The axons of pyramidal cells are longer than those of interneurons and thus, these cells are more vulnerable to the toxic effects of chemicals that disrupt axonal transport. Many electrophilic alkylating agents covalently can bind to cellular macromolecules and thereby disrupt axonal transport. This can induce a distal dying back neuropathy without killing the cell per se.
The extent of neuronal damage can be achieved by controlling the damaging stimulus for example.
(1) The extent of neuronal damage by status epilepticus (SE) can be controlled by limiting the duration of SE
(2) Using pharmacological tools, selective chronic slow progressive neuronal death can also be achieved e.g. chronic activation of glutamate receptors (by AMPA, kainic acid) is capable of inducing dose dependent slow progressive neuronal death
(3) Heavy metals resulted in slow and progressive dose dependent neurotoxicity