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2314 entries

Progressive effects of cholinergic depletion on cortical functional properties in the somatosensory cortex of rats

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)

Purkinje cell depletion by ox7-saporin impairs eyeblink conditioned excitation and inhibition in rats.

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)

Hindbrain noradrenergic lesions attenuate anorexia and alter central cFos expression in rats after gastric viscerosensory stimulation.

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)

Attentional functions of cortical cholinergic inputs: what does it mean for learning and memory

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)

Extrinsic regulation of injury/growth-related gene expression in the inferior olive of the adult rat.

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)

Early microglial activation following neonatal excitotoxic brain damage in mice: a potential target for neuroprotection.

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)

Cholinergic activity enhances hippocampal long-term potentiation in CA1 during walking in rats.

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)

Featured Article: Subplate neurons and functional maturation of thalamocortical synapses

Kanold PO (2003) Featured Article: Subplate neurons and functional maturation of thalamocortical synapses. Targeting Trends 4(4)

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

Read the featured article in Targeting Trends.

See Also:

Featured Article: CCK-SAP in binding studies

Porreca F, Hruby V, Lai J (2003) Featured Article: CCK-SAP in binding studies. Targeting Trends 4(4)

Related Products: CCK-SAP (Cat. #IT-31)

Read the featured article in Targeting Trends.

Destruction of midbrain dopaminergic neurons by using an immunotoxin to the dopamine transporter.

Wiley RG, Harrison MB, Levey A, Lappi DA (2003) Destruction of midbrain dopaminergic neurons by using an immunotoxin to the dopamine transporter. Cell Mol Neurobiol 23:839-850. doi: 10.1023/a:1025065306264

Summary: The authors demonstrate the effective and specific removal of neurons expressing the dopamine transporter in the substantia nigra pars compacta and the ventral tegmental area with anti-DAT-SAP (Cat. #IT-25). A 21-µg icv injection produced a highly significant loss of midbrain dopaminergic neurons, creating a useful model for Parkinson’s disease.

Related Products: Anti-DAT-SAP (Cat. #IT-25)

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