• Journal of Korean Biological Nursing Science
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• v.24 no.2
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• pp.77-85
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• 2022

Purpose: Aging process comes with cognitive impairment due to decreased neuronal cell number, activity, and neuronal circuit. Alteration of inhibitory neurons contributes to cognitive impairment in normal aging and is responsible for disrupting the excitation/inhibition balance by reducing the synthesis of gamma-aminobutyric acid (GABA). Morus nigra (Mulberry) is a natural physiologically active substance that has been proven to have anti-oxidant, anti-diabetic, and anti-inflammatory effects through many studies. This study aimed to evaluate the effects of the mulberry extract (ME) on cognitive function through anti-oxidant enzyme and GABAergic neuronal activity in aged rat brain. Methods: Sprague Dawley rats were randomly assigned as the young group (8 weeks, n= 8), aging group (67 weeks, n= 8), and aging+ mulberry extract group (67 weeks, n= 8). The aging+ mulberry extract group was orally administered 500 mg/kg/d mulberry extract for 6 weeks. Results: The aging+ mulberry extract group improved spatial and short-term memory. The antioxidant potential of ME increased the expression of superoxide dismutase-1 (SOD-1) and decreased inducible nitric oxide synthase (iNOS). Also, the aging+ mulberry extract group significantly increased the expression of GABAergic interneuron in hippocampus cornu ammonis1 (CA1) compared to the aging group. Conclusion: The number of GABAergic inhibitory interneurons was deceased and memory functions in the aging process, but those symptoms were improved and restored by mulberry extract administration.

• Journal of Life Science
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• v.16 no.5
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• pp.750-758
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• 2006

Calcium-binding protein calretinin is thought to play important roles in calcium buffering. Recently, we reported on the distribution, morphology of calretinin-immunoreactive (IR) neurons and the effects of eye enucleation on the immunoreactivity of calretinin in the superficial layers of the hamster superior colliculus (SC). In the present study, we describe the distributions and types of labeled cells and effects of enucleation in the deeper layers by immunocytochemistry. We also compare this labeling to that of GABA, the major inhibitory neurotransmitter in the central nervous system. In contrast to the superficial layers, the deeper layers contained many calretinin-IR neurons which formed two tiers. The first tier, which was very distinctive, was found within the intermediate gray layer. The second tier was found in the deep gray layer. Labeled neurons varied dramatically in morphology and included vertical fusiform, stellate, round/oval, and horizontal neurons. In contrast to the superficial layers, enucleation appeared to have no effect on the distribution of calretinin immunoreactivity in the deeper layers. Two-color immunofluorescence revealed that none of calretinin-IR neurons were labeled with an antibody to GABA. The present results demonstrate that calretinin identifies unique neuronal sublaminar organizations in the hamster SC. The present results also demonstrate that none of the calretinin-IR neurons in the hamster SC is GABAergic interneurons. As many calretinin-IR cells are GABAergic interneurons in most other brain areas, this phenomenon in hamster SC is exceptional.

• Journal of the korean academy of Pediatric Dentistry
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• v.27 no.1
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• pp.7-14
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• 2000

Inhibitory cells are critically involved in shaping normal hippocampal function and are thought to be important elements in the development of hippocampal pathologies. The present study was carried out in hippocampal CA1 area in vivo to compare with hippocampal slice studies. Intracellular and extracellular recordings with or without bicuculline electrodes were obtained in the intact brain of anesthetized rats, and cells were intracellularty labelled with neurobiotin. Electrical stimulation of fimbria-fornix resulted in an initial short-latency population spike. In the presence of $10{\mu}M$ bicuculline, orthodromic stimulation resulted in bursts of population spikes. The amplitude of population spikes in the CA1 region increased with stimulus intensity, as did the number of population spikes when the field recording electrode contained $10{\mu}M$ bicuculline. We measured the level of excitability in the CA1 area, using a paired-pulse stimulus paradigm to evoke population spikes. Population spikes showed strong paired-pulse inhibition at short interstimulus intervals. Burst afterdischarges up to 400 ms were observed after paired-pulse stimulus. These result suggest that hippocampal CA1 inhibitory interneurons can affect the excitability of pyramidal neurons that can not be appreciated in conventional in vitro preparation.

• Applied Microscopy
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• v.41 no.4
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• pp.235-248
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• 2011

Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adults and is a major risk factor for the development of posttraumatic epilepsy (PTE). Recent studies have provided significant insight into the pathophysiological mechanisms underlying the development of epilepsy. Although the link between brain trauma and epilepsy is well recognized, the complex biological mechanisms that result in PTE following TBI have not been fully elucidated. Therefore, this study investigated in order to identify whether or not the abnormal expression of calcium-binding proteins in the lesioned hippocampus plays a role in neuronal damage by brain trauma and whether or not the expressions may change in the contralateral hippocampus during the adaptive stage as early time point following TBI. During early time point following TBI, both parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities were decreased with in the lesioned hippocampus. However, these expressions were recovered to control levels as depend on time courses. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced as compared to the control levels, whereas CB expression was unchanged. These findings indicate that the alterations of the calcium-binding proteins, especially PV and CB, may contribute to the neuronal death and/or damage induced by abnormal inhibitory neurotransmission at early time period following brain trauma and the development of epileptogenesis in patients with traumatic brain injury.