ABSTRACT
As the number of CA-MRSA skin and soft tissue infections continues to grow, it's important to know which patients are at greatest risk and which evidence-based treatment protocols to turn to when needed.
Subject(s)
Methicillin-Resistant Staphylococcus aureus/isolation & purification , Staphylococcal Infections/diagnosis , Staphylococcal Infections/drug therapy , Acetamides/economics , Acetamides/therapeutic use , Administration, Topical , Anti-Bacterial Agents/economics , Anti-Bacterial Agents/therapeutic use , Clindamycin/economics , Clindamycin/therapeutic use , Community-Acquired Infections/diagnosis , Community-Acquired Infections/drug therapy , Continuity of Patient Care , Cross Infection/diagnosis , Ethnicity , Humans , Linezolid , Medical History Taking , Mupirocin/administration & dosage , Oxazolidinones/economics , Oxazolidinones/therapeutic use , Patient Education as Topic , Physical Examination , Practice Guidelines as Topic , Rifampin/therapeutic use , Risk Factors , Secondary Prevention , Skin/injuries , Staphylococcal Infections/transmission , Trimethoprim, Sulfamethoxazole Drug Combination/economics , Trimethoprim, Sulfamethoxazole Drug Combination/therapeutic useABSTRACT
Lesions of the gustatory thalamus (GT) prevent the occurrence of between-session contrast effects (i.e., anticipatory negative contrast and consummatory successive negative contrast [cSNC]) involving liquid rewards. These deficits are attributed to a disruption of the reward comparison mechanism that computes the value of the current reward relative to the expected reward. Instrumental successive negative contrast (iSNC), which occurs following a surprising reduction in the magnitude of a solid food reward, is also keyed off the detection of a disparity between the value of the expected and actual rewards. The present study examined whether neurotoxic lesions of the GT prevent the occurrence of iSNC just as they abolish cSNC. In Experiment 1, both GT-lesioned and neurologically intact rats trained with 10 food pellets and shifted to one food pellet showed a significant iSNC effect. In Experiment 2, the same GT-lesioned rats failed to show cSNC when shifted from 1.0M sucrose to 0.15% sodium saccharin. The obtained pattern of results suggests that separate reward comparison mechanisms with different neural substrates underlie expression of cSNC and iSNC.
Subject(s)
Appetitive Behavior/drug effects , Conditioning, Operant/physiology , Excitatory Amino Acid Agonists/toxicity , Motivation , N-Methylaspartate/toxicity , Reward , Taste/physiology , Thalamus/physiology , Animals , Appetitive Behavior/physiology , Brain Mapping , Conditioning, Operant/drug effects , Dominance, Cerebral/drug effects , Dominance, Cerebral/physiology , Drinking/drug effects , Drinking/physiology , Feeding Behavior/drug effects , Feeding Behavior/physiology , Male , Rats , Rats, Sprague-Dawley , Taste/drug effects , Thalamus/drug effectsABSTRACT
The effects of permanent forebrain lesions on conditioned taste aversions (CTAs) and conditioned odor aversions (COAs) were examined in 3 experiments. In Experiment 1, lesions of the bed nucleus of the stria terminalis had no influence on CTA or COA acquisition. Although lesions of the lateral hypothalamus induced severe hypodipsia in Experiment 2, they did not prevent the acquisition of CTAs or COAs. Finally, in Experiment 3, lesions of the insular cortex retarded CTA acquisition but had no influence on COA acquisition. The implications of these findings are discussed with regard to the forebrain influence on parabrachial nucleus function during CTA acquisition.
