Janine I. Rossato

ORCID: 0000-0002-7980-5842
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Sleep and Wakefulness Research
  • Receptor Mechanisms and Signaling
  • Stress Responses and Cortisol
  • Memory Processes and Influences
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroendocrine regulation and behavior
  • Genetics and Neurodevelopmental Disorders
  • Nicotinic Acetylcholine Receptors Study
  • Organoselenium and organotellurium chemistry
  • Prion Diseases and Protein Misfolding
  • Adenosine and Purinergic Signaling
  • Alzheimer's disease research and treatments
  • Free Radicals and Antioxidants
  • Anesthesia and Neurotoxicity Research
  • Zebrafish Biomedical Research Applications
  • Photoreceptor and optogenetics research
  • Nerve injury and regeneration
  • Selenium in Biological Systems
  • Sociology and Education in Brazil
  • Cholinesterase and Neurodegenerative Diseases
  • Neurological diseases and metabolism
  • Molecular Sensors and Ion Detection

Universidade Federal do Rio Grande do Norte
2014-2025

Universidade Estadual do Oeste do Paraná
2023-2024

University of Edinburgh
2017-2023

University of Buenos Aires
2003-2013

Pontifícia Universidade Católica do Rio Grande do Sul
2005-2013

National Council for Scientific and Technological Development
2003-2010

Instituto Nacional de Ciência e Tecnologia de Neurociência Translacional
2009

Instituto do Cérebro
2009

Universidade Federal do Rio Grande do Sul
2003-2007

Hospital São Lucas da PUCRS
2006-2007

Persistence is a characteristic attribute of long-term memories (LTMs). However, little known about the molecular mechanisms that mediate this process. We recently showed persistence LTM requires late protein synthesis- and BDNF-dependent phase in hippocampus. Here, we show intrahippocampal delivery BDNF reverses deficit memory caused by inhibition hippocampal synthesis. Importantly, demonstrate induces itself, transforming nonlasting trace into persistent one an ERK-dependent manner. Thus,...

10.1073/pnas.0711863105 article EN Proceedings of the National Academy of Sciences 2008-02-09

The paradigmatic feature of long-term memory (LTM) is its persistence. However, little known about the mechanisms that make some LTMs last longer than others. In rats, a long-lasting fear LTM vanished rapidly when D1 dopamine receptor antagonist SCH23390 was injected into dorsal hippocampus 12 hours, but not immediately or 9 after fearful experience. Conversely, intrahippocampal application agonist SK38393 at same critical post-training time converted decaying persistent one. This effect...

10.1126/science.1172545 article EN Science 2009-08-20

Upon retrieval, consolidated memories are again rendered vulnerable to the action of metabolic blockers, notably protein synthesis inhibitors. This has led hypothesis that reconsolidated at time and this depends on synthesis. Ample evidence indicates hippocampus plays a key role both in consolidation reconsolidation different memories. Despite fact, present there no studies about consequences hippocampal inhibition storage post-retrieval persistence object recognition memory. Here we report...

10.1101/lm.422607 article EN Learning & Memory 2007-01-01

Nonreinforced retrieval can cause extinction and/or reconsolidation, two processes that affect subsequent in opposite ways. Using the Morris water maze task we show that, rat, repeated nonreinforced expression of spatial memory causes extinction, which is unaffected by inhibition protein synthesis within CA1 region dorsal hippocampus. However, if number trials insufficient to induce long-lasting then a hippocampal synthesis-dependent reconsolidation process recovers original memory....

10.1101/lm.315206 article EN Learning & Memory 2006-07-01

The retrosplenial cortex (RSC) is involved in a range of cognitive functions. However, its precise involvement memory processing unknown. Pharmacological and behavioral experiments demonstrate that protein synthesis c-Fos expression the anterior part RSC (aRSC) are necessary late after training to maintain for many days fear-motivated memory. Long-lasting storage regulated by D1/D5 dopamine receptors aRSC depends on functional interplay between dorsal hippocampus aRSC. These results suggest...

