Age-related changes in the function of somatic membrane potassium channels of neurons in the mollusc Lymnaea stagnalis

Frolkis, V.V.; Martynenko, O. A.; Timchenko, A.N.

doi:10.1016/0047-6374(89)90006-7

Cited by 13 publications

(4 citation statements)

References 5 publications

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“…Indeed, there is empirical evidence that several active channel conductances are altered with aging in L3 monkey LPFC neurons, including the Ca 2+ -dependent current that underlies the slow afterhyperpolarization, sI AHP (Luebke and Amatrudo 2012), as well as HCN and KCNQ channels (Wang et al 2011). In other brain areas, age-related reductions in a K + conductance (Niesen et al 1988) and delayed rectifier K + current (Frolkis et al 1989), increased calcium influx and amplitude of calcium-dependent sAHPs (for review: (Faber and Sah 2003; Foster 2007; Thibault et al 2007)) and density of high-voltage activated L-type Ca 2+ channels (Thibault and Landfield 1996; Porter et al 1997; Blalock et al 1999; Thibault et al 2001; Oh et al 2013) have all been described. The relationship between age-related changes in excitatory and inhibitory synaptic responses and firing rates also need further investigation: the present study showed that synaptic responses likely attenuate less in aged neurons, but a previous study established that the frequency of spontaneous EPSCs is reduced in these neurons with aging but the frequency of spontaneous inhibitory EPSCs is increased (Luebke et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Functional consequences of age-related morphologic changes to pyramidal neurons of the rhesus monkey prefrontal cortex

et al. 2014

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Layer 3 (L3) pyramidal neurons in the lateral prefrontal cortex (LPFC) of rhesus monkeys exhibit dendritic regression, spine loss and increased action potential (AP) firing rates during normal aging. The relationship between these structural and functional alterations, if any, is unknown. To address this issue, morphological and electrophysiological properties of L3 LPFC pyramidal neurons from young and aged rhesus monkeys were characterized using in vitro whole-cell patch-clamp recordings and high-resolution digital reconstruction of neurons. Consistent with our previous studies, aged neurons exhibited significantly reduced dendritic arbor length and spine density, as well as increased input resistance and firing rates. Computational models using the digital reconstructions with Hodgkin-Huxley and AMPA channels allowed us to assess relationships between demonstrated age-related changes and to predict physiological changes that have not yet been tested empirically. For example, the models predict that in both backpropagating APs and excitatory postsynaptic currents (EPSCs), attenuation is lower in aged versus young neurons. Importantly, when identical densities of passive parameters and voltage- and calcium-gated conductances were used in young and aged model neurons, neither input resistance nor firing rates differed between the two age groups. Tuning passive parameters for each model predicted significantly higher membrane resistance (Rm) in aged versus young neurons. This Rm increase alone did not account for increased firing rates in aged models, but coupling these Rm values with subtle differences in morphology and membrane capacitance did. The predicted differences in passive parameters (or parameters with similar effects) are mathematically plausible, but must be tested empirically.

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Section: Discussionmentioning

confidence: 99%

Functional consequences of age-related morphologic changes to pyramidal neurons of the rhesus monkey prefrontal cortex

et al. 2014

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“…For example, Frolkis et al (1991 , 1995 ) reported increased voltage-gated Ca 2+ current densities and changes in other aspects of intrinsic electrical excitability in aged Lymnaea neurons. The same group reported changes in voltage-gated K + currents amplitudes and inactivation kinetics in old Lymnaea neurons ( Frolkis et al, 1989 ). Patel et al (2006) reported a decline in intrinsic excitability associated with a decline in input resistance and an increase in AHP magnitude and duration in CGGs of older Lymnaea and Klaassen et al (1998) observed a decline in excitability associated with a reduction in input resistance in aging RPeD1.…”

