A deep understanding of the degenerative processes that lead to the loss of nigral dopaminergic neurons and its effect on the neuronal network is key for the development of potential disease-delaying treatments. Toxins such as 6-hydroxydopamine (6-OHDA) or N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) have long been known to cause Parkinson’s disease in susceptible humans when ingested accidentally. The neurotoxin 6-OHDA was used to create the first animal model of PD and is today widely used to create situs-specific lesions in rodents, non-human primates, and dogs. 6-OHDA does not cross the blood-brain barrier (BBB) in significant quantities; thus, stereotactic injections into the brain are necessary to achieve the desired specific nigrostriatal lesion in order to induce parkinsonism. In addition to inducing molecular alterations comparable to those seen in PD, 6-OHDA models have also been shown to reproduce some of the electrophysiological and clinical hallmarks of PD. This chapter presents the animal models with an emphasis on toxic-induced parkinsonism and discusses the induced molecular electrophysiological and clinical features.