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Review
. 2020 Aug 25;12(9):546.
doi: 10.3390/toxins12090546.

Saporin from Saponaria officinalis as a Tool for Experimental Research, Modeling, and Therapy in Neuroscience

Alexey P Bolshakov  1 , Mikhail Yu Stepanichev  2 , Yulia V Dobryakova  3 , Yulia S Spivak  1 , Vladimir A Markevich  3
Affiliations
Review

Saporin from Saponaria officinalis as a Tool for Experimental Research, Modeling, and Therapy in Neuroscience

Alexey P Bolshakov et al. Toxins (Basel). .

Abstract

Saporin, which is extracted from Saponaria officinalis, is a protein toxin that inactivates ribosomes. Saporin itself is non-selective toxin but acquires high specificity after conjugation with different ligands such as signaling peptides or antibodies to some surface proteins expressed in a chosen cell subpopulation. The saporin-based conjugated toxins were widely adopted in neuroscience as a convenient tool to induce highly selective degeneration of desired cell subpopulation. Induction of selective cell death is one of approaches used to model neurodegenerative diseases, study functions of certain cell subpopulations in the brain, and therapy. Here, we review studies where saporin-based conjugates were used to analyze cell mechanisms of sleep, general anesthesia, epilepsy, pain, and development of Parkinson's and Alzheimer's diseases. Limitations and future perspectives of use of saporin-based toxins in neuroscience are discussed.

Keywords: 192IgG-saporin; Alzheimer’s disease; orexin-saporin; pain; saporin; saporin-based toxins; sleep.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The sleep-related effects of orexin-saporin injection in various parts of the brain. The effects caused by death of neurons that receive orexinergic inputs from the lateral hypothalamus (LH) are shown next to the structure that was destroyed by the toxin. MS, medial septum; VLPO, ventrolateral preoptic area; SN, substantia nigra; VLPAG, Ventrolateral Periaquaductal Gray.
Figure 2
Figure 2
Effects of different saporin-based conjugates on the nociceptive system in the spinal cord. Panel (A), basic connectivity of two major types of nociceptive neurons. Panel (B), a compensatory increase in the expression of NK1 receptors in the spinal cord neurons after elimination of IB4-positive neurons in the dorsal root ganglion. Note that IB4-saporin may also cause degeneration of microglia in the spinal cord and affect pain sensitivity. Panel (C), intrathecal injection of SP-saporin causes degeneration of NK1-positive neurons in the spinal cord and reduces sensitivity to noxious stimuli.
Figure 3
Figure 3
Compensation of cholinergic deficit in the hippocampus after death of cholinergic neurons in the medial septum and diagonal band of Broca (DBB). Panel (A), normal pattern of innervation. Panel (B), loss of cholinergic input leads to an increase in NGF level. Panel (C), compensatory sprouting of sympathetic fibers in the hippocampus resulting from elevated NGF level.
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