Seizure-induced structural and functional changes in the rat hippocampal formation: Comparison between brief seizures and status epilepticus

Cardoso, Armando; Lukoyanova, Elena A.; Madeira, M. Dulce; Lukoyanov, Nikolay

doi:10.1016/j.bbr.2011.07.057

Cited by 35 publications

(41 citation statements)

References 78 publications

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“…Similar findings were also obtained in animals that had chemically-induced status epilepticus (Gröticke et al 2008, Furtado et al 2010, Aniol et al 2013, Schultz et al 2014, Rojas et al 2016 or brief seizures after treatment with electroshock kindled seizures (Cavazos et al 1994, Bengzon et al 1997, Cardoso et al 2011. Consistent with these results, it has been shown that recurrent seizures in patients with epilepsy are associated with progressive atrophic changes in some brain regions (Bernhardt et al 2009) which are suggested to cause behavioral alterations and impaired cognitive performance (Jokeit andEbner 2002, Vingerhoets 2006).…”

Section: Introductionmentioning

confidence: 53%

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Antimuscarinic-induced convulsions in fasted mice after food intake: no evidence of spontaneous seizures, behavioral changes or neuronal damage

Enginar¹,

Nurten²,

Türkmen³

et al. 2017

Acta Neurobiologiae Experimentalis

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Prolonged or repeated seizures have been shown to cause spontaneous recurrent seizures, increased anxiety-related behavior, locomotor hyperactivity, impaired functions of learning and memory, and neuronal damage in the hippocampus and other brain regions in animals. Mice and rats treated with antimuscarinic drugs after fasting for two days or less develop convulsions after being allowed to eat ad libitum. To address whether such behavioral and neuroanatomic changes occur following these convulsions, mice treated i.p. with saline (control) or 2.4 mg/kg atropine and given food after 24 h of fasting were grouped according to seizure scores for behavioral and histological analysis. Following convulsions, the occurrence of spontaneous recurrent seizures was observed for 30 days. Motor activity and grooming behavior were assessed in the open field, and memory was assessed using the novel object recognition test 4 and 7 days after onset of convulsions, respectively. Animals allocated for the histological analysis were decapitated 7 days after onset of convulsions and hippocampal slices were evaluated for the percentage of degenerating neurons stained with Fluoro-Jade C. Spontaneous recurrent seizures, locomotor alterations, anxiety-related behavior, memory impairment, and neuronal loss in the granular layer of the dentate gyrus were not detected in the animals with seizure score 1-2 or 3-5. These results are in accordance with those related to the absence of behavioral changes, cognitive deficits, and hippocampal neuronal damage after single brief seizures in animals and patients with epilepsy.

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Section: Introductionmentioning

confidence: 53%

“…Accordingly, various learning and memory tests showed seizure-induced memory impairments in animals (Szyndler et al 2006, Akula et al 2007, Müller et al 2009a, 2009b, Cardoso et al 2011. The novel object recognition test was used to assess memory performance in the present study.…”

Section: Discussionmentioning

confidence: 88%

Antimuscarinic-induced convulsions in fasted mice after food intake: no evidence of spontaneous seizures, behavioral changes or neuronal damage

Enginar¹,

Nurten²,

Türkmen³

et al. 2017

Acta Neurobiologiae Experimentalis

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“…Indeed, it has been shown that aging is associated with a reduction of the GABAergic subpopulations that express neuropeptide Y (NPY) and somatostatin (SS) in several brain areas such as the hypothalamus, striatum, and cortical regions (Kowalski et al 1992;Cha et al 1996;Zhang et al 1998;Cadacio et al 2003;Cardoso et al 2006;Stanley et al 2012;Spiegel et al 2013). One of those cortical regions is the hippocampal formation (HF), a limbic area involved in several cognitive functions, including spatial learning and memory (Morris 1984;Eichenbaum 1999;Aggleton and Brown 2006;Cardoso et al 2011). In fact, the interneurons of the HF expressing NPY and SS represent one of the neuronal populations most affected by aging (Cadacio et al 2003;Vela et al 2003;Patrylo et al 2007).…”

Section: Introductionmentioning

confidence: 99%

“…In other words, we aimed to verify if caloric restriction started at this advanced age presents at least some of the numerous benefits observed in younger rats (Andrade et al 2002;Rich et al 2010;Roth and Polotsky 2012;Cardoso et al 2013). We centered this study of old-onset caloric restriction in the HF because it is one of the brain regions most affected by nutritional deficits (Cintra et al 1990;Hipólito-Reis et al 2013) and aging (Cadacio et al 2003;Stanley et al 2012), added to its importance in cognitive functions (Morris 1984;Eichenbaum 1999;Aggleton and Brown 2006;Cardoso et al 2011). …”

