D1/D5 dopamine receptors modulate spatial memory formation

AbstractWe investigated the effect of the intra-CA1 administration of the D1/D5 receptor antagonist SCH23390 and the D1/D5 receptor agonist SKF38393 on spatial memory in the water maze. When given immediately, but not 3h after training, SCH23390 hindered long-term spatial memory formation without affecting non-spatial memory or the normal functionality of the hippocampus. On the contrary, post-training infusion of SKF38393 enhanced retention and facilitated the spontaneous recovery of the original spatial preference after reversal learning. Our findings demonstrate that hippocampal D1/D5 receptors play an essential role in spatial memory processing

Prior learning of relevant non-aversive information is a boundary condition for avoidance memory reconsolidation in the rat hippocampus

Reactivated memories can be modified during reconsolidation, making this process a potential therapeutic target for post-traumatic stress disorder (PTSD), a mental illness characterized by the recurring avoidance of situations that evoke trauma-related fears. However, avoidance memory reconsolidation depends on a set of still loosely defined boundary conditions, limiting the translational value of basic research. In particular, the involvement of the hippocampus in fear-motivated avoidance memory reconsolidation remains controversial. Combining behavioral and electrophysiological analyses in male Wistar rats, we found that previous learning of relevant non-aversive information is essential to elicit the participation of the hippocampus in avoidance memory reconsolidation, which is associated with an increase in theta and gamma oscillations power and cross-frequency coupling in dorsal CA1 during reactivation of the avoidance response. Our results indicate that the hippocampus is involved in memory reconsolidation only when reactivation results in contradictory representations regarding the consequences of avoidance, and suggest that robust nesting of hippocampal theta-gamma rhythms at the time of retrieval is a specific reconsolidation marker.2018-03-1

Nicotine modulates the long-lasting storage of fear memory

Late post-training activation of the ventral tegmental area (VTA)–hippocampus dopaminergic loop controls the entry of information into long-term memory (LTM). Nicotinic acetylcholine receptors (nAChR) modulate VTA function, but their involvement in LTM storage is unknown. Using pharmacological and behavioral tools, we found that α7-nAChR-mediated cholinergic interactions between the pedunculopontine tegmental nucleus and the medial prefrontal cortex modulate the duration of fear-motivated memories, maybe by regulating the activation state of VTA–hippocampus dopamine connections.Fil: Lima, Ramón H.. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; ArgentinaFil: Radiske, Andressa. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; ArgentinaFil: Köhler, Cristiano A.. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; ArgentinaFil: González, María Carolina. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Rossato, Janine Inez. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bevilaqua, Lia R.. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; ArgentinaFil: Medina, Jorge Horacio. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cammarota, Martin Pablo. Pontificia Universidade Catolica Do Rio Grande Do Sul; Brasil. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Reconsolida??o da mem?ria de extin??o : an?lise farmacol?gica, bioqu?mica e molecular

