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Central administration of thyrotropin-releasing hormone and histidyl-proline-diketopiperazine disrupts the acquisition of a food rewarded task by a non-aversive action
| Content Provider | Semantic Scholar |
|---|---|
| Author | Andrews, J. S. Sahgal, Arun |
| Copyright Year | 1983 |
| Abstract | The effects of thyrotropin-releasing hormone (TRH) and its metabolites on operant behaviour have rarely been explored. In this study, the effects of intracerebroventricular (icv) administration of TRH and histidyl-proline-diketopiperazine (DKP), a metabolite of TRH, on the acquisition of a food-rewarded lever-press task were compared with saline-treated controls. TRH and DKP severely retarded the acquisition of lever pressing. The effects of systemically administered D-amphetamine were also examined in order to test whether this result was due to any stimulant properties of these peptides. These results suggest that stimulatory effects do not adequately account for impaired acquisition. The possibility that the disruption of learning was due to an aversive effect of icv administration of these peptides was tested by means of a conditioned place paradigm. Neither peptide induced an avoidance of the environment with which it had previously been paired. Several possible reasons for the peptides' adverse effect on learning are discussed, including the possibility that TRH and DKP act on attentional mechanisms. |
| Starting Page | 373 |
| Ending Page | 383 |
| Page Count | 11 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/0167-0115(83)90109-X |
| PubMed reference number | 6422515 |
| Journal | Medline |
| Volume Number | 7 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/016701158390109X |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/016701158390109X?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/0167-0115%2883%2990109-X |
| Journal | Regulatory Peptides |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
