Dopaminergic mechanisms in memory consolidation and antidepressant reversal of a chronic mild stress-induced cognitive impairment'
| Autor: | Mariusz Papp, Monika Niemczyk, Ewa Litwa, Piotr Gruca, Paul Willner, Katarzyna Tota-Glowczyk, Magdalena Lason-Tyburkiewicz |
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| Rok vydání: | 2017 |
| Předmět: |
Male
Agonist medicine.drug_class Novel object recognition D1 receptors Prefrontal Cortex Hippocampus Nucleus accumbens Nucleus Accumbens 03 medical and health sciences Chronic mild stress 0302 clinical medicine Dopamine receptor D2 medicine Animals Cognitive Dysfunction Rats Wistar D3 receptors Receptor Prefrontal cortex Memory Consolidation Original Investigation D2 receptors Pharmacology Depression Receptors Dopamine D2 Receptors Dopamine D1 Venlafaxine Risperidone Antidepressive Agents 030227 psychiatry Dopamine Agonists Dopamine Antagonists Rat Antidepressant Memory consolidation Psychology Neuroscience Stress Psychological 030217 neurology & neurosurgery |
| Zdroj: | Psychopharmacology |
| ISSN: | 1432-2072 0033-3158 |
| DOI: | 10.1007/s00213-017-4651-4 |
| Popis: | Cognitive deficits in depression can be modelled using the novel object recognition (NOR) test, performance in which is impaired by chronic mild stress (CMS). We aimed to examine the involvement of mesocorticolimbic DA terminal regions, and to establish the substrate for CMS-induced impairment of NOR and its reversal by chronic antidepressant treatment. In experiments 1 and 2, we examined the effect of infusions into medial PFC, dorsal hippocampus (HPC), and nucleus accumbens (NAc) shell of D1 and D2 antagonists and D3 agonist, which were predicted to impair NOR with a short (1 h) delay, and of D1 and D2 agonists and D3 antagonist, which were predicted to facilitate NOR with a long (24 h) delay. Using optimal doses identified in experiment 2, in experiments 3 and 4, we examined effects on drug-stimulated NOR of CMS and chronic treatment with venlafaxine (VFX) or risperidone (RSP). We found a wide involvement of DA systems in memory for NOR: D1 receptors in PFC, HPC, and NAc; D3 receptors in PFC and HPC; and D2 receptors in PFC. CMS impaired D2- and D3-mediated effects in PFC and HPC; antidepressants rescued those effects in PFC but not HPC. The involvement of DA in NOR is multifaceted, but the effects of CMS and antidepressants are more discrete, involving D2 and D3 receptors in PFC specifically. While raising many difficult questions, these results suggest that the D2 and D3 receptors in the medial PFC may be an important substrate for cognitive deficits in depression and their remediation. Electronic supplementary material The online version of this article (doi:10.1007/s00213-017-4651-4) contains supplementary material, which is available to authorized users. |
| Databáze: | OpenAIRE |
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