Pâmela Billig Mello-Carpes

The Nucleus of the Solitary Tract → Nucleus Paragigantocellularis → Locus Coeruleus → CA1 region of dorsal hippocampus pathway is important for consolidation of object recognition memory.

The Nucleus of the Solitary Tract (NTS) receives gustatory and visceral information from afferent fibers in the vagus and projects to the Nucleus Paragigantocellularis (PGi), among several other brain region. PGi sends excitatory fibers, mostly glutamatergic, to the Locus Coeruleus (LC). In turn, LC sends noradrenergic projections to many areas of the brain, including hippocampus (HIPP) and amygdala. Here we show that the NTS-PGi-LC-HIPP pathway is required for the memory consolidation of object recognition (OR). The inhibition of NTS, PGi or LC by microinfusion of the GABA(A) receptor agonist, muscimol, into each of these structures up to 3h after object recognition memory training impairs its consolidation as assessed in a retention test 24h later. The posttraining microinfusion of the β-blocker, timolol into CA1 mimics this effect. Intra-CA1 NA microinfusion does not alter retention per se, but reverses the disruptive effect of muscimol given into NTS, PGi or LC. This effect of NA is shared by a microinfusion of NMDA into LC. These results support the idea that the NTS-PGi-LC-CA1 pathway contributes to memory consolidation through a β-noradrenergic mechanism in CA1.

Facilitation of fear extinction by novelty depends on dopamine acting on D1-subtype dopamine receptors in hippocampus

Significance A brief exposure to a novel environment was recently shown to enhance the extinction of contextual fear probably through a protein synthesis-dependent process of synaptic tagging and capture in the hippocampus. Here we report that this finding can be generalized to the extinction of another fear-motivated task, one-trial inhibitory avoidance. This generalization is important because extinction is used in exposure therapy to treat posttraumatic stress disorder in humans, and this may derive from various forms of fear-related stress. In addition, here we show that the effect of novelty on fear extinction is dependent on dopamine D1 but not D5 receptors in the hippocampus. These findings could be applicable to the exposure therapy of fear memory disorders. Extinction is the learned inhibition of retrieval. Recently it was shown that a brief exposure to a novel environment enhances the extinction of contextual fear in rats, an effect explainable by a synaptic tagging-and-capture process. Here we examine whether this also happens with the extinction of another fear-motivated task, inhibitory avoidance (IA), and whether it depends on dopamine acting on D1 or D5 receptors. Rats were trained first in IA and then in extinction of this task. The retention of extinction was measured 24 h later. A 5-min exposure to a novel environment 30 min before extinction training enhanced its retention. Right after exposure to the novelty, animals were given bilateral intrahippocampal infusions of vehicle (VEH), of the protein synthesis inhibitor anisomycin, of the D1/D5 dopaminergic antagonist SCH23390, of the PKA inhibitor Rp-cAMP or of the PKC inhibitor Gö6976, and of the PKA stimulator Sp-cAMP or of the PKC stimulator PMA. The novelty increased hippocampal dopamine levels and facilitated the extinction, which was inhibited by intrahippocampal protein synthesis inhibitor anisomysin, D1/D5 dopaminerdic antagonist SCH23390, or PKA inhibitor Rp-cAMP and unaffected by PKC inhibitor Gö6976; additionally, the hippocampal infusion of PKA stimulator Sp-cAMP reverts the effect of D1/D5 dopaminergic antagonist SCH 23390, but the infusion of PKC stimulator PMA does not. The results attest to the generality of the novelty effect on fear extinction, suggest that it relies on synaptic tagging and capture, and show that it depends on hippocampal dopamine D1 but not D5 receptors.

Memory deficits and oxidative stress in cerebral ischemia–reperfusion: Neuroprotective role of physical exercise and green tea supplementation

Ischemic stroke is a major cause of morbidity and mortality all over the world. Among impairments observed in survivors there is a significant cognitive learning and memory deficit. Neuroprotective strategies are being investigated to minimize such deficits after an ischemia event. Here we investigated the neuroprotective potential of physical exercise and green tea in an animal model of ischemia-reperfusion. Eighty male rats were divided in 8 groups and submitted to either transient brain ischemia-reperfusion or a sham surgery after 8 weeks of physical exercise and/or green tea supplementation. Ischemia-reperfusion was performed by bilateral occlusion of the common carotid arteries during 30 min. Later, their memory was evaluated in an aversive and in a non-aversive task, and hippocampus and prefrontal cortex were removed for biochemical analyses of possible oxidative stress effects. Ischemia-reperfusion impaired learning and memory. Reactive oxygen species were increased in the hippocampus and prefrontal cortex. Eight weeks of physical exercise and/or green tea supplementation before the ischemia-reperfusion event showed a neuroprotective effect; both treatments in separate or together reduced the cognitive deficits and were able to maintain the functional levels of antioxidant enzymes and glutathione.

Hippocampal noradrenergic activation is necessary for object recognition memory consolidation and can promote BDNF increase and memory persistence.

Previously we showed that activation of the Nucleus of the Solitary Tract (NTS)-Nucleus Paragigantocellularis (PGi)-Locus coeruleus (LC) pathway, which theoretically culminates with norepinephrine (NE) release in dorsal hippocampus (CA1 region) and basolateral amygdala (BLA) is necessary for the consolidation of object recognition (OR) memory. Here we show that, while the microinjection of the beta-noradrenergic receptor blocker timolol into CA1 impairs OR memory consolidation, the microinjection of norepinephrine (NE) promotes the persistence of this type of memory. Further, we show that OR consolidation is attended by an increase of norepinephrine (NE) levels and of the expression of brain derived neurotrophic factor (BDNF) in hippocampus, which are impaired by inactivation of the NTS-PGi-LC pathway by the infusion of muscimol into the NTS.

