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Abstract
Prenatal stress (PS) has long-term sequelae for the morphological and functional status of the central nervous system of the progeny. A PS-induced proinflammatory status of the organism may result in an impairment of both hippocampal synaptic plasticity and hippocampus-dependent memory formation in adults. We addressed here the question of how PS-induced alterations in the immune response in young and old mice may contribute to changes in hippocampal function in aging. Immune stimulation (via LPS injection) significantly affected the ability of the hippocampal CA3-CA1 synapse of PS mice to undergo long-term potentiation (LTP). Elevated corticosterone level in the blood of aged PS mice that is known to influence LTP magnitude indicates a chronic activation of the HPA axis due to the in utero stress exposure. We investigated the contribution of adrenergic receptors to the modulation of hippocampal synaptic plasticity of aged mice and found that impaired LTP in the PS-LPS group was indeed rescued by application of isoproterenol (a nonspecific noradrenergic agonist). Further exploration of the mechanisms of the observed phenomena will add to our understanding of the interaction between PS and proinflammatory immune activation and its contribution to the functional and structural integrity of the aging brain.
Highlights
In recent years it became evident that early-life adversities have a strong impact on the development of different organ systems, including the nervous and the immune systems [1,2,3,4,5,6,7]
It has been shown that prenatal stress (PS) of different intensities, experienced in a certain time window, might have long-term sequelae for the morphological and functional status of the central nervous system (CNS) of the offspring [8,9,10]
We examined the processes of synaptic plasticity of CA3-CA1 synapse in the hippocampus by recording evoked field excitatory postsynaptic potentials from the stratum radiatum of acute hippocampal slices taken from one-year-old mice
Summary
In recent years it became evident that early-life adversities have a strong impact on the development of different organ systems, including the nervous and the immune systems [1,2,3,4,5,6,7]. There is a tight correlation between significant alterations in brain morphology [11,12,13] and impaired synaptic plasticity in the hippocampus and frontal cortex of the PS prepubertal as well as adult animals [14,15,16,17,18,19]. One of the important neuromodulators that is involved in mediating age-dependent changes in synaptic plasticity and is associated with the stress response is norepinephrine (NE) [27,28,29,30,31,32,33,34]. We observed differential modulation of LTP mediated by activation of β1-adrenergic receptors in the hippocampus of young PS rats [35, 36]
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