- 12th December
- 24th November
Asked by: jonathansadlowe
I referenced to research that is unpublished but was presented at SfN this year. I’m supposed to get a copy of the poster from the author soon, but I haven’t. The best I can do know is copy/paste the author abstract from the SfN meeting planner. If you are not a member, you cannot access the link.
Author Abstract: S.D. Preston. Want vs. Should: Neural and behavioral effects of affect and cognition on decisions about material goods. 2010 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2010. Online.
Research across species and domains suggests a common proximate, neural mechanism for making decisions about resources. Prior experiments on food storing in rodents, as well as human studies of compulsive hoarding, shopping, and gambling implicates the mesolimbocortical system, particularly the nucleus accumbens (NAcc) and orbital frontal cortex (OFC). Our own work confirms that this system is implicated in decisions to acquire as well as discard material goods, whether for personal use or monetary profit. This suggests that this system is more generally engaged by consumption decisions regardless of the frame. However, the degree of engagement of various regions does shift with the frame of the decision, as does the type of items subjects prefer. Personal decisions activate the self-referential, default midline systems more while decisions for financial benefit activate more lateral, cognitive control regions associated with comparing and calculating the value of items. In addition, using more natural and impulsive response formats causes subjects to highlight more immediately rewarding items like food and small change while more comparative and reflective response formats cause subjects to highlight items that one “should” have, but are less inherently rewarding. Demonstrating for the first time that animal and human hoarding are related by more than just a metaphor, the degree of NAcc activation in our task also scales with participants’ trait tendencies for human compulsive hoarding (particularly trouble parting with goods for emotional reasons). Additional work in our lab confirms that acquisitive tendencies are normally distributed in the population and are particularly associated with underlying differences in anxiety, which fuels the more deliberative system to emphasize the future utility of items that are not inherently rewarding. This research is consistent with prior work in rodents, monkeys, and humans, but additionally specifies how intrinsic, natural or pharmacological rewards differ from those associated with goods that are only conceptually consumed, but nonetheless motivate people to acquire them and exhibit features like addictions to drugs of abuse. Research on material goods is critical to understand a process that humans engage in daily, which is critical to our economy, our quality of life, and the environment.
Perhaps a search would yield extra results?
- 23rd November
Want vs. Should: Neural and behavioral effects of affect and cognition on decisions about material goods (Preston)
What brain areas are involved in deciding what we want to keep, what we can discard, what has meaning for us, and what has monetary value?
A study carried out by Preston set out to explore the neuroanatomical substrates for these decisions by performing an fMRI task in which subjects made force-decisions between everyday goods.
Before that, let’s familiarize ourselves with the term acquisitiveness, which is characterized by a strong desire to possess, gain or retain. Acquisitiveness is a trait that may be beneficial for heatlh, quality of life, and the environment.
Personal decisions: According to Preston, “personal decisions activate the self-referential, default midline systems more while decisions for financial benefit activate more lateral, cognitive control regions associated with comparing and calculating the value of items.” Because these decisions are of an intuitive and affective nature, they engage affective and self-relevant regions like the orbitofrontal cortex, right angular gyrus, right middle temporal gyrus (MTG) and others. These decision are marked by increased activity in the medial prefrontal cortex (mPFC) and the anterior cingulate cortex (ACC), a self-processing area.
Monetary decisions: are controlled and economical. They involve the right insula (value-judgement area), the dorsolateral prefrontal cortex (dLPFC), an evaluative area, and Broca’s area (analysis and planning).
Acquisition decisions: act like a hedonic (pleasure) signal are marked by an increase in desirability and engage the medial orbitofrontal cortex (mOFC) and nucleus accumbens (reward area) engagement. Decisions in which reward may be acquired are also related to associated with mesolimbocortical (MLC) regions.
Discarding decisions: have elements of additional control and evaluation. Individuals usually think in utilitarian terms to establish preference and possessiveness has been shown to increase an object’s desirability. These are taken in basis of monetary value and involves the insula and the ACC.
- All decision types (personal, monetary, acquire, discard) engage the mPFC.
- Acquisitiveness involves both acquisition and failure to discard.
- Acquisitiveness entails incentive salience (motivational, wanting attribute due to the brain’s prediction for reward) for even mundane, utilitarian items.
- Hoarding behaviors are associated with the OFC.
- 17th November
- 17th November
- The ventral tegmental area (VTA) and the basolateral amygdala (BLA) have long been regarded as key components in the brain reward circuit.
- Chronic opiate administration switches the functional role of intra-BLA dopamine (DA) transmission from a D1-dependent substrate to a D2-dependent substrates.
