Kainic acid lesion-induced nigral neuronal death

Neuroprotective Effects of the MAO‐B Inhibitor, PF9601N, in an In Vivo Model of Excitotoxicity

“…The death of nigral dopaminergic neurons caused by kainate has been previously reported, but this appears to be a secondary phenomenon that does not arise for many days after the initial insult and represents a consequence of the primary toxic events, see . The mechanisms underlying this indirect dopaminergic toxicity are not fully understood, and it has been suggested that it may result from the loss of striatal interneurones , although the high levels of released dopamine and the gliosis observed in the present work could also contribute.…”

Advancements in the Quest to Map, Monitor, and Manipulate Neural Circuitry

“…Initially, studies of the brain relied on gross anatomy, defining large structures at relatively low resolution, without knowledge of cell type (Scoville and Milner, 1957). Coarsely targeted lesions using electrical current or chemicals allowed researchers to impart functional significance to these anatomically distinct brain regions (Foster et al, 2003;Lavond and Steinmetz, 2003). Early studies also used dyes and microscopy to identify and trace neurons, characterize their morphology, and identify connectivity patterns within discrete brain regions (Golgi, 1886).…”

Kainic acid lesion-induced spatial memory deficits of rats

“…Administration of KA into the rat striatum causes neuronal degeneration, neurochemical alterations and behavioral responses [5][6][7][8][9]. With regard to spatial memory deficits, previous studies have suggested that intracerebroventricular (i.c.v.)…”

“…administration of KA induced severe neuronal damage in limbic areas (amygdala, hippocampus) in rats, produced differential impairments of spatial learning memory and social behavior [10] and induced long-term loss of hippocampal plasticity manifested as reduced capacity for long-term potentiation [11]. There are also studies which have shown that intrastriatally KA administration caused the short-term direct death of striatal neurons while sparing nerve terminals [5]. Intrastriatal injections of the related excitotoxin, ibotenic acid, is known to result in death of nigral neurons [12,13].…”

“…In addition, nigral neuronal death following intrastriatal KA has been reported [15]. Striatal KA lesion resulted in progressive, long-term death of dopamine neurons in the SN [5]. Injection of KA in the VTA induced spontaneous recurrent seizure (SRS) in rats and impaired spatial learning memory, suggesting that loss of dopaminergic neurons in the VTA might contribute to spatial learning memory deficits induced by SRS [16].…”