Spatial learning induces neurotrophin receptor and synapsin I in the hippocampus

Gómez‐Pinilla, Fernando; So, Vannarith; Kesslak, J. Patrick

doi:10.1016/s0006-8993(01)02394-0

Cited by 100 publications

(79 citation statements)

References 27 publications

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“…First, the effect of swimming on growth factors is most prominent for massed training that involves higher levels of physical activity than the spaced training used in our experiments. [29][30][31] Second, the number of BrdU-labeled cells in Yoked animals, which were submitted to exactly the same level of physical activity as that of the Learning group, did not statistically differ from that of Unmanipulated controls. Higher levels of activity such as the ones observed in a running wheel are necessary for modifying hippocampal neurogenesis.…”

Section: Discussionmentioning

confidence: 86%

“…The results are expressed as mean7SEM. In order to control for a nonspecific effect of learning, BrdU-IR cells were also counted (batch 2) within the dorsolateral corner of the subventricular zone [22][23][24][25][26][27][28][29][30][31][32] …”

Section: Quantitative Evaluation Of Peroxidase Stainingmentioning

confidence: 99%

“…In this task, two phases of learning can be distinguished: an early phase during which performance improves rapidly, and a late phase during which asymptotic levels of performance are reached. These two phases seem to involve different brain processes [28][29][30][31] and, consequently, may differentially influence neurogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Differential effects of learning on neurogenesis: learning increases or decreases the number of newly born cells depending on their birth date

et al. 2003

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The hippocampal formation, to which new neurons are added on a daily basis throughout life, is important in spatial learning. Surviving de novo produced cells integrate into the functional circuitry, where they can influence both normal and pathological behaviors. In this study, we examined the effect of the water-maze (a hippocampal-dependent spatial task) on neurogenesis. Learning in this task can be divided into two phases, an early phase during which performance improves rapidly, and a late phase during which asymptotic levels of performance are reached. Here we demonstrate that the late phase of learning has a multifaceted effect on neurogenesis depending on the birth date of new neurons. The number of newly born cells increased contingently with the late phase and a large proportion of these cells survived for at least 4 weeks and differentiated into neurons. In contrast, late-phase learning decreased the number of newly born cells produced during the early phase. This decline in neurogenesis was positively correlated with performance in the water-maze. Thus, rats with the highest de novo cell number were less able to acquire and use spatial information than those with low numbers of new cells. These results show that learning has a complex effect on hippocampal neurogenesis, and reveals a novel mechanism through which neurogenesis may influence normal and pathological behaviors. Molecular Psychiatry (2003) 8, 974-982.

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Section: Discussionmentioning

confidence: 86%

Section: Quantitative Evaluation Of Peroxidase Stainingmentioning

confidence: 99%

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Differential effects of learning on neurogenesis: learning increases or decreases the number of newly born cells depending on their birth date

et al. 2003

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“…BDNF protein was quantified using an enzyme linked immunosorbent assay (ELISA; BDNF Emax ImmunoAssay system Kit; Promega Inc., Madison, WI, USA) as per manufacturer's protocol. Synapsin I, phosphosynapsin I, total-CREB, and phospho-CREB proteins were analyzed by Western blot as previously described (Gó mez-Pinilla et al, 2001), quantified by densitometric scanning of the film under linear exposure conditions and normalized for actin levels. Membranes were incubated with the following primary antibodies: antisynapsin I (1:2000; Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA), anti-phospho-synapsin I (1:2000; Santa Cruz Biotechnology), anti-total CREB (1:1000; Cell Signaling Technology, Inc., Beverly, MA, USA), anti-phospho-CREB (1:1000; Cell Signaling Technology, Inc.), anti-actin (1:2000; Santa Cruz Biotechnology) followed by anti-goat IgG horseradish peroxidase conjugate for synapsin, phospho-synapsin and actin or anti-rabbit IgG horseradish peroxidase conjugate for total CREB and phospho-CREB (Santa Cruz Biotechnology).…”

Section: Protein Measurementsmentioning

confidence: 99%

Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor

et al. 2004

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“…Exercise induces synaptic plasticity markers in the hippocampus through a BDNF-mediated mechanism, particularly increasing the mRNA levels of the transcriptional factor involved in memory, and cAMP responseelement-binding (CREB) protein (Vaynman et al, 2003;Gomez-Pinilla et al, 2001;Vaynman et al, 2004), in a dose response manner to increasing BDNF mRNA levels (Vaynman et al, 2004). Importantly, CAMKII is able to regulate CREB-dependent transcription (Lonze & Ginty, 2002).…”

Section: Introductionmentioning

confidence: 99%

The select action of hippocampal calcium calmodulin protein kinase II in mediating exercise-enhanced cognitive function

Vaynman¹,

Ying²,

Gómez‐Pinilla³

2007

Neuroscience

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We found that a single week of exercise enhanced cognitive function on the Morris water maze (MWM), such that exercise animals were significantly better than sedentary controls at learning and recalling the location of the platform. In order to elucidate the role that calcium calmodulin protein kinase II (CAMKII) holds in mediating the exercise-induced enhancement in learning and memory, a specific antagonist of CAMKII, KN-62, was used to block CAMKII in the hippocampus during a 1-week voluntary exercise period. Following, a 2-trial-per-day MWM was performed for 5 consecutive days, succeeded by a probe trial 2 days later. Inhibiting CAMKII action during exercise blocked the ability of exercise to enhance memory retention on the MWM; the recall abilities of exercise animals receiving the CAMKII blocker were significantly worse than those of both sedentary and exercise controls. Conversely, CAMKII may not play a significant role in mediating the effects of exercise on learning acquisition as inhibiting CAMKII failed to block the exercise-induced enhancement in learning acquisition. Our results also show that CAMKII activation early during MWM learning may be counterproductive to learning acquisition, as exercising animals given the CAMKII inhibitor performed significantly (p < 0.001) better than exercising control animals and sedentary controls only on day 2 of the MWM. Inhibiting CAMKII also blocked the exercise-induced upregulation of molecules critical for learning and memory, BDNF and the transcription activator CREB, which is regulated by and downstream to BDNF action. These findings indicate that hippocampal CAMKII may have a refined role in mediating the effects of exercise on cognition, selectively functioning to regulate memory retention.

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Spatial learning induces neurotrophin receptor and synapsin I in the hippocampus

Cited by 100 publications

References 27 publications

Differential effects of learning on neurogenesis: learning increases or decreases the number of newly born cells depending on their birth date

Differential effects of learning on neurogenesis: learning increases or decreases the number of newly born cells depending on their birth date

Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor

The select action of hippocampal calcium calmodulin protein kinase II in mediating exercise-enhanced cognitive function

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