Neurotoxic Effects of Kainic Acid on Substantia Nigra Neurons in Rat Brain Slices

Johnson, Stephen M.; Luo, Xiang; Bywood, Petra Teresia

doi:10.1006/exnr.1997.6578

Cited by 8 publications

(4 citation statements)

References 37 publications

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“…Using both immunohistochemical techniques and electromicroscopy, we found that loss of the dendritic arbor in SN neurons is a sensitive index for detecting and measuring damage (Johnson and Bywood, 1998a;Johnson et al, 1997). Loss of dendrites as an early event in degeneration was also observed by others both in vitro (Kikuchi and Kim, 1993;Park et al, 1996) and in vivo (Irving et al, 1996;Matesic and Lin, 1994).…”

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confidence: 52%

“…In our own experiments, EAA-induced cell death was associated with chromatin clumping (Johnson et al, 1997), a characteristic of apoptosis. We have not yet examined other potential indicators of apoptosis, such as terminal transferase (TdT)-mediated deoxy-UTP-biotin nick-end labelling (TUNEL) histochemistry.…”

Section: Discussionmentioning

confidence: 97%

“…3E). These immunohistochemical changes reflect an increasing degree of severity of damage assessed using electromicroscopic or histological procedures (Johnson and Bywood, 1998b;Johnson et al, 1997). In contrast to SNd neurons, those of the All group showed only modest dendritic damage after treatment with 10~M NMDA (Fig.…”

Section: Effects Of Excitatory Amino Acidsmentioning

confidence: 97%

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Catecholamine neuron groups in rat brain slices differ in their susceptibility to excitatory amino acid induced dendritic degeneration

Bywood

Johnson

2001

neurotox res

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We investigated whether specific types of catecholamine neurons were differentially vulnerable to damage induced by excitatory amino acids (EAAs) in vitro in a rat brain slice preparation. Brain slices, 300 micro m thick, were cut horizontally, exposed to either N-methyl-D-aspartate (NMDA) or kainic acid (KA) for 2h, fixed and then cut into thin (30 micro m) sections in the same (horizontal) plane as the slice. The sections were immunolabelled for tyrosine hydroxylase to identify different groups of catecholamine neurons (substantia nigra (SN), paranigral (PN), interfascicular (IF) and hypothalamic A11, A13 and A14) which exhibited prominent dendritic projections in the horizontal plane. Loss of dendrites was used as a sensitive index of damage that precedes the loss of the cell body. Catecholamine neurons differed strikingly in their vulnerability of EAA-induced dendrite degeneration. The most vulnerable were those in the dorsal tier of the SN, whereas the most resistant were those in the hypothalamic A11 group. For example, in the dorsal tier of SN, NMDA (50 micro M) reduced the proportion of neurons with dendrites from 64% (+/- 8% SEM) in controls to 13% (+/- 7%) whereas the majority of A11 neurons (69 +/- 10%) retained their dendrites compared to controls (89% +/- 8%). The other groups of catecholamine neurons exhibited intermediate vulnerability. An essentially similar pattern of differential vulnerability was observed with KA. An understanding of the cellular mechanisms that underlie the particular vulnerability of SN neurons in the slice will aid the discovery of pharmacological therapies to prevent or slow the pathological process in neurodegenerative diseases which involve these neurons.

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confidence: 52%

Section: Discussionmentioning

confidence: 97%

Section: Effects Of Excitatory Amino Acidsmentioning

confidence: 97%

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Catecholamine neuron groups in rat brain slices differ in their susceptibility to excitatory amino acid induced dendritic degeneration

Bywood

Johnson

2001

neurotox res

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“…Morphological changes were detected, including disrupted dendritic arbor development and truncated dendrites after KA incubation. These are early indicators of neurodegeneration, demonstrating that neurons had begun to lose dendrites, cell bodies appeared to shrink, and cytoplasmic material was lost and detached from neighboring cells or the culture surface (54, 55). Previous studies suggested that KA caused damage to the cell body and degeneration in the nucleus, causing darkening in color and truncated dendrites as early cellular changes in response to toxic insult (56).…”

Section: Discussionmentioning

confidence: 99%

Trkb-IP3 Pathway Mediating Neuroprotection in Rat Hippocampal Neuronal Cell Culture Following Induction of Kainic Acid

Chong

Muthuraju

Huat

et al. 2018

MJMS

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BackgroundFollowing brain injury, development of hippocampal sclerosis often led to the temporal lobe epilepsy which is sometimes resistant to common anti-epileptic drugs. Cellular and molecular changes underlying epileptogenesis in animal models were studied, however, the underlying mechanisms of kainic acid (KA) mediated neuronal damage in rat hippocampal neuron cell culture alone has not been elucidated yet.MethodsEmbryonic day 18 (E-18) rat hippocampus neurons were cultured with poly-L-lysine coated glass coverslips. Following optimisation, KA (0.5 μM), a chemoconvulsant agent, was administered at three different time-points (30, 60 and 90 min) to induce seizure in rat hippocampal neuronal cell culture. We examined cell viability, neurite outgrowth density and immunoreactivity of the hippocampus neuron culture by measuring brain derived neurotrophic factor (BDNF), γ-amino butyric acid A (GABAA) subunit α-1 (GABRA1), tyrosine receptor kinase B (TrkB), and inositol trisphosphate receptor (IP3R/IP3) levels.ResultsThe results revealed significantly decreased and increased immunoreactivity changes in TrkB (a BDNF receptor) and IP3R, respectively, at 60 min time point.ConclusionThe current findings suggest that TrkB and IP3 could have a neuroprotective role which could be a potential pharmacological target for anti-epilepsy drugs.

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Degeneration of the Dendritic Arbor as an Index of Neurotoxicity in Identified Catecholamine Neurons in Rat Brain Slices

Johnson

Bywood

1998

Experimental Neurology

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Neurotoxic Effects of Kainic Acid on Substantia Nigra Neurons in Rat Brain Slices

Cited by 8 publications

References 37 publications

Catecholamine neuron groups in rat brain slices differ in their susceptibility to excitatory amino acid induced dendritic degeneration

Catecholamine neuron groups in rat brain slices differ in their susceptibility to excitatory amino acid induced dendritic degeneration

Trkb-IP3 Pathway Mediating Neuroprotection in Rat Hippocampal Neuronal Cell Culture Following Induction of Kainic Acid

Degeneration of the Dendritic Arbor as an Index of Neurotoxicity in Identified Catecholamine Neurons in Rat Brain Slices

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