The hippocampus is a critical area for converting short-term memories into long-term memories and it plays a pivotal role in encoding, consolidation and retrieval of associations responsible for episodic memory. In dentate gyrus of mammalian hippocampus, neuron production carries on throughout adult life. In fact, at he border of granule cell layer (GCL) facing hilus, there are neural precursors, identified as astrocyte-like cells, that proliferate; a number of daughter cells die, while others differentiate into morphologically, biochemically and functionally characterized mature granule neurons. These new neurons send their projections to CA3 field and receive synapses, becoming a part of functional networks. The role of hippocampus in learning and the occurrence of neurogenesis in GCL suggest an active role of new neurons in memory formation. In order for newborn cells to be able to be involved in learning processes, they must be rescued from death and they must become a part of functional networks. Therefore, the knowledge of the effects of learning on survival of differentiating cells is the first step to making hypotheses about their role in learning. The acquisition of a hippocampus-dependent task enhances newborn cell survival in GCL during the period in which several newborn cells die. In this paper the effect of learning, occurring after the maximal period of newborn cell death, on newborn cells was investigated. Rats were trained for hippocampus-dependent learning in Morris water maze. 5-bromo-2'-deoxyuridine was administered 8-10 days before training beginning and labeled cells were counted after training. Learning decreased BrdU-labeled cell density in GCL, and increased TUNEL-positive cells. Moreover, learning diminished immature neuron density prevalently in the internal blade of GCL. Therefore, a different effect of learning on immature neuron survival, depending on the time elapsing from mitosis to learning, is suggested.

Learning may reduce neurogenesis in adult rat dentate gyrus

AMBROGINI, PATRIZIA;FERRI, PAOLA;CIARONI, SANDRA;CUPPINI, RICCARDO
2004

Abstract

The hippocampus is a critical area for converting short-term memories into long-term memories and it plays a pivotal role in encoding, consolidation and retrieval of associations responsible for episodic memory. In dentate gyrus of mammalian hippocampus, neuron production carries on throughout adult life. In fact, at he border of granule cell layer (GCL) facing hilus, there are neural precursors, identified as astrocyte-like cells, that proliferate; a number of daughter cells die, while others differentiate into morphologically, biochemically and functionally characterized mature granule neurons. These new neurons send their projections to CA3 field and receive synapses, becoming a part of functional networks. The role of hippocampus in learning and the occurrence of neurogenesis in GCL suggest an active role of new neurons in memory formation. In order for newborn cells to be able to be involved in learning processes, they must be rescued from death and they must become a part of functional networks. Therefore, the knowledge of the effects of learning on survival of differentiating cells is the first step to making hypotheses about their role in learning. The acquisition of a hippocampus-dependent task enhances newborn cell survival in GCL during the period in which several newborn cells die. In this paper the effect of learning, occurring after the maximal period of newborn cell death, on newborn cells was investigated. Rats were trained for hippocampus-dependent learning in Morris water maze. 5-bromo-2'-deoxyuridine was administered 8-10 days before training beginning and labeled cells were counted after training. Learning decreased BrdU-labeled cell density in GCL, and increased TUNEL-positive cells. Moreover, learning diminished immature neuron density prevalently in the internal blade of GCL. Therefore, a different effect of learning on immature neuron survival, depending on the time elapsing from mitosis to learning, is suggested.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11576/1880635
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