Brain plasticity refers to the brainis ability to change structure and function Experience is a major stimulant of brain plasticity in animal species as diverse as insects and humans It is now clear that experience produces multiple, dissociable changes in the brain including increases in dendritic length, increases (or decreases) in spine density, synapse formation, increased glial activity, and altered metabolic activity These anatomical changes are correlated with behavioral differences between subjects with and without the changes Experience-dependent changes in neurons are affected by various factors including aging, gonadal hormones, trophic factors, stress, and brain pathology We discuss the important role that changes in dendritic arborization play in brain plasticity and behavior, and we consider these changes in the context of changing intrinsic circuitry of the cortex in processes such as learning

/pdf/brain-plasticity-and-behavior-eh85uqto8k.pdf

Brain plasticity and behavior

Young neurons born in the subventricular zone (SVZ) of adult mice migrate to the olfactory bulb (OB) where they differentiate into granule cells (GCs) and periglomerular interneurons. Using retroviral labeling of precursors in the SVZ, we describe five stages and the timing for the maturation of newly formed GCs: (1) tangentially migrating neuroblasts (days 2-7); (2) radially migrating young neurons (days 5-7); (3) GCs with a simple unbranched dendrite that does not extend beyond the mitral cell layer (days 9-13); (4) GCs with a nonspiny branched dendrite in the external plexiform layer (days 11-22); and (5) mature GCs (days 15-30). Using [3H]thymidine, we show that the maximum number of labeled GCs is observed around day 15 after injection. Interestingly, between days 15 and 45 after birth, soon after the cells developed spines, the number of [3H]thymidine-labeled GCs declined by 50%. Using anosmic mice, we found that sensory input was critical for the survival of GCs from day 15 to 45 after labeling. However, the number and morphology of 15-d-old cells in the granule cell layer was similar in anosmic and wild-type mice. We infer that the lack of activity did not have an effect on the generation, migration, and early differentiation of granule cells. Soon after young GCs matured, and presumably became synaptically connected, their survival depended on the level of activity that they received. This selection mechanism might allow the construction of specific OB circuits based on olfactory experience and suggests possible functions of OB cell replacement.

https://www.jneurosci.org/content/jneuro/22/14/6106.full.pdf

Maturation and Death of Adult-Born Olfactory Bulb Granule Neurons: Role of Olfaction

In the mammalian forebrain, most neurons originate from proliferating cells in the ventricular zone lining the lateral ventricles, including a discrete area of the subventricular zone (SVZ). In this region, neurogenesis continues into adulthood. Most of the cells generated in the SVZ are neuronal precursors with progeny that migrate rostrally along a pathway known as the rostral migratory stream before they reach the main olfactory bulb (MOB) where they differentiate into local interneurons. The olfactory system thus provides an attractive model to investigate neuronal production and survival, processes involving interplay between genetic and epigenetic influences. The present study was conducted to investigate whether exposure to an odor-enriched environment affects neurogenesis and learning in adult mice. Animals housed in either a standard or an odor-enriched environment for 40 d were injected intraperitoneally with bromodeoxyuridine (BrdU) to detect proliferation among progenitor cells and to follow their survival in the MOB. The number of BrdU-labeled neurons was not altered 4 hr after a single BrdU injection. In contrast, the number of surviving progenitors 3 weeks after BrdU injection was markedly increased in animals housed in an enriched environment. This effect was specific because enriched odor exposure did not influence hippocampal neurogenesis. Finally, we showed that adult mice housed in odor-enriched cages display improved olfactory memory without a change in spatial learning performance. By maintaining a constitutive turnover of granule cells subjected to modulation by environmental cues, ongoing bulbar neurogenesis could be associated with improved olfactory memory.

https://www.jneurosci.org/content/jneuro/22/7/2679.full.pdf

Enriched Odor Exposure Increases the Number of Newborn Neurons in the Adult Olfactory Bulb and Improves Odor Memory