10.1002/hipo.22092 article EN Hippocampus 2013-01-28

Therapies based on the impairment of reconsolidation or enhancement extinction offer possibility decreasing persistent recollection distressing memories. However, direct interplay between and has rarely been considered. Previously, we reported that reactivation induces fear memory. Here, using a step-down inhibitory avoidance learning paradigm in rats, show intrahippocampus infusion function-blocking anti-BDNF antibody immediately 6 h after memory impairs extinction. Extinction increases pro...

10.1523/jneurosci.4093-14.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-04-22

ABSTRACT Object recognition memory (ORM) is a hippocampus‐dependent form of essential for distinguishing items and constructing episodic representations the past. Ca2+/calmodulin‐dependent protein kinase II (CaMKII) serine/threonine‐specific highly enriched in hippocampal formation, where it acts as memory‐relevant calcium effector. We found that, rats, training an ORM inducing learning task rapidly increased CaMKII autophosphorylation CA1 region dorsal hippocampus. Moreover, early...

10.1111/ejn.70049 article EN European Journal of Neuroscience 2025-03-01

Cellular prion protein (PrPc) has a pivotal role in diseases. PrPc is specific receptor for laminin (LN) gamma1 peptide and several lines of evidence indicate that it also involved neural plasticity. Here we investigated whether the interaction between LN plays rat memory formation. We found post-training intrahippocampal infusion PrPc-derived peptides contain binding site (PrPc163-182 PrPc173-192) or anti-PrPc anti-LN antibodies inhibit PrPc-LN impaired inhibitory avoidance retention. The...

10.1111/j.1460-9568.2006.05156.x article EN European Journal of Neuroscience 2006-12-01

The nitric oxide (NO)/soluble guanylyl cyclase (sGC)/protein kinase G (PKG) pathway is important for memory processing, but the identity of its downstream effectors as well actual participation in consolidation nonaversive declarative long-term (LTM) remain unknown. Here, we show that training rats an object recognition (OR) learning task rapidly increased nitrites/nitrates (NOx) content CA1 region dorsal hippocampus while posttraining intra-CA1 microinfusion neuronal NO synthase (nNOS)...

10.1002/hipo.20656 article EN Hippocampus 2009-06-16

Storage of acetylcholine in synaptic vesicles plays a key role maintaining cholinergic function. Here we used mice with targeted mutation the vesicular transporter (VAChT) gene that reduces expression by 40% to investigate cognitive processing under conditions VAChT deficiency. Motor skill learning rotarod revealed mutant were slower learn this task, but once they reached maximum performance indistinguishable from wild-type mice. Interestingly, motor maintenance after 10 days was unaffected...

10.1111/j.1601-183x.2008.00439.x article EN Genes Brain & Behavior 2008-09-06

While hippocampal and cortical mechanisms of memory consolidation have long been studied, their interaction is poorly understood. We sought to investigate potential interactions with respect trace dominance, strengthening, interference associated postencoding novelty or sleep. A learning procedure was scheduled in a watermaze that placed the impact sleep opposition. Distinct behavioural manipulations—context preexposure during retrieval—differentially affected dominance survival,...

10.1371/journal.pbio.2000531 article EN cc-by PLoS Biology 2017-01-13

The gamma aminobutyric acid-A (GABA-sub(A)) agonist, muscimol, the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosphonopentanoic acid (AP5), and inhibitor of extracellularly regulated kinases (ERKs), UO 126, cause retrograde amnesia when administered to hippocampus. In present study, authors found that they all for 1-trial inhibitory avoidance, not only infused into dorsal CA1 region hippocampus, but also basolateral amygdala or entorhinal, parietal, posterior...

10.1037/0735-7044.118.3.563 article EN Behavioral Neuroscience 2004-01-01
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