2002 Targeting Trends Review

Zhu XO, de Permentier PJ, Waite PM (2002) Cholinergic depletion by IgG 192-saporin retards development of rat barrel cortex. Brain Res Dev Brain Res 136:1-16. doi: 10.1016/s0165-3806(02)00301-2

Summary: It has been shown that cholinergic afferents from the basal forebrain are necessary for normal cortical morphogenesis. However, the role of these projections in the development of the thalamocortical topographical map has not been investigated. Using the facial whisker barrel field in the rat somatosensory cortex as a development model, the authors administered 192-Saporin to newborn pups (0.1 µg, Cat. #IT-01). The data show a transient delay in the development of the barrel pattern over the first postnatal week.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Birthelmer A, Dommes E, Jeltsch H, Cassel JC, Jackisch R (2002) Septal grafts and evoked acetylcholine release in the rat hippocampus after 192 IgG-saporin lesions. Neuroreport 13(7):973-976. doi: 10.1097/00001756-200205240-00015

Summary: The authors investigate the structural and behavioral effects of intrahippocampal grafts containing cholinergic neurons into a lesioned region of the brain. Previous studies in rats were complicated by the lack of a specific cholinergic lesioning agent. 0.4 µg 192-Saporin (Cat. #IT-01) in 0.4 µl was injected into the vertical limb of the diagonal band of Broca in rats, then 6 to 10 months later the animals received intrahippocampal grafts of septal cells containing cholinergic neurons. Measurement of noradrenaline and serotonin uptake indicate that the grafts were able to produce only modest cholinergic effects. The authors conclude that this may be a result of performing the graft too soon following administration of the immunotoxin.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Burk JA, Herzog CD, Porter MC, Sarter M (2002) Interactions between aging and cortical cholinergic deafferentation on attention. Neurobiol Aging 23:467-477. doi: 10.1016/s0197-4580(01)00315-3

Summary: Trauma to forebrain cholinergic neurons is suspected to make these neurons more susceptible to future age-related loss of function. The authors tested this theory by making incomplete lesions of the basal forebrain cholinergic system using bilateral infusions of 192-Saporin (0.5 µl of 0.15 µg/µl, Cat. #IT-01) in rats trained prior to surgery. The attentional performance of the treated rats did not differ from control animals until the age of 31 months. The data indicate that pre-existing damage to the cholinergic basal forebrain region yields age-related attentional impairments.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Galani R, Lehmann O, Bolmont T, Aloy E, Bertrand F, Lazarus C, Jeltsch H, Cassel JC (2002) Selective immunolesions of CH4 cholinergic neurons do not disrupt spatial memory in rats. Physiol Behav 76:75-90. doi: 10.1016/s0031-9384(02)00674-1

Summary: Lesioning of the nucleus basalis magnocellularis (NBM) with 192-Saporin (Cat. #IT-01) has produced varied cognitive effects in numerous studies. The authors of this work suggest that several factors such as lesion procedure and the type of behavioral test used may cause these variations. Thirty-one rats were lesioned using 0.2 or 0.4 µg of 192-Saporin infused into the NBM, and locomotor activity, learning, and memory capabilities were tested using several test methods. Spatial memory appeared to remain intact, but evidence suggests that attentional processing is affected by NBM lesioning with 192-Saporin.

Usage: Rat NBM was lesioned using 0.2 or 0.4 µg of 192-Saporin (Cat. #IT-01).

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Wang H, Germanson TP, Guyenet PG (2002) Depressor and tachypneic responses to chemical stimulation of the ventral respiratory group are reduced by ablation of neurokinin-1 receptor-expressing neurons. J Neurosci 22(9):3755-3764. doi: 10.1523/JNEUROSCI.22-09-03755.2002

Summary: The pre-Bötzinger complex is a region of the ventral respiratory group (VRG) in the brain. Injection of excitatory amino acids into this region can cause a variety of responses such as rapid breathing, hypotension, and elevated arterial pressure. The authors used SSP-SAP (Cat. #IT-11) to eliminate the neurokinin-1 receptor (NK-1r) positive neurons in the VRG to determine their role in control of respiration and arterial pressure. Intraparenchymal injection of 0.313 ng/50 nl SSP-SAP produced several abnormal respiratory effects in rats treated with excitatory amino acids. The results indicate that NK-1r positive neurons in the ventrolateral medulla play an important role in respiratory rhythm and blood pressure.

