Patricia S. Grigson
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Academic title Associate Professor of Neural and Behavioral Sciences
College College of Medicine
Campuses Penn State Milton S. Hershey Medical Center
Department Neural and Behavioral Sciences
Graduate programs MD/PhD Degree Program
Integrative Biosciences
Neuroscience
Email Phone
  psg6@psu.edu
  717 531 5772
 
Educational background
  Ph.D., Rutgers University, 1990
Postdoctoral Training, Pennsylvania State University College of Medicine, 1990-1993
Research interests
 

The Neural Basis of Reward Comparison

A great deal is known about the neural pathways involved in responding to the rewarding properties of food, water, or drugs of abuse, for example. However, these rewards are not typically experienced in a vacuum. At any given time, an animal can engage in a number of different activities, each of which may lead to a different rewarding outcome. The choice to select one behavior over another serves as evidence that very different rewards must be compared by some common neural substrate. However, there currently is little known about the neural pathways involved in such reward comparison processes. It is the focus of this laboratory to identify the substrate.

Rewards are compared in three ways over time. First, a reward can be compared with a different reward that is available closely in time. This form of reward comparison requires short-term memory processes. We have found that a brainstem relay, in particular the nucleus of the solitary tract, is involved in making this type of short-term memory dependent comparison process and that the effect is reflected in the activity of single taste cells in this nucleus (see figures). Second, a reward can be compared with the "memory" of another reward received 24h earlier. This form of reward comparison relies upon long-term memory and necessitates the involvement of the second gustatory relay, the parabrachial nucleus of the pons. Finally, a reward can be compared with another that is expected in the future. The anticipated reward may be a preferred gustatory stimulus or a drug of abuse, such as morphine or cocaine. This phenomenon seems to rely upon more complex associative processes occurring in the forebrain.

Given that drug addiction often is accompanied by an apparent devaluation of that which is naturally rewarding (e.g., relationships, employment, food...), we hope that these efforts will begin to illuminate the neural substrates by which natural rewards and drugs of abuse are compared.

Graphic
  Graphic
  An example of a typical record generated by a sucrose-best neuron in the nucleus of the solitary tract when the tongue is stimulated with 0.1 M sucrose (top) or 1.0 M sucrose (bottom). The arrows indicate the point of stimulus onset. The number of spikes/sec elicited by a single cell in the nucleus of the solitary tract for the low (0.1 M) and for the high (1.0 M) concentration of sucrose during the non-comparison condition (middle panels: CL and CH) and during the comparison condition (outer panels: AL and AH). Note that the difference in responding for the two concentrations of sucrose was greater during the comparison (difference = 16.12 spikes/sec + 1.04) than during the non-comparison (difference = 6.68 spike/sec + 1.04) condition. These data show that, while single cells in the brainstem track the concentration of a tastant, the code for that tastant can be altered by the recent availability of a solution of a different concentration (i.e., "value").
Areas of expertise
 
Morphine DependenceLithium Chloride
Dopamine Uptake InhibitorsAntimanic Agents
Food PreferencesStreet Drugs
MotivationHeroin
SucroseAppetitive Behavior
Mental RecallTaste
Conditioning (Psychology)Substance-Related Disorders
Conditioning, ClassicalConditioning, Operant
Dietary SucroseAvoidance Learning
Solitary NucleusExploratory Behavior
PonsWater Deprivation
CorticosteroneDrinking
Drinking BehaviorEating
SaccharinAmygdala
SmellFood Deprivation
Decerebrate StateTaste Threshold
Sweetening AgentsReward
AppetiteCocaine
Association LearningRetention (Psychology)
ThalamusNarcotics
CuesMorphine
Brain StemFeeding Behavior
Iron, DietaryIron
Cocaine-Related DisordersDietary Carbohydrates
Substance Withdrawal SyndromeGoals
Heroin DependenceCentral Nervous System
Gene ExpressionBehavior, Addictive
FoodProto-Oncogene Proteins c-fos
Extinction, PsychologicalGene Expression Profiling
Nerve Tissue Proteins
Publication author name
  Grigson PS
Select publications
  Grigson PS. Cornelius K. Wheeler DS. The suppressive effects of intraperitoneal cocaine are augmented when evaluated in nondeprived rats. 2001 May-Jun. Pharmacol Biochem Behav. 69(1-2):117-23.
National Institute on Drug Abuse
Grigson PS. Freet CS. The suppressive effects of sucrose and cocaine, but not lithium chloride, are greater in Lewis than in Fischer rats: evidence for the reward comparison hypothesis. 2000 Apr. Behav Neurosci. 114(2):353-63.
National Institute on Drug Abuse
National Institute on Deafness and other Communication Disorders
Grigson PS. Lyuboslavsky PN. Tanase D. Wheeler RA. Water-deprivation prevents morphine-, but not LiCl-induced, suppression of sucrose intake. 1999 Aug. Physiol Behav. 67(2):277-86.
National Institute on Drug Abuse
National Institute on Deafness and other Communication Disorders
Grigson PS. Like drugs for chocolate: separate rewards modulated by common mechanisms? 2002 Jul. Physiol Behav. 76(3):389-95.
National Institute on Drug Abuse
Grigson PS. Twining RC. Cocaine-induced suppression of saccharin intake: a model of drug-induced devaluation of natural rewards. 2002 Apr. Behav Neurosci. 116(2):321-33.
National Institute on Drug Abuse
National Institute on Deafness and other Communication Disorders

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