56 research outputs found
Immunology and microbiology. How do they affect social cognition and emotion recognition?
Social interactions profoundly influence animals' life. The quality of social interactions and many everyday life decisions are determined by a proper perception, processing and reaction to others' emotions. Notably, alterations in these social processes characterize a number of neurodevelopmental disorders, including autism spectrum disorders and schizophrenia. Increasing evidences support an implication of immune system vulnerability and inflammatory processes in disparate behavioral functions and the aforementioned neurodevelopmental disorders. In this review, we show a possible unifying view on how immune responses, within and outside the brain, and the communication between the immune system and brain responses might influence emotion recognition and related social responses. In particular, we highlight the importance of combining genetics, immunology and microbiology factors in understanding social behaviors. We underline the importance of better disentangling the whole machinery between brain-immune system interactions to better address the complexity of social processes
Lesion of medial prefrontal dopamine terminals abolishes habituation of accumbens shell dopamine responsiveness to taste stimuli
Taste stimuli increase extracellular dopamine (DA) in the nucleus accumbens (NAc) and in the medial prefrontal cortex (mPFC). This effect shows single-trial habituation in NAc shell but not in core or in mPFC. Morphine sensitization abolishes habituation of DA responsiveness in NAc shell but induces it in mPFC. These observations support the hypothesis of an inhibitory influence of mPFC DA on NAc DA. To test this hypothesis, we used in vivo microdialysis to investigate the effect of mPFC 6-hydroxy-dopamine (6-OHDA) lesions on the NAc DA responsiveness to taste stimuli. 6-OHDA was infused bilaterally in the mPFC of rats implanted with guide cannulae. After 1 week, rats were implanted with an intraoral catheter, microdialysis probes were inserted into the guide cannulae, and dialysate DA was monitored in NAc shell/core after intraoral chocolate. 6-OHDA infusion reduced tissue DA in the mPFC by 75%. Tyrosine hydroxylase immunohistochemistry showed that lesions were confined to the mPFC. mPFC 6-OHDA lesion did not affect the NAc shell DA responsiveness to chocolate in naive rats but abolished habituation in rats pre-exposed to the taste. In the NAc core, mPFC lesion potentiated, delayed and prolonged the stimulatory DA response to taste but failed to affect DA in pre-exposed rats. Behavioural taste reactions and motor activity were not affected. The results indicate a top-down control of NAc DA by mPFC and a reciprocal relationship between DA transmission in these two areas. Moreover, habituation of DA responsiveness in the NAc shell is dependent upon an intact DA input to the mPFC
Influence of morphine sensitization on the responsiveness of mesolimbic and mesocortical dopamine transmission to appetitive and aversive gustatory stimuli
RATIONALE: Repeated treatment with morphine has been shown to sensitize rats to its stimulant effects on motor activity and mesolimbic dopamine (DA) transmission.
OBJECTIVES: The aim of this study is to investigate if morphine sensitization is associated to changes in the behavioral reactions to appetitive and aversive taste stimuli and in the response of in vivo DA transmission in the nucleus accumbens (NAc) shell and core and medial prefrontal cortex (PFCX) to the same stimuli.
METHODS: Rats were administered twice a day for three consecutive days with increasing doses of morphine [10, 20, and 40 mg/kg, subcutaneously (sc)] or with saline. After 15 days of withdrawal, rats were infused intraorally with either an appetitive (sweet chocolate, 1 ml) or an aversive solution (quinine HCl 5 × 10(-4) M, 1 ml). The behavioral taste reactions were recorded during microdialysis of DA in the NAc shell and core and PFCX.
RESULTS: Opiate sensitization did not affect behavioral reactions to intraoral chocolate or quinine. In rats naive to the taste stimuli, morphine sensitization was associated to potentiation of stimulatory DA response to appetitive and aversive taste stimuli in the NAc core. Morphine sensitization reciprocally affected habituation of DA responsiveness after one trial exposure to appetitive and aversive taste stimuli (abolition it in the shell, induction in the PFCX). No habituation of DA responsiveness to taste was observed in the NAc core in controls as well as in morphine-sensitized rats.
CONCLUSIONS: These results suggest that opiate sensitization is associated to differential adaptive changes of the responsiveness of DA transmission to taste stimuli in DA terminal areas
Effect of medial prefrontal cortex 6-OHDA lesions on behavioral and neurochemical responses to gustatory stimuli
Appetitive sweet tastes increase dopamine (DA) in the nucleus accumbens (NAc) shell and core and in the medial prefrontal cortex (mPFC) in relation to their motivational valence, salience and novelty; the DA increase in the NAc shell is subjected to single trial habituation while in the NAc core and in the mPFC is not. Recently it was shown that sensitization to morphine can reverse these phenomena in the NAc shell and in the mPFC; abolishment of the habituation phenomenon was observed in the NAc shell while in the mPFC single trial habituation took place. Medial prefrontal cortex is an area well known to interact with subcortical areas such as the VTA and the NAc and it has been proposed that DA depletion in the mPFC can alter the mode of function of subcortical areas, including the NAc DAergic responses to pharmacological and environmental challenges of the system. In fact, 6-OHDA lesions of the mPFC have been shown to produce sensitization to the neurochemical and behavioral responses to cocaine and to alter the NAc DAergic transmission in response to natural reinforcers. In the present thesis it was studied the effect of 6-OHDA lesions in the mPFC in the NAc DAergic response to a taste stimulus (sweet chocolate) using in vivo microdialysis. Moreover, behavioral taste reactivity and motor behavior studies were held out to investigate whether the lesions influence this type of behaviors. As in sensitized to morphine animals, lesions produced abolishment of habituation in the NAc shell in the pre-exposed to taste animals, while in the NAc core produced a higher and delayed increase in DA in the naive animals. No differences between lesioned and sham operated animals where observed in naive and pre-exposed animals in the DAergic response of NAc shell and core, respectively. No differences were observed between the groups in taste reactivity test and in the motor activity studies. TH immunoreactivity studies were performed and tissue neurotransmitter levels were quantified in order to evaluate the extension and percentage of the lesions in the mPFC
Effect of medial prefrontal cortex 6-hydroxy-dopamine on the nucleus accumbens dopamine responsiveness to appetitive stimuli
Neurocircuitry of Reward and Addiction : Potential Impact of Dopamine-Glutamate Co-release as Future Target in Substance Use Disorder
Dopamine-glutamate co-release is a unique property of midbrain neurons primarily located in the ventral tegmental area (VTA). Dopamine neurons of the VTA are important for behavioral regulation in response to rewarding substances, including natural rewards and addictive drugs. The impact of glutamate co-release on behaviors regulated by VTA dopamine neurons has been challenging to probe due to lack of selective methodology. However, several studies implementing conditional knockout and optogenetics technologies in transgenic mice have during the past decade pointed towards a role for glutamate co-release in multiple physiological and behavioral processes of importance to substance use and abuse. In this review, we discuss these studies to highlight findings that may be critical when considering mechanisms of importance for prevention and treatment of substance abuse
JWH-018: a cannabinoid compound of Spice drugs stimulates dopamine transmission in the nucleus accumbens shell
Responsiveness of nucleus accumbens and prefrontal cortex dopamine transmission to appetitive and aversive gustatory stimuli in rats sensitized to morphine
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