Submitted by Setor de Tratamento da Informa??o - BC/PUCRS ([email protected]) on 2015-07-15T15:03:02Z No. of bitstreams: 1 472298 - Texto Completo.pdf: 677948 bytes, checksum: 96bddf252e88732ab099f3a5a6fc7a54 (MD5)Made available in DSpace on 2015-07-15T15:03:02Z (GMT). No. of bitstreams: 1 472298 - Texto Completo.pdf: 677948 bytes, checksum: 96bddf252e88732ab099f3a5a6fc7a54 (MD5) Previous issue date: 2015-05-08Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior - CAPESBackground : Therapies based on the impairment of memory reconsolidation or the enhancement of extinction learning offer the possibility of diminishing the impact caused by the persistent recollection of traumatic events. Nonetheless, the possible interaction between reconsolidation and extinction has rarely been considered. Previously, we reported that reactivation induces reconsolidation of fear extinction, but the molecular bases of this process are largely unknown. Brain-derived neurotrophic factor (BDNF) has been repeatedly linked to fear extinction; therefore we analyzed the possible involvement of this neurotrophin in fear extinction memory reconsolidation. Methods : With a step-down inhibitory avoidance-learning task (IA) and selective pharmacological tools, we investigated the effect of gene expression, protein synthesis and BDNF signaling inhibition on the persistent storage of the reactivated fear extinction memory trace in rats. Results : When given in dorsal CA1 immediately after IA extinction reactivation, the protein synthesis inhibitor anisomycin (ANI), the gene expression inhibitor ?- amanitin (AMA), the BDNF maturation blocker PAI-1, and function-blocking anti- BDNF antibody hindered extinction memory persistence. Pro-BDNF and BDNF levels were altered in dorsal CA1 after extinction memory reactivation. Coinfusion of recombinant BDNF reversed the recovery of fear induced by intra-CA1 ANI and AMA. Conclusion : These data suggest that hippocampal BDNF is sufficient to sustain fear extinction memory reconsolidation and indicate that increasing BDNF signaling after extinction memory retrieval impedes the recurrence of fear caused by impairing this process.Introdu??o : Terapias baseadas no bloqueio da reconsolida??o ou no fortalecimento da extin??o oferecem a possibilidade terap?utica de diminuir o impacto causado pela persist?ncia das lembran?as de eventos traum?ticos. No entanto, a intera??o entre a reconsolida??o e a extin??o tem sido pouco analisada. Previamente, nosso grupo demonstrou que a mem?ria de extin??o do medo pode ser reconsolidada, por?m as bases moleculares que sustentam esse processo ainda s?o desconhecidas. O fator neurotr?fico dependente do c?rebro (BDNF) tem sido frequentemente relacionado com a extin??o do medo; por isso, n?s analisamos o poss?vel envolvimento dessa neurotrofina na reconsolida??o da mem?ria de extin??o do medo. M?todos : Com a tarefa de esquiva inibit?ria como modelo experimental junto com ferramentas farmacol?gicas espec?ficas, n?s investigamos o efeito da express?o g?nica, s?ntese de prote?nas e da inibi??o da sinaliza??o de BDNF sobre a persist?ncia da mem?ria de extin??o ap?s a sua reativa??o em ratos. Resultados : Quando injetado imediatamente ap?s a reativa??o da mem?ria de extin??o, o inibidor de s?ntese proteica anisomicina (ANI), inibidor de express?o g?nica ?-amanitina (AMA), o bloqueador da matura??o de BDNF (PAI-1) e um anticorpo bloqueador da fun??o de BDNF (anti-BDNF), prejudicaram a persist?ncia da mem?ria de extin??o. Os n?veis de pr?-BDNF, BDNF e pTrKB foram alterados na regi?o CA1 do hipocampo dorsal ap?s a reativa??o da mem?ria de extin??o. A Co-infus?o de BDNF recombinante reverteu o reaparecimento do medo induzido pela infus?o de ANI e AMA na regi?o CA1 do hipocampo dorsal. Conclus?o : Esses dados sugerem que o BDNF hipocampal ? suficiente para sustentar a reconsolida??o da mem?ria de extin??o do medo e indicam que o aumento da sua sinaliza??o ap?s a reativa??o da mem?ria de extin??o impede a reincid?ncia do medo causado por inibidores desse processo

Caracteriza??o dos processos bioqu?micos e farmacol?gicos da reconsolida??o da mem?ria de extin??o

Made available in DSpace on 2015-04-14T13:35:19Z (GMT). No. of bitstreams: 1 434469.pdf: 522845 bytes, checksum: 1a6aa11b2380d6b39eabb139c21770ae (MD5) Previous issue date: 2011-09-27A express?o de uma mem?ria j? consolidada pode levar ? ocorr?ncia de dois processos opostos, que requerem a s?ntese de novo de prote?nas nas mesmas ?reas do c?rebro: a extin??o e a reconsolida??o. A extin??o debilita a express?o da mem?ria original, enquanto que a reconsolida??o permite a incorpora??o de nova informa??o a ela. O conhecimento acerca destes dois processos acumulou-se durante os ?ltimos anos, por?m a poss?vel intera??o entre ambos ainda n?o foi avaliada. Neste trabalho demonstramos que a inibi??o da s?ntese prot?ica e express?o g?nica hipocampal imediatamente ap?s a reativa??o prejudicam a express?o da mem?ria de extin??o sem afetar a mem?ria original aversiva. A partir desses dados, sugere-se que, assim como a reconsolida??o, a mem?ria de extin??o ap?s a reativa??o tamb?m requer a participa??o de s?ntese prot?ica e express?o g?nica para sua manuten??o na regi?o CA1 do hipocamp

Editorial: On the destabilization of maladaptive memory: updates and future perspectives

Peer reviewed: Tru