References

Woods M, Whiteside G, Pearson M, Pomonis J, Turchin P, Walker K (2003) Ablation of a population of NK-1 expressing neurons in the dorsal horn of the spinal cord does not induce αβ sprouting into lamina II. Neuroscience 2003 Abstracts 64.11. Society for Neuroscience, New Orleans, LA.

Summary: Peripheral nerve injury results in hyperalgesia and allodynia. It has been proposed that sprouting of myelinated touch responsive Aβ-fibers into the innervation territory of pain sensitive C fibers in the spinal cord contributes to these abnormal behaviors. In has further been postulated that excitatory cell death of spinal cord neurons may result in “vacant synapses” that induce sprouting (Woolf et al., 1992). We have investigated whether selectively ablating a population of cells in laminae I and II, using intrathecal (i.t.) SP-saporin (SP-SAP), will induce sprouting from deeper laminae. Male Sprague-Dawley rats were either injected i.t. at the lumbar region with SP-SAP (1 μl, 5 μM) or the sciatic nerve was axotomised at the mid-thigh level. Two weeks later the sciatic nerve was injected with the retrograde tracer, cholera toxin-β subunit (CTB) (2 μl, 2%) which selectively traces Aβ-fibers. Three days post CTB the animals were perfused, the lumbar ganglia and spinal cord harvested, sectioned and stained immunohistochemically for NK-1 and CTB. As previously described axotomy resulted in considerable CTB immunostaining in laminae I, II and III compared to non-axotomised controls in which it was present only in I and III. SP-SAP i.t. resulted in a substantial reduction of NK-1 like immunostaining in the spinal cord compared to saline injected controls. CTB was not detected in lamina II of spinal cords from animals with an ablation of NK-1 expressing cells. These results suggest that the death of dorsal horn neurons does not induce sprouting of Aβ-fibers into lamina II.

Related Products: SP-SAP (Cat. #IT-07)

Herron P, Ismail NS (2003) Progressive effects of cholinergic depletion on cortical functional properties in the somatosensory cortex of rats. Neuroscience 2003 Abstracts 61.11. Society for Neuroscience, New Orleans, LA.

Summary: The amount and duration of cholinergic depletion of basal forebrain input appear to be important for how significant the functional capacity of cortical neurons and behavior are affected. Firstly, it is not known whether there is a correlative relationship between the level of cholinergic depletion and the level of degraded functional properties or whether there is a threshold of depletion, beyond which no further degradation occurs. Secondly, it is not known whether similar levels of cholinergic depletion over different periods cause the similar or different effects on functional capacities and behavior. These experiments were done in the posteromedial barrel subfield (PMBSF) cortex of young adult Sprague-Dawley rats. Selective lesion of cholinergic neurons in the NBM was achieved with cortical or intraventricular injections of the immunotoxin (IT), 192 IgG saporin. Electrophysiological recordings and whisker use in exploratory behavior were monitored for different post-injection survival periods. Results show that cholinergic depletion causes a significant decrease in the magnitude of evoked activity and an increase in the size of receptive fields for different periods. Observations of exploratory behavior showed that animals used whiskers controlled by cholinergic depleted cortex less than the whiskers controlled by non-cholinergic depleted cortex. Thus, cholinergic depletion leads to effects that significantly alter the functional capacity of the cortex and the behavioral use of those whiskers.

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

Nolan BC, Freeman JH (2003) Purkinje cell depletion by ox7-saporin impairs eyeblink conditioned excitation and inhibition in rats. Neuroscience 2003 Abstracts 87.3. Society for Neuroscience, New Orleans, LA.

