amphetamine
It is hypothesize that this drug-induced release of endorphins may contribute to the positive reinforcing and motivating properties of ethanol and psychostimulants.
Acute nicotine changes dynorphin and prodynorphin mRNA in the striatum
It is proposed that nicotine influences Dyn primarily through dopamine release and that glutamate plays a modulatory role and a heightened dynorphinergic tone may contribute to the aversive effects of nicotine in naive animals and first-time tobacco smokers.