Catalpol attenuates MPTP induced neuronal degeneration of nigral-striatal dopaminergic pathway in mice through elevating glial cell derived neurotrophic factor in striatum

Catalpol Induces Neuroprotection and Prevents Memory Dysfunction through the Cholinergic System and BDNF

“…BDNF interaction with tropomyosin-related kinase B receptors and presynaptic muscarinic receptors modulates transmitter release in adult rodent motor nerve terminal, which can improve stroke motor function recovery [51]. Previous studies reported that catalpol increased the hippocampal neuroplasticity in the aged rats [52] and attenuated MPTP-induced neuronal degeneration of nigral-striatal dopaminergic pathway in mice [53] partly attributed to BDNF upregulation. At the same time, higher BDNF level, together with ACh, is beneficial to brain plasticity and the induction of specific, associative detail behavioral memory [54, 55] and synaptogenesis [56].…”

Expression of GDNF receptors GFRα1 and RET is preserved in substantia nigra pars compacta of aging Asian Indians

“…Recently, Xu et al (2010) while demonstrating the protective effect of a Chinese drug Catalpol showed that it raised the striatal GDNF levels in MPTP injected animals, which increased the TH immunoreactive neuronal numbers in SNpc and striatal DAT density, whereas blocking RET reduced its protective effect. Ma et al (1999a) demonstrated an age-related reduction in the number of dopamine transporter (DAT) immunoreactive nigral neurons and linked it to the occurrence of age-related extrapyramidal signs.…”

Chronic MPTP treatment produces hyperactivity in male mice which is not alleviated by concurrent trehalose treatment

“…For example, when assessed within 48 h of the last MPTP treatment, male mice exhibit increased latencies in pole descent, decreased latencies to remain on a rotating rod, decreased locomotor activity, increased foot faults during beam crossing or grid tests, poor swimming ability, increased tail suspension immobility, increased akinesia and catalepsy, memory impairments in an avoidance task, and olfactory deficits [3,[6][7][8][9][10][11][12]. Similar treatment has also been described to cause long-lasting impairments (up to 6 months post-treatment) on latencies to remain on a rotating rod [2,13,14], in foot slips or gait alterations [15,16], on performance of the cued, but not spatial, version of a water maze task [16], and on baseline and amphetamine-induced locomotor activity [16].…”