- This D1/D2 opiate reward switch in the BLA can directly modulate opiate reward information from the VTA. Furthermore, the DA reward processing occurs in the nucleus accumbens shell (not core)
Author Abstract (Lintas, et. al) : Transmission through dopamine D1 versus D2 receptors in the basolateral amygdala represents an opiate addiction switching mechanism controlling opiate memory encoding in the drug naïve versus dependent state
The basolateral nucleus of the amygdala (BLA) receives innervation from dopaminergic fibers, and dopamine (DA) D1 and D2 receptors are expressed in this region. BLA sends excitatory afferents to the nucleus accumbens (NAcc), to both shell and core regions. The NAcore and NAshell are both implicated in the processing of various associative reward stimuli. However, the precise role of D1 versus D2 receptor transmission in the processing of associative, opiate-related reward learning is not presently understood. Using a combination of in vivo single unit extracellular recording in the NAcc combined with behavioural pharmacology studies, we have identified a double dissociation in the functional role of DA D1 versus D2 receptor transmission in the BLA, as a function of opiate exposure state: thus, in previously opiate-naïve rats, blockade of intra-BLA D1, but not D2, receptor transmission blocks the rewarding effects of morphine (5mg/kg;i.p.) measured in an unbiased conditioned place preference (CPP) procedure. In direct contrast, in rats made opiate dependent and in a state of withdrawal, intra-BLA D2, but not D1 receptor blockade completely blocks opiate reward encoding. We find the same double dissociation with intra-BLA D1/D2 activation: in opiate-naïve rats, pharmacological activation of intra-BLA D1 (but not D2) receptors strongly potentiates sub-threshold morphine (0.05mg/kg;i.p.) reward encoding while activation of D2 receptors (but not D1 receptors) potentiates sub-threshold morphine reward transmission in opiate dependent/withdrawn rats. Single unit recordings performed in neurons of the NAcc shell (but not core) confirm the modulatory role of BLA D1/D2 transmission in NAcc neuronal responses to morphine (1mg/kg;i.v.). Thus, blockade of intra-BLA D1 (but not D2) transmission blocks NAcc neuronal responding to morphine in opiate naïve rats, while blockade of BLA D2 (but not D1) receptors blocks neuronal responding to morphine in opiate dependent/withdrawn rats. Our results characterize and identify a novel and unique opiate addiction switching mechanism directly in the BLA, that can control the encoding of opiate reward information (behaviourally and neuronally) as a direct function of opiate exposure state, via D1 or D2 receptor signalling.
- 16th November
The Effects of Corticotropin-Releasing Factor on Dopamine Release: Implications for Reward and Effort
Take home messages:
- Corticotropin releasing factor (CRF) acts in the ventral tegmental area (VTA), a primary source of dopaminergic neurons and an integral part of the mesolimbic reward pathway, to regulate dopamine (DA) neurotransmission.
- A large reward (large reward magnitude) will enhance motivated behavior.
- A large reward magnitude also enhances DA release in response to cues and rewards.
- CRF, a hormone and neurotransmitter implicated in the stress response (HPA axis), in the VTA will attenuate motivated behavior in a dose-dependent manner and this effect is not due to motor suppression.
- CRF in the VTA attenuates phasic DA release (burst DA release as opposed to a more gradual release) specifically to rewards, not the cues related to the rewards.
- Satiety (being full) will reduce motivated behavior (in this case the reward was food pellets) as well as DA release to rewards (but not cues).
Author Abstract (Phillips, et. al) : Phasic dopamine release during reward and effort manipulations: Effects of corticotropin release factor.
The effort an individual is willing to exert to obtain a reward is dependent upon one’s motivational state as well as the value of the reward. Contemporary theories of dopamine function suggest that dopamine release, particularly in the striatum, is involved with enabling high-effort behaviors. Motivated behaviors can be influenced by stressful stimuli and stress-released neuropeptides such as corticotropin-releasing factor (CRF). The behavioral effects of stress on motivation could involve the midbrain dopamine system as (i) stress increases dopamine levels, (ii) CRF is released into the midbrain during stress, and (iii) CRF increases the firing rate and potentiates glutamate receptor current in dopamine neurons. Thus, we hypothesized that CRF in the VTA will elevate phasic dopamine release and increase the effort exerted to obtain a reward. However, before addressing this pharmacological question it was important to first determine how natural manipulations of motivational state and reward magnitude influence phasic dopamine release during high-effort behaviors.
We utilized fast-scan cyclic voltammetry to examine phasic striatal dopamine release to rewards and reward-predictive cues in rats performing an operant task under a progressive ratio (PR) reinforcement schedule for natural reinforcers. In separate sessions, we assessed behavior and dopamine release in rats under different motivational states (food-deprived or free-fed) or working for rewards of different magnitudes. The cumulative number of rewards earned scaled with the reward size in a given PR session. Interestingly, we found that motivational state and reward size robustly scaled reward-evoked dopamine release, while cue-evoked dopamine release was less sensitive to these manipulations. After establishing the effect of natural manipulations, we next examined how CRF injections into the midbrain affected behavior and dopamine release during PR sessions. Contrary to our hypothesis, CRF injected into the midbrain lowered the breakpoint in PR sessions. Furthermore, CRF injections attenuated reward-evoked dopamine release but did not affect cue-evoked dopamine release. Together, these results suggest that CRF modulates motivated behavior by affecting either dopamine neurons responsive to reward delivery and/or inputs to the midbrain representing the delivery of rewards.