Section: Introductionmentioning

confidence: 99%

Old-onset caloric restriction effects on neuropeptide Y- and somatostatin-containing neurons and on cholinergic varicosities in the rat hippocampal formation

Cardoso

Silva

Magano

et al. 2014

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Caloric restriction is able to delay age-related neurodegenerative diseases and cognitive impairment. In this study, we analyzed the effects of old-onset caloric restriction that started at 18 months of age, in the number of neuropeptide Y (NPY)-and somatostatin (SS)-containing neurons of the hippocampal formation. Knowing that these neuropeptidergic systems seem to be dependent of the cholinergic system, we also analyzed the number of cholinergic varicosities. Animals with 6 months of age (adult controls) and with 18 months of age were used. The animals aged 18 months were randomly assigned to controls or to caloric-restricted groups. Adult and old control rats were maintained in the ad libitum regimen during 6 months. Caloric-restricted rats were fed, during 6 months, with 60 % of the amount of food consumed by controls. We found that aging induced a reduction of the total number of NPY-and SS-positive neurons in the hippocampal formation accompanied by a decrease of the cholinergic varicosities. Conversely, the 24-month-oldonset caloric-restricted animals maintained the number of those peptidergic neurons and the density of the cholinergic varicosities similar to the 12-month control rats. These results suggest that the aging-associated reduction of these neuropeptide-expressing neurons is not due to neuronal loss and may be dependent of the cholinergic system. More importantly, caloric restriction has beneficial effects in the NPY-and SS-expressing neurons and in the cholinergic system, even when applied in old age.

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“…Additionally, the interval of 10 days between end of treatment and cognitive assessment may have led to early post treatment differences between UBP and BP groups no longer being apparent, reflecting recovery of hippocampal cognitive function over time following ECS as occurs in patients treated with ECT (Semkovska et al, 2011;Semkovska and McLoughlin, 2010). Interestingly, some recent studies attempting to cause neuronal loss using ECS have found that repeated brief seizures can cause specific neuronal death within hippocampal structures under certain conditions (Cardoso et al, 2011). However, these same studies also report that cell loss does not occur when ECS is administered on a 24-48 hour schedule (Cardoso et al, 2008).…”

mentioning

confidence: 99%

A comparison of brief pulse and ultrabrief pulse electroconvulsive stimulation on rodent brain and behaviour

O’Donovan

Kennedy

Guinan

et al. 2012

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Brief pulse electroconvulsive therapy (BP ECT; pulse width 0.5-1.5 msec) is a very effective treatment for severe depression but is associated with cognitive side-effects. It has been proposed that ultrabrief pulse (UBP; pulse width 0.25-0.30 msec) ECT may be as effective as BP ECT but have less cognitive effects because it is a more physiological form of neuronal stimulation. To investigate this further, we treated normal rats with a 10 session course of either BP (0.5 msec), UBP (0.3 msec), or sham electroconvulsive stimulation (ECS) and measured antidepressant-related changes in dentate gyrus cell proliferation and hippocampal BDNF protein levels as well as hippocampal-dependant spatial reference memory using the water plus maze and immobility time on the forced swim test. Both BP and UBP ECS induced very similar types of motor seizures. However, BP ECS but not UBP ECS treatment led to a significant, near 3-fold, increase in cell proliferation (p=0.026) and BDNF levels (p=0.01). In the forced swim test, only BP ECS treated animals had a significantly lower immobility time (p=0.046). There was a trend for similarly reduced hippocampal-dependent memory function in both BP and UBP groups but overall there was not a significant difference between treatment and control animals when tested 10 days after completing allocated treatment. These findings show that, even though both forms of ECS elicited similar motor seizures, UBP ECS was less efficient than BP ECS in inducing antidepressant-related molecular, cellular and behavioural changes.

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Seizure-induced structural and functional changes in the rat hippocampal formation: Comparison between brief seizures and status epilepticus

Cited by 35 publications

References 78 publications

Antimuscarinic-induced convulsions in fasted mice after food intake: no evidence of spontaneous seizures, behavioral changes or neuronal damage

Antimuscarinic-induced convulsions in fasted mice after food intake: no evidence of spontaneous seizures, behavioral changes or neuronal damage

Old-onset caloric restriction effects on neuropeptide Y- and somatostatin-containing neurons and on cholinergic varicosities in the rat hippocampal formation

A comparison of brief pulse and ultrabrief pulse electroconvulsive stimulation on rodent brain and behaviour

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