TY - JOUR
T1 - Age-related learning deficits can be reversible in honeybees Apis mellifera
AU - Baker, Nicholas
AU - Wolschin, Florian
AU - Amdam, Gro
N1 - Funding Information:
We thank R. Scheiner, B Smith and W Tyler for discussions, C Koehler, L Mandarino, B Thiede and Z Yi for technical resources and support, and B Rascón, C Burden and D Münch for comments on the manuscript. This work was supported by the Alexander-von-Humboldt Foundation (to FW), and the PEW Charitable Trust , the Norwegian Research Council ( 180504 , 185306 , 191699 ) and the National Institute on Aging ( PO1AG22500 , to GVA).
PY - 2012/10
Y1 - 2012/10
N2 - Many animals are characterized by declining brain function at advanced ages, including honeybees (Apis mellifera). Variation in honeybee social development, moreover, results in individual differences in the progression of aging that may be accelerated, delayed, and sometimes reversed by changes in behavior. Here, we combine manipulations of social development with a measurement of sensory sensitivity, Pavlovian (associative) learning, and a proteomic technique to study the brain of aged honeybees. First, we confirm that sensory sensitivity can remain intact during aging, and that age-associated learning deficits are specific to bees that forage, a behavior typically expressed after a period of nursing activity. These initial data go beyond previous findings by showing how foragers age in social groups of different age compositions and sizes. Thereafter, we establish that learning ability can recover in aged foragers that revert to nursing tasks. Finally, we use liquid chromatography coupled to tandem mass spectrometry (LC-MS2) to describe proteomic differences between central brains, from reverted former foragers that varied in recovery of learning performance, and from nurse bees that varied in learning ability but never foraged. We find that recovery is positively associated with levels of stress response/cellular maintenance proteins in the central brain, while variation in learning before aging is negatively associated with the amounts of metabolic enzymes in the brain tissue. Our work provides the strongest evidence, thus far, for reversibility of learning deficits in aged honeybees, and indicates that recovery-related brain plasticity is connected to cellular stress resilience, maintenance and repair processes.
AB - Many animals are characterized by declining brain function at advanced ages, including honeybees (Apis mellifera). Variation in honeybee social development, moreover, results in individual differences in the progression of aging that may be accelerated, delayed, and sometimes reversed by changes in behavior. Here, we combine manipulations of social development with a measurement of sensory sensitivity, Pavlovian (associative) learning, and a proteomic technique to study the brain of aged honeybees. First, we confirm that sensory sensitivity can remain intact during aging, and that age-associated learning deficits are specific to bees that forage, a behavior typically expressed after a period of nursing activity. These initial data go beyond previous findings by showing how foragers age in social groups of different age compositions and sizes. Thereafter, we establish that learning ability can recover in aged foragers that revert to nursing tasks. Finally, we use liquid chromatography coupled to tandem mass spectrometry (LC-MS2) to describe proteomic differences between central brains, from reverted former foragers that varied in recovery of learning performance, and from nurse bees that varied in learning ability but never foraged. We find that recovery is positively associated with levels of stress response/cellular maintenance proteins in the central brain, while variation in learning before aging is negatively associated with the amounts of metabolic enzymes in the brain tissue. Our work provides the strongest evidence, thus far, for reversibility of learning deficits in aged honeybees, and indicates that recovery-related brain plasticity is connected to cellular stress resilience, maintenance and repair processes.
KW - Brain senescence
KW - Cytochrome P450
KW - Heat shock protein 8
KW - LC-MS proteomics
KW - Pavlovian learning
KW - Peroxiredoxin
KW - Recovery-related plasticity
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U2 - 10.1016/j.exger.2012.05.011
DO - 10.1016/j.exger.2012.05.011
M3 - Article
C2 - 22626973
AN - SCOPUS:84865764277
SN - 0531-5565
VL - 47
SP - 764
EP - 772
JO - Experimental Gerontology
JF - Experimental Gerontology
IS - 10
ER -