Toxin-Induced Experimental Models of Learning and Memory Impairment

Abstract

Animal models for learning and memory have significantly contributed to novel strategies for drug development and hence are an imperative part in the assessment of therapeutics. Learning and memory involve different stages including acquisition, consolidation, and retrieval and each stage can be characterized using specific toxin. Recent studies have postulated the molecular basis of these processes and have also demonstrated many signaling molecules that are involved in several stages of memory. Most insights into learning and memory impairment and to develop a novel compound stems from the investigations performed in experimental models, especially those produced by neurotoxins models. Several toxins have been utilized based on their mechanism of action for learning and memory impairment such as scopolamine, streptozotocin, quinolinic acid, and domoic acid. Further, some toxins like 6-hydroxy dopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and amyloid-β are known to cause specific learning and memory impairment which imitate the disease pathology of Parkinson’s disease dementia and Alzheimer’s disease dementia. Apart from these toxins, several other toxins come under a miscellaneous category like an environmental pollutant, snake venoms, botulinum, and lipopolysaccharide. This review will focus on the various classes of neurotoxin models for learning and memory impairment with their specific mechanism of action that could assist the process of drug discovery and development for dementia and cognitive disorders.

Repurposing of the β-Lactam Antibiotic, Ceftriaxone for Neurological Disorders: A Review

“…After induction of different models of neurological illness by lesioning or chemicals, it is known that animals manifest behavioral alterations in early onset and in the long-term they might also exhibit memory deficits (Van Dam and De Deyn, 2011;Savio et al, 2012;More et al, 2016). Numerous studies evidenced that CEF substantially improved such chemicalinduced behavioral alteration and memory impairments in different rodent models of neurological conditions (Lai et al, 2011;Wei et al, 2012;Akina et al, 2013;Chotibut et al, 2014;Feng et al, 2014;Hsieh et al, 2017;Kaur and Prakash, 2017;Fan et al, 2018).…”

Chemicals used for the induction of Alzheimer’s disease-like cognitive dysfunctions in rodents

“…Some of the common chemicals used for modelling AD are scopolamine, streptozotocin, and alcohol, as well as dysregulation of heavy metals, such as aluminum (Al), copper (Cu), zinc (Zn), lead (Pb, and reducing sugar (D-galactose) 99 , among others ( Tables 1, 2…”

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

“…By blocking axoplasmic transport, colchicine critically damages hippocampal granule cells, ultimately leading to neuronal loss, which manifests with cognitive impairment and spontaneous motor activity. Intracerebroventricular (ICV) injection (15 g in 5 L/7.5 g in 10 L) of colchicine in rats could induce AD-like pathology with consequent cognitive and behavioral alterations similar to AD [89,[93][94][95]. The drug selectively blocks acetylcholine transferase in the basal forebrain and hippocampus, which are regions responsible for memory [90].…”