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Li X, Conklin D, Ma W, Zhu X, Eisenach JC (2002) Spinal noradrenergic activation mediates allodynia reduction from an allosteric adenosine modulator in a rat model of neuropathic pain. Pain 97:117-125. doi: 10.1016/s0304-3959(02)00011-8

Summary: T62 is a thiobene compound that enhances adenosine agonist binding to the A1 receptor. Activation of the adenosine receptor has been effective in several different pain models. The authors used a spinal nerve ligation model for mechanical allodynia to assess T62 efficacy and mode of action. Rats treated with anti-DBH-SAP (4 µg in 5 µl, Cat. #IT-03) experienced no anti-allodynia effects from T62 administration, indicating that modulation of mechanical allodynia by T62 utilizes the spinal noradrenergic system.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Berchtold NC, Kesslak JP, Cotman CW (2002) Hippocampal brain-derived neurotrophic factor gene regulation by exercise and the medial septum. J Neurosci Res 68(5):511-521. doi: 10.1002/jnr.10256

Summary: Brain-derived neurotrophic factor (BDNF) enhances neuron function and plasticity. The authors lesioned rats with medial septal injections of 192-Saporin (Cat #IT-01, 375 ng in 0.5 µl PBS) or OX7-SAP (Cat #IT-02, 12.5 or 25 ng in 0.5 µl PBS). 192-Saporin affected the sedentary, but not exercise-induced levels of BDNF. OX7-SAP reduced levels in both groups in a dose-dependent manner.

Related Products: 192-IgG-SAP (Cat. #IT-01), OX7-SAP (Cat. #IT-02)

Butt AE, Noble MM, Rogers JL, Rea TE (2002) Impairments in negative patterning, but not simple discrimination learning, in rats with 192 IgG-Saporin lesions of the nucleus basalis magnocellularis. Behav Neurosci 116(2):241-255. doi: 10.1037//0735-7044.116.2.241

Summary: 192-Saporin (Cat. #IT-01) administration to the basal forebrain has frequently been used in rats to create a model for Alzheimer’s disease. The authors used 0.2 µl bilateral injections of 0.4 µg/µl 192-SAP into the nucleus basalis magnocellularis (NBM). Previous studies using non-specific excitotoxic agents have suggested the involvement of the NBM in learning and memory. The authors confirm more recent findings that indicate some of the deficits produced by these excitotoxins are due to the non-specific lesioning caused by these agents. The highly selective cholinergic lesioning produced by 192-Saporin left simple association learning intact but impaired more complicated configural association processes.

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Butt AE, Bowman TD (2002) Transverse patterning reveals a dissociation of simple and configural association learning abilities in rats with 192 IgG-saporin lesions of the nucleus basalis magnocellularis. Neurobiol Learn Mem 77:211-233. doi: 10.1006/nlme.2001.4013

Summary: Using 80 ng bilateral infusions of 192-Saporin (Cat. #IT-01) into each of the medial and lateral target sites of the nucleus basalis magnocellularis (NBM) in rats, the authors demonstrate that lesioning the cholinergic systems of the NBM impairs a more complicated learning technique, while leaving simple association learning intact. The results also show that the transition between these two learning strategies is impaired in lesioned animals.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Mattsson A, Ögren SO, Olson L (2002) Facilitation of dopamine-mediated locomotor activity in adult rats following cholinergic denervation. Exp Neurol 174:96-108. doi: 10.1006/exnr.2001.7850

Summary: Using 80 ng bilateral infusions of 192-Saporin (Cat. #IT-01) into each of the medial and lateral target sites of the nucleus basalis magnocellularis (NBM) in rats, the authors demonstrate that lesioning the cholinergic systems of the NBM impairs a more complicated learning technique, while leaving simple association learning intact. The results also show that the transition between these two learning strategies is impaired in lesioned animals.

Related Products: 192-IgG-SAP (Cat. #IT-01)