Section: Evidence For Age-associated Alterations In Intrinsic Electrimentioning

confidence: 94%

“…Lymnaea ’s application in aging studies dates back to the 1980s with the publication of several neurophysiological studies ( Frolkis et al, 1984 ; Nagy et al, 1985 ; Janse et al, 1986 ), the first report of age effects on associative memory performance ( Audesirk et al, 1982 ) and work on the general biology and population-level aspects of the species’ aging process ( Janse et al, 1988 ; Slob and Janse, 1988 ). Since then publications on various cell biological, endocrinological, neurophysiological, biophysical, behavioral, and reproductive aspects of aging in Lymnaea have appeared ( Frolkis et al, 1989 , 1991 ; Janse et al, 1989 , 1999 ; Wildering et al, 1991 ; Klaassen et al, 1998 ; Janse and van der Roest, 2001 ; Arundell et al, 2006 ; Patel et al, 2006 , 2010 ). Its use in research of the molecular and cellular foundations of AMI started in earnest with Hermann et al (2007) followed by a series of other publications from our laboratory linking AMI and neuronal excitability changes to oxidative stress, inflammation, lipid peroxidation and declining glutathione (GSH) availability, and identifying PLA 2 as a central player in these phenomena ( Watson et al, 2012a , b , 2013 , 2014 ; Hermann et al, 2013 ; Beaulieu et al, 2014 ).…”

Section: The Need For Simplification: Lymnaea Stagnalis mentioning

confidence: 99%

Phospholipase A2 â€“ nexus of aging, oxidative stress, neuronal excitability, and functional decline of the aging nervous system? Insights from a snail model system of neuronal aging and age-associated memory impairment

2014

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The aging brain undergoes a range of changes varying from subtle structural and physiological changes causing only minor functional decline under healthy normal aging conditions, to severe cognitive or neurological impairment associated with extensive loss of neurons and circuits due to age-associated neurodegenerative disease conditions. Understanding how biological aging processes affect the brain and how they contribute to the onset and progress of age-associated neurodegenerative diseases is a core research goal in contemporary neuroscience. This review focuses on the idea that changes in intrinsic neuronal electrical excitability associated with (per)oxidation of membrane lipids and activation of phospholipase A2 (PLA2) enzymes are an important mechanism of learning and memory failure under normal aging conditions. Specifically, in the context of this special issue on the biology of cognitive aging we portray the opportunities offered by the identifiable neurons and behaviorally characterized neural circuits of the freshwater snail Lymnaea stagnalis in neuronal aging research and recapitulate recent insights indicating a key role of lipid peroxidation-induced PLA2 as instruments of aging, oxidative stress and inflammation in age-associated neuronal and memory impairment in this model system. The findings are discussed in view of accumulating evidence suggesting involvement of analogous mechanisms in the etiology of age-associated dysfunction and disease of the human and mammalian brain.

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“…Detailed studies on the parietal neurons in L. stagnalis by Frolkis and co-workers revealed decreases in maximal amplitude of fast and delayed outward potassium currents, in maximal potassium conductance, and in kinetics of inactivation of the delayed outward current, furthermore, increases in the amplitude of potential-dependent calcium channels (46,47). These findings indicate that during ageing essential neuron-specific changes occur in the electric properties of neurons (Table 2).…”

Section: Age-related Findings At the Level Of Single Neuronsmentioning

confidence: 92%

The Great Pond Snail (Lymnaea stagnalis) as a Model of Aging and Age-Related Memory Impairment: An Overview

Fodor

Svigruha

Kemenes

et al. 2021

The Journals of Gerontology: Series A

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With the increase of life span, normal ageing and age-related memory decline are affecting an increasing number of people; however, many aspects of these processes are still not fully understood. Although vertebrate models have provided considerable insights into the molecular and electrophysiological changes associated with brain ageing, invertebrates, including the widely recognised molluscan model organism, the great pond snail (Lymnaea stagnalis) have proven to be extremely useful for studying mechanisms of ageing at the level of identified individual neurons and well-defined circuits. It’s numerically simpler nervous system, well-characterized life cycle and relatively long lifespan make it an ideal organism to study age-related changes in the nervous system. Here, we provide an overview of age-related studies on L. stagnalis and showcase this species as a contemporary choice for modelling the molecular, cellular, circuit, and behavioural mechanisms of ageing and age-related memory impairment.

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Age-related changes in the function of somatic membrane potassium channels of neurons in the mollusc Lymnaea stagnalis

Cited by 13 publications

References 5 publications

Functional consequences of age-related morphologic changes to pyramidal neurons of the rhesus monkey prefrontal cortex

Functional consequences of age-related morphologic changes to pyramidal neurons of the rhesus monkey prefrontal cortex

Phospholipase A2 â€“ nexus of aging, oxidative stress, neuronal excitability, and functional decline of the aging nervous system? Insights from a snail model system of neuronal aging and age-associated memory impairment

The Great Pond Snail (Lymnaea stagnalis) as a Model of Aging and Age-Related Memory Impairment: An Overview

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