Summary: The role of the cerebellar cortex in conditioned excitation has been demonstrated by studies that used lesions, inactivation, and electrical stimulation (e.g., Attwell, Rahman, & Yeo, 2001, J Neurosci, 21, 5715-5722). However, very little evidence exists concerning the role of the cerebellar cortex in conditioned inhibition. Moreover, there are multiple blink control zones in the cerebellar cortex (Hesslow, 1994, J Physiol, 476, 229-244), which complicates the interpretation of studies that use localized lesions. In the current study, rats were infused with the immunotoxin OX7-saporin into the lateral ventricles to selectively destroy Purkinje cells throughout the cerebellar cortex (Angner, et.al, 2000, Neurotox, 21, 395-404). The OX7- saporin method provides advantages relative to other methods, including the ability to deplete Purkinje cells after initial training. In Experiment 1, rats were given saline or OX7-saporin prior to excitatory conditioning training, which was established using a tone conditioned stimulus (CS) paired with a periorbital shock unconditioned stimulus (US). Rats given OX7-saporin had nearly complete Purkinje cell loss and acquisition of excitatory conditioning was severely impaired. In Experiment 2, rats were first trained with excitatory conditioning procedures, followed by infusion of either saline or OX7-saporin. After a two-week post-infusion period, the rats were given reacquisition training. After reacquiring excitatory conditioning, the rats were trained using a feature-negative discrimination procedure consisting of trials with CS-US pairings and trials with a non-reinforced tone-light compound stimulus. Rats treated with OX7-saporin showed a significant impairment in reacquisition and acquisition of conditioned inhibition. The results suggest that Purkinje cells are critically involved in the acquisition of both conditioned excitation and inhibition in rats.

Related Products: OX7-SAP (Cat. #IT-02)

Rinaman L (2003) Hindbrain noradrenergic lesions attenuate anorexia and alter central cFos expression in rats after gastric viscerosensory stimulation. J Neurosci 23(31):10084-10092. doi: 10.1523/JNEUROSCI.23-31-10084.2003

Summary: Using 5-ng injections of anti-DBH-SAP (Cat. #IT-03) into hindbrain nucleus of the solitary tract in rats, the author investigated the role of DBH-positive neurons in the mediation of anorexigenic and central nervous system activation effects due to exogenous CCK.

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

Sarter M, Bruno J, Givens B (2003) Attentional functions of cortical cholinergic inputs: what does it mean for learning and memory. Neurobiol Learn Mem 80:245-256. doi: 10.1016/s1074-7427(03)00070-4

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

Pagliardini S, Ren J, Greer JJ (2003) Ontogeny of the pre-Bötzinger complex in perinatal rats. J Neurosci 23(29):9575-9584. doi: 10.1523/JNEUROSCI.23-29-09575.2003 PMID: 14573537

Related Products: Antibody to NK-1 Receptor (Cat. #AB-N04)

Buffo A, Carulli D, Rossi F, Strata P (2003) Extrinsic regulation of injury/growth-related gene expression in the inferior olive of the adult rat. Eur J Neurosci 18(8):2146-2158. doi: 10.1046/j.1460-9568.2003.02940.x

Summary: Inferior olive (IO) cells of the CNS have the ability to regenerate axons after injury, even when the injury is close to the terminal field. After administration of 2.2 µg of 192-Saporin (Cat. #IT-01) and a control immunotoxin (mouse IgG-SAP, Cat #IT-18) to each ventricle in rats, two subsets of IO cells were discovered. Each subset responded differently to injury indicating that multiple mechanisms are responsible for their intrinsic regenerative potential.

Related Products: 192-IgG-SAP (Cat. #IT-01), Mouse IgG-SAP (Cat. #IT-18)

Leung LS, Shen B, Rajakumar N, Ma J (2003) Cholinergic activity enhances hippocampal long-term potentiation in CA1 during walking in rats. J Neurosci 23(28):9297-9304. doi: 10.1523/JNEUROSCI.23-28-09297.2003

Summary: To investigate the role of the cholinergic system in long term potentiation (LTP) the authors lesioned the left and right medial septum of rats with 0.14 µg of 192-Saporin (Cat. #IT-01). LTP induced in lesioned walking animals is less robust than in control animals.

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

Dommergues MA, Plaisant F, Verney C, Gressens P (2003) Early microglial activation following neonatal excitotoxic brain damage in mice: a potential target for neuroprotection. Neuroscience 121(3):619-628. doi: 10.1016/s0306-4522(03)00558-x

Summary: Brain lesions that mimic damage from cerebral palsy in mice are characterized by microglial activation within 24 hours of insult. Using intraperitoneal injections of Mac-1-SAP (90 µg/kg, Cat. #IT-06), a reduction in the density of resident microglial and blood-derived monocytes was obtained.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)

Dudkin KN, Chueva IV, Makarov FN (2003) [Interaction between sensory and cognitive processes in visual recognition: the role of the associative areas of the cerebral cortex] Russian. Ross Fiziol Zh Im I M Sechenova 89(10):1226-1239.

Summary: The authors used ME20.4-SAP(Cat. #IT-15).

Related Products: ME20.4-SAP (Cat. #IT-15)