Effects of green tea and physical exercise on memory impairments associated with aging.

We investigated the effects of physical exercise and green tea supplementation (associated or not) on biochemical and behavioral parameters in the time course of normal aging. Male Wistar rats aged 9 months were divided into groups: control, physical exercise (treadmill running), and supplemented with green tea while either performing physical exercise or not. A young control group was also studied. Physical exercise and green tea supplementation lasted 3 months. Afterwards, behavioral and biochemical tests were performed. Biochemical measurements revealed differences in antioxidant and oxidant responses in hippocampus, prefrontal cortex and striatum. Behavioral testing showed age-related memory impairments reversed by physical exercise. The association of green tea supplementation and physical exercise did not provide aged rats with additional improvements in memory or brain oxidative markers. Green tea per se significantly decreased reactive oxygen species levels and improved antioxidant defenses although it did not reverse memory deficits associated with normal aging.

Chronic exposure to low mercury chloride concentration induces object recognition and aversive memories deficits in rats

This work examines the effects of chronic exposure to low inorganic mercury (mercury chloride, HgCl2) concentration on the recognition and aversive memories. Forty male Wistar rats were divided into 4 groups treated during 30 or 60 days with saline (control) or HgCl2 doses. After treated the animals were tested considering object recognition and inhibitory avoidance behavioral memory paradigms. Elevated plus maze, open field and tail flick tests were used to assess anxiety, locomotor and exploratory activity and pain thresholds. Only exposure for 60 days to HgCl2 induced in memory deficits quantified in the object recognition task. In the inhibitory avoidance all the animals exposed to mercury (for 30 or 60 days) presented worst performance than control animals. Our results suggest that chronic exposure to low mercury chloride concentrations impairs memory formation.

The use of Facebook as a tool to increase the interest of undergraduate students in physiology in an interdisciplinary way

the process of teaching and learning at the undergraduate level is challenged by an increasing amount of content ([1][1]). Now its not enough to convey knowledge; its also necessary to seek alternative ways to motivate and capture the interest of students both during class and outside of class.

Supplementation with different teas from Camellia sinensis prevents memory deficits and hippocampus oxidative stress in ischemia-reperfusion

&NA; Memory and cognition impairments resultant of ischemic stroke could be minimized or avoided by antioxidant supplementation. In this regard, the neuroprotective potential of Green tea from Camellia sinensis has been investigated. However, there is a lack of information regarding the neuroprotective potential of others teas processed from the Camellia sinensis. Here we investigate the neuroprotective role of green, red, white and black tea on memory deficits and brain oxidative stress in a model of ischemic stroke in rats. Our findings show that green and red teas prevent deficits in object and social recognition memories, but only green tea protects against deficits in spatial memory and avoids hippocampal oxidative status and intense necrosis and others alterations in the brain tissue. In summary, green tea shows better neuroprotection in ischemic stroke than the others teas from Camellia sinensis. HighlightsWhite, green and red teas protect recognition memory deficit after ischemic stroke.Only green tea protects against ischemic stroke induced spatial memory deficit.Only green tea protects against hippocampal oxidative stress after ischemic stroke.Neuroprotection is higher after green tea supplementation.

Physical exercise prevents motor disorders and striatal oxidative imbalance after cerebral ischemia-reperfusion.

Stroke is the third most common cause of death worldwide, and most stroke survivors present some functional impairment. We assessed the striatal oxidative balance and motor alterations resulting from stroke in a rat model to investigate the neuroprotective role of physical exercise. Forty male Wistar rats were assigned to 4 groups: a) control, b) ischemia, c) physical exercise, and d) physical exercise and ischemia. Physical exercise was conducted using a treadmill for 8 weeks. Ischemia-reperfusion surgery involved transient bilateral occlusion of the common carotid arteries for 30 min. Neuromotor performance (open-field and rotarod performance tests) and pain sensitivity were evaluated beginning at 24 h after the surgery. Rats were euthanized and the corpora striata was removed for assay of reactive oxygen species, lipoperoxidation activity, and antioxidant markers. Ischemia-reperfusion caused changes in motor activity. The ischemia-induced alterations observed in the open-field test were fully reversed, and those observed in the rotarod test were partially reversed, by physical exercise. Pain sensitivity was similar among all groups. Levels of reactive oxygen species and lipoperoxidation increased after ischemia; physical exercise decreased reactive oxygen species levels. None of the treatments altered the levels of antioxidant markers. In summary, ischemia-reperfusion resulted in motor impairment and altered striatal oxidative balance in this animal model, but those changes were moderated by physical exercise.

Influence of mental practice and movement observation on motor memory, cognitive function and motor performance in the elderly

Background With aging, it is important to maintain cognitive and motor functions to ensure autonomy and quality of life. During the acquisition of motor skills, it is necessary for the elderly to understand the purpose of the proposed activities. Physical and mental practice, as well as demonstrations, are strategies used to learn movements. Objectives To investigate the influence of mental practice and the observation of movement on motor memory and to understand the relationship between cognitive function and motor performance in the execution of a sequence of digital movements in the elderly. Method This was a cross-sectional study conducted with 45 young and 45 aged subjects. The instruments used were Mini-Mental State Examination (MMSE), Manual Preference Inventory and a Digital Motor Task (composed of a training of a sequence of movements, an interval and a test phase). The subjects were divided into three subgroups: control, mental practice and observation of movement. Results The elderly depend more strongly on mental practice for the acquisition of a motor memory. In comparing the performances of people in different age groups, we found that in the elderly, there was a negative correlation between the MMSE score and the execution time as well as the number of errors in the motor task. Conclusions For the elderly, mental practice can advantage motor performance. Also, there is a significant relationship between cognitive function, learning and the execution of new motor skills.