Footshock stress alters early postnatal development of electrophysiological responses and caspase-3 activity in rat hippocampus

Kudryashov, I. E.; Yakovlev, A. A.; Kudryashova, I. V.; Gulyaeva, N. V.

doi:10.1016/s0304-3940(02)00937-0

Cited by 16 publications

(6 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several recent reports support a possible role of caspase‐3 in neuroplasticity of mammals (Mattson & Duan, 1999; Mattson, 2000; Kudryashov et al. , 2001, 2002; Shimohama et al.…”

Section: Discussionmentioning

confidence: 82%

Caspase‐like activity is essential for long‐term synaptic plasticity in the terrestrial snail Helix

Bravarenko

Онуфриев

Stepanichev

et al. 2006

Eur J of Neuroscience

View full text Add to dashboard Cite

Although caspase activity in the nervous system of mollusks has not been described before, we suggested that these cysteine proteases might be involved in the phenomena of neuroplasticity in mollusks. We directly measured caspase-3 (DEVDase) activity in the Helix lucorum central nervous system (CNS) using a fluorometrical approach and showed that the caspase-3-like immunoreactivity is present in the central neurons of Helix. Western blots revealed the presence of caspase-3-immunoreactive proteins with a molecular mass of 29 kDa. Staurosporin application, routinely used to induce apoptosis in mammalian neurons through the activating cleavage of caspase-3, did not result in the appearance of a smaller subunit corresponding to the active caspase in the snail. However, it did increase the enzyme activity in the snail CNS. This suggests differences in the regulation of caspase-3 activity in mammals and snails. In the snail CNS, the caspase homolog seems to possess an active center without activating cleavage typical for mammals. In electrophysiological experiments with identified snail neurons, selective blockade of the caspase-3 with the irreversible and cell-permeable inhibitor of caspase-3 N-benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp-(OMe)-fluoro-methylketone prevented development of the long-term stage of synaptic input sensitization, suggesting that caspase is necessary for normal synaptic plasticity in snails. The results of our study give the first direct evidence that the caspase-3-like activity is essential for long-term plasticity in the invertebrate neurons. This activity is presumably involved in removing inhibitory constraints on the storage of long-term memory.

show abstract

“…Several recent reports support a possible role of caspase‐3 in neuroplasticity of mammals (Mattson & Duan, 1999; Mattson, 2000; Kudryashov et al. , 2001, 2002; Shimohama et al.…”

Section: Discussionmentioning

confidence: 82%

Caspase‐like activity is essential for long‐term synaptic plasticity in the terrestrial snail Helix

Bravarenko

Онуфриев

Stepanichev

et al. 2006

Eur J of Neuroscience

View full text Add to dashboard Cite

show abstract

“…Several recent reports support a possible role of caspase‐3 in neuroplasticity (Mattson et al, 1998; Chan et al, 1999; Chan and Mattson, 1999; Mattson and Duan, 1999; Glazner et al, 2000; Mattson, 2000; Kudryashov et al, 2001, 2002; Shimohama et al, 2001a, b; Yan et al, 2001; Gilman and Mattson, 2002; Lu et al, 2002). The results of our study are in accordance with the above‐mentioned work, and give the first direct evidence that caspase‐3 activity is essential for LTP in hippocampal CA1.…”

Section: Discussionmentioning

confidence: 90%

“…Thus, active caspase‐3 may play a role in cellular processes such as neuronal differentiation, migration, and plasticity. Recently, we have demonstrated that in early postnatal ontogenesis, a transient decline in CA1 population spike amplitude in the rat hippocampal slices coincides with caspase‐3 activation during a period not related to an increase in apoptosis, suggesting involvement of caspase‐3 in synaptic plasticity (Kudryashov et al, 2001, 2002).…”

mentioning

confidence: 99%

Caspase activity is essential for long‐term potentiation

Gulyaeva

Kudryashov

Kudryashova

2003

J of Neuroscience Research

View full text Add to dashboard Cite

Slices from rat hippocampus were incubated with the caspase-3 inhibitor N-benzyloxycarbonyl-Asp-Glu-Val-Asp fluoromethylketone (Z-DEVD-FMK) or with the inactive peptide N-benzyloxycarbonyl-Phe-Ala fluoromethylketone (Z-Phe-Ala-FMK) for 30 min. The peptides changed neither input-output curves nor paired-pulse effects at 70-msec interpulse intervals, nor amplitudes of pop spikes in the CA1 region 1.0-6.9 hr after the incubation. Slices taken 1.0-1.4 hr after Z-DEVD-FMK or inactive peptide treatment demonstrated similar long-term potentiation (LTP) curves; however, LTP was suppressed significantly (P<0.001) 1.5-3.4 hr after Z-DEVD-FMK treatment when compared to the corresponding inactive peptide group. LTP magnitude correlated with time after Z-DEVD-FMK (r= -0.74; P<0.02) but did not depend on time after the inactive peptide treatment. After 3.5 hr, LTP was blocked completely. Z-DEVD-FMK did not have a significant effect on presynaptic function. The results are the first evidence that inhibition of caspase-3 significantly decreases or fully blocks LTP in the CA1 region and suggest that caspase-3 is essential for LTP. Candidate caspase-3 substrates that may be cleaved for LTP induction and maintenance are discussed.

show abstract

“…Thus, mechanisms of apoptosis without caspase-3 activation have been observed [14]. Caspase activation in turn does not always lead to apoptosis, but may be involved in the mech anisms of neuroplasticity [3,4,20,[26][27][28]. Data obtained by Mattson et aL [32,33] indicate that the enzymes of the apoptotic cascade may alter signaling associated with synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

Electroconvulsive Shock Induces Neuron Death in the Mouse Hippocampus: Correlation of Neurodegeneration with Convulsive Activity

Zarubenko

Yakovlev

Stepanichev

et al. 2005

Neurosci Behav Physiol

View full text Add to dashboard Cite

The relationship between convulsive activity evoked by repeated electric shocks and structural changes in the hippocampus of Balb/C mice was studied. Brains were fixed two and seven days after the completion of electric shocks, and sections were stained by the Nissl method and immunohistochemically for apop totic nuclei (the TUNEL method). In addition, the activity of caspase-3, the key enzyme of apoptosis, was measured in brain areas immediately after completion of electric shoeks. The number of neurons decreased significantly in fIeld CAl and the dentate fascia, but not in hippocampal field CA3. The num bers of cells in CAl and CA3 were inversely coudated with the intensity of convulsions. Signs of apop totic neuron death were not seen, while caspase-3 activity was significantly decreased in the hippocampus after electric shocks. These data support the notion that functional changes affect neurons after electric shock and deepen our understanding of this view, providing direct evidence that there are moderate (up to 10%) but significant levels of neuron death in defined areas of the hippocampus. Inverse correlations of the numbers of cells with the extent of eonvulsive activity suggest that the main cause of neuron death is convulsions evoked by electric shocks.

show abstract

Footshock stress alters early postnatal development of electrophysiological responses and caspase-3 activity in rat hippocampus

Cited by 16 publications

References 21 publications

Caspase‐like activity is essential for long‐term synaptic plasticity in the terrestrial snail Helix

Caspase‐like activity is essential for long‐term synaptic plasticity in the terrestrial snail Helix

Caspase activity is essential for long‐term potentiation

Electroconvulsive Shock Induces Neuron Death in the Mouse Hippocampus: Correlation of Neurodegeneration with Convulsive Activity

Contact Info

Product

Resources

About