Responses to reward in monkey dorsal and ventral striatum

Abstract

The sources of input and the behavioral effects of lesions and drug administration suggest that the striatum participates in motivational processes. We investigated the activity of single striatal neurons of monkeys in response to reward delivered for performing in a go-nogo task. A drop of liquid was given each time the animal correctly executed or withheld an arm movement in reaction to a visual stimulus. Of 1593 neurons, 115 showed increased activity in response to delivery of liquid reward in both go and nogo trials. Responding neurons were predominantly located in dorsal and ventromedial parts of anterior putamen, in dorsal and ventral caudate, and in nucleus accumbens. They were twice as frequent in ventral as compared to dorsal striatal areas. Responses occurred at a median latency of 337 ms and lasted for 525 ms, with insignificant differences between dorsal and ventral striatum. Reward responses differed from activity recorded in the face area of posterior putamen which varied synchronously with individual mouth movements. Responses were directly related to delivery of primary liquid reward and not to auditory stimuli associated with it. Most of them also occurred when reward was delivered outside of the task. These results demonstrate that neurons of dorsal and particularly ventral striatum are involved in processing information concerning the attribution of primary reward.

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

“…Reward-related neurons are found in both the dorsal and ventral striatum, but they are more frequently found in the ventral striatum [7]. These cells respond to both the anticipation [55,104] and presentation of reward stimuli [7,16,55], and show activity levels that reflects the appetitive value of the reward [7,104].…”

“…While the prior discussion proposes DA gating of reward inputs from the orbitofrontal cortex and amygdala, it is possible that DA may have symmetrical effects on inputs to the striatum carrying information about rewarding and aversive events. It should also be emphasized that while reward-responsive neurons are more often found in the ventral relative to the dorsal striatum [7], ventral striatal DA disruption interferes with some [36], but not all [28], aspects of reward processing. Reward-related responses are also found in the dorsal striatum [7,56], and dorsal striatal DA disruption attenuates some aspects of reinforcement [11].…”

“…It should also be emphasized that while reward-responsive neurons are more often found in the ventral relative to the dorsal striatum [7], ventral striatal DA disruption interferes with some [36], but not all [28], aspects of reward processing. Reward-related responses are also found in the dorsal striatum [7,56], and dorsal striatal DA disruption attenuates some aspects of reinforcement [11]. DA modulates both the striatal response to current glutamate inputs [27,67,87] and long-term changes in synaptic strength of these inputs [21,22,65].…”

Cocaine and Amphetamine Depress Striatal GABAergic Synaptic Transmission through D2 Dopamine Receptors

“…These non-motor connections account, at least in part, for the involvement of the striatum in memory formation, mnemonic guidance of behavior and rewarding processes (Whishaw et al 1987;Saint-Cyr et al 1988;Knowlton et al 1996;Graybiel 1998;Apicella et al 1991). Interestingly, most recent investigations into the molecular neurobiology of addiction have emphasized the view that addictive drugs lead to the compulsive nature of drug abuse and to the persistent tendency to relapse by engaging a set of molecular mechanisms normally involved in striatally based associative learning and reward.…”

Steps to a neurochemistry of personality

“…Particularly high rates of intracranial self-stimulation and energy use (2-deoxyglucose uptake) during self-stimulation are found mainly in the NAS shell . Although NAS cells decrease firing during periods of focused attention and consummatory events, they increase firing to primary and conditioned signals of reward and novelty, and during intervals when reward is expected and during engagement in rewarding social and aggressive activity (Apicella et al 1991;Henriksen & Giacchino 1993;Le Moal & Simon 1991;Schultz et al 1992;. In contrast, pharmacologic impairment of NAS shell functioning leads to an extinction-like response on established reinforcement schedules, long-lasting decreases in the self-administration of reinforcing drugs, and reduced effort in working for drug reward (Lyness et al 1979;Lyness & Smith 1992;Roberts et al 1980).…”