Brain plasticity refers to the brain's ability to change structure and function. Experience is a major stimulant of brain plasticity in animal species as diverse as insects and humans. It is now clear that experience produces multiple, dissociable changes in the brain including increases in dendritic length, increases (or decreases) in spine density, synapse formation, increased glial activity, and altered metabolic activity. These anatomical changes are correlated with behavioral differences between subjects with and without the changes. Experience-dependent changes in neurons are affected by various factors including aging, gonadal hormones, trophic factors, stress, and brain pathology. We discuss the important role that changes in dendritic arborization play in brain plasticity and behavior, and we consider these changes in the context of changing intrinsic circuitry of the cortex in processes such as learning.

/pdf/brain-plasticity-and-behavior-3512cjh0ly.pdf

Brain plasticity and behavior.

In adult rodents, neurons are continually generated in the subventricular zone of the forebrain, from where they migrate tangentially toward the olfactory bulb, the only known target for these neuronal precursors. Within the main olfactory bulb, they ascend radially into the granule and periglomerular cell layers, where they differentiate mainly into local interneurons. The functional consequences of this permanent generation and integration of new neurons into existing circuits are unknown. To address this question, we used neural cell adhesion molecule-deficient mice that have documented deficits in the migration of olfactory-bulb neuron precursors, leading to about 40% size reduction of this structure. Our anatomical study reveals that this reduction is restricted to the granule cell layer, a structure that contains exclusively γ-aminobutyric acid (GABA)ergic interneurons. Furthermore, mutant mice were subjected to experiments designed to examine the behavioral consequences of such anatomical alteration. We found that the specific reduction in the newly generated interneuron population resulted in an impairment of discrimination between odors. In contrast, both the detection thresholds for odors and short-term olfactory memory were unaltered, demonstrating that a critical number of bulbar granule cells is crucial only for odor discrimination but not for general olfactory functions.

https://www.pnas.org/content/pnas/97/4/1823.full.pdf

Importance of newly generated neurons in the adult olfactory bulb for odor discrimination

Enriched neonatal odor exposure leads to increased numbers of olfactory bulb mitral and granule cells

Neuromorphological changes in mouse olfactory bulb after neonatal exposure to phenobarbital

Early postnatal development of the rat accessory olfactory bulb

Lead-exposed neonatal rats are frequently used as a model for plumbism in children. In most studies,PPb is administered to the dam, and it is assumed that the pups are exposed to Pb primarily from the dam's milk. Rat pups, however, are coprophagic and begin to consume the maternal feces in their second postnatal week. This experiment was designed to determine whether the maternal feces are a significant source of Pb in pups exposed via the lactating dam. Dams were administered Pb as lead acetate (PbAc), either through their drinking water (500 ppm PbAc) or through twice daily intubations (3 mg PbAc/Kg body wt) from postpartum d 1 (P1) to P21 (P0=day of birth). Control dams were administered deionized water. The dams were housed with their litters in stainless-steel hanging cages with wire-screened bottoms. Litters of exposed and control dams treated through their drinking water had access to either Pb-containing or Pb-free maternal fecal matter for 2 h/d during the late lactation period. Half of the litters from intubated dams had continuous access to maternal feces throughout the lactation period, whereas access was curtailed at P14 in the other litters. Lead content of the feces from Pb-exposed dams ranged from 1000 to 5000 μg Pb/g wet wt. At P21, Pb concentrations were 2–4 times higher in blood, brain, bone, and liver of pups that had access to Pb-contaminated feces than in pups that were exposed to Pb primarily through the mother's milk. When estimating exposure levels in pups receiving Pb through the lactating dam, coprophagy and the high content of Pb in the dam's feces must be taken into consideration.

Linda Rosselli-Austin

Papers

Enriched neonatal odor exposure leads to increased numbers of olfactory bulb mitral and granule cells

Neuromorphological changes in mouse olfactory bulb after neonatal exposure to phenobarbital

Early postnatal development of the rat accessory olfactory bulb

Lead-exposure of neonatal rats through maternal milk : A confounded model.