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Behavioral and neurochemical modification of mesocortical and mesolimbic DA monitored by acute and chronic microdialysis probes after drug and food conditioned stimuli
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Modulation of feeding-induced activation of mesolimbic dopamine transmission by appetitive stimuli and its relation to motivational state
No full textWe have previously shown in non-deprived rats that feeding of an unfamiliar palatable food (Fonzies((R))) phasically stimulates in vivo dopamine (DA) transmission in the medial nucleus accumbens (NAc) and this effect undergoes habituation after a previous (24 h) Fonzies meal (Bassareo & Di Chiara 1997, J. Neurosci., 17, 851-861). The present study shows that an unfamiliar food (Kinder((R))) with a taste and composition (milk chocolate) different from that of Fonzies, also induces a release of DA in the NAc subjected to one-trial habituation. Habituation was taste specific as no cross-habituation was observed between Fonzies and Kinder. In undeprived rats, a 40-min exposure to an intrinsic appetitive stimulus (food smell arising from a Fonzies-filled plastic box) also prevented the increase in dialysate DA associated with Fonzies feeding, and this effect was partially reversed by food deprivation. Food deprivation also prevented habituation of Fonzies-induced increase of dialysate DA in the NAc. Predictive association of an empty plastic box to Fonzies feeding resulted in the acquisition of appetitive properties by the box and in facilitation (rather than inhibition) of the phasic responsiveness of DA transmission to Fonzies feeding. A 10-min pre-exposure to appetitive olfactory stimuli intrinsic to Fonzies still prevented, like a 40-min pre-exposure, the NAc DA response to Fonzies feeding; however, a 5-min pre-exposure to these appetitive stimuli did not prevent the DA response in the NAc. These results show that the phasic responsiveness of NAc DA transmission to an unfamiliar palatable food is under strong modulatory control by primary (consummatory) and secondary (appetitive) stimuli, and that the sign and extent of this control depends on the nature of the appetitive stimulus, delay of reward and motivational state (deprivation)
Reward system and addiction: what dopamine does and doesn't do
No full textAddictive drugs share with palatable food the property of
increasing extracellular dopamine (DA), preferentially in the
nucleus accumbens shell rather than in the core. However, by
acting directly on the brain, drugs bypass the adaptive
mechanisms (habituation) that constrain the responsiveness of
accumbens shell DA to food reward, abnormally facilitating
Pavlovian incentive learning and promoting the acquisition of
abnormal DA-releasing properties by drug conditioned stimuli.
Thus, whereas Pavlovian food conditioned stimuli release core
but not shell DA, drug conditioned stimuli do the opposite,
releasing shell but not core DA. This process, which results in
the acquisition of excessive incentive–motivational properties
by drug conditioned stimuli, initiates the drug addiction
process. Neuroadaptive processes related to the chronic
influence of drugs on subcortical DA might secondarily impair
the function of prefronto-striatal loops, resulting in impairments
in impulse control and decision making that form the basis for
the compulsive feature of drug seeking and its relapsing
character
Adaptive changes of dopamine responsiveness to palatable food: differences between accumbens shell, core and prefrontal cortex
No full textDrugs of abuse and highly palatable food share the property to stimulate dopamine (DA) transmission preferentially in the nucleus accumbens (NAc) shell. But while the stimulation of DA shell by non-drug reward (food) undergoes rapid habituation, that exerted by drugs of abuse does not. The lack of habituation of shell DA in response to drugs of abuse is hypothesized to abnormally strengthen stimulus-drug association and result in the attribution of excessive motivational value to discrete stimuli or contexts predictive of drug availability. Several studies reported that, in food and water deprived rats, repeated sugar consumption continuously increase DA trasmission in the NAc shell as well as drugs of abuse.
The aim of our research was to study the adaptive changes in the reactivity of DA transmission in the shell and core and prefrontal cortex (PFCX) of non deprived animals to higly palatable food after long term feeding with it.
Male Sprague-Dawley rats were trained to drink chocolate solution (sugar solution for control group) that was made available for two or 1 week from 8 p.m. to 8 a.m., apart from weekends. At the end of the training period, microdialysis experiments were performed for three consecutive days. Behavioral responses to chocolate infused by intraoral catheter were observed and DA modifications were monitored by chronic microdialysis probes. The main finding of our study is that no habituation was observed in the response of shell DA to intraoral infusion of chocolate in trained rats.
In agreement with previous studies, no habituaton was observed in the response of DA in the NAc core and PFCX. In conclusion repeated exposure of the same palatable food abolishes the habituation of DA responsiveness in the NAc shell, and potentiates it in the NAc core and we can speculate that disturbances of feeding behavior are related to loss of adaptive regulation of food-stimulated release of DA in the NAc shell
Anxiogenic drugs and drugs of abuse differentially influence limbic versus cortical dopamine transmission: evidence for specific motivational roles of mesolimbic and mesocortical dopamine systems
No full textNot just from ethanol. Tetrahydroisoquinolinic (TIQ) derivatives: from neurotoxicity to neuroprotection
No full textThe 1,2,3,4-tetrahydroisoquinolines (TIQs) are compounds frequently described as alkaloids that can be found in the human body fluids and/or tissues including the brain. In most circumstances, TIQs may be originated as a consequence of reactions, known as Pictet-Spengler condensations, between biogenic amines and electrophilic carbonyl compounds, including ethanol’s main metabolite, acetaldehyde. Several TIQs may also be synthesized enzymatically whilst others may be formed in the body as by-products of other compounds including TIQs themselves. The biological actions of TIQs appear critically dependent on their metabolism, and nowadays, among TIQs, 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), N-methyl-1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (N-methyl-(R)-salsolinol), 1-[(3,4-dihydroxyphenyl)methyl]-1,2,3,4-tetrahydroisoquinoline-6,7-diol (norlaudanosoline or tetrahydropapaveroline or THP) and 1-benzyl-1,2,3,4-tetrahydroisoquinoline (1BnTIQ) are considered as those endowed with the most potent neurotoxic actions. However, it remains to be established whether a continuous exposure to TIQs or to their metabolites might carry toxicological consequences in the short- or long-term period. Remarkably, recent findings suggest that some TIQs such as (1-[(4-hydroxyphenyl)methyl]-1,2,3,4-tetrahydroisoquinoline-6,7-diol) (higenamine) and 1-methyl-1,2,3,4-tetrahydroisoquinoline (1-MeTIQ) as well as N-methyl-tetrahydroisoquinoline (N-methyl-TIQ) exert unique neuroprotective and neurorestorative actions. The present review article provides an overview on these aspects of TIQs and summarizes those that presently appear the most significant highlights on this puzzling topic
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