Neonatal 192 IgG-saporin lesion of forebrain cholinergic neurons: focus on the life span?

Pappas, Bruce A.; Sherren, Nicole

doi:10.1016/s0149-7634(03)00067-8

Cited by 13 publications

(12 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5A, F) reveals patterns of ChAT-positive cells similar to those reported previously for normal animals (Butcher and Woolf, 2004; Mesulam et al, 1983; Robertson et al, 1998), with strongly labeled multipolar neurons and a few bipolar neurons seen in medial septum and in the vertical and horizontal limbs of the diagonal band. As reported previously (Johnson et al, 2002; Marques Pereira et al, 2005; Pappas and Sherren, 2003; Robertson et al, 1998) saporin treatment results in the loss of many BFCNs. In the present experiments, figures 5B and 5G illustrate a marked loss of ChAT-positive cells in the medial septum and in the nuclei of the diagonal band of the Sap+Sal animals.…”

Section: Resultssupporting

confidence: 83%

“…Treatment with the 192 IgG saporin leads to the loss of a large portion of the BFCNs (Ha et al, 1999; Johnson et al, 2002; Pappas and Sherren, 2003; Ricceri et al, 2004; Robertson et al, 1998; Szigeti et al, 2013). Although it is known that saporin is able to kill cells by inactivating ribosomes and thereby shutting down protein synthesis (Daniels-Wells et al, 2013), it is not yet clear how a partial, sublethal (to the cell) dose may affect the cell.…”

Section: Discussionmentioning

confidence: 99%

“…This treatment dosage is a relatively low dose (Johnson et al, 2002; Marques Pereira et al, 2005; Pappas and Sherren, 2003; Robertson et al, 1998). Six different sets of animals were used, with 5 conditions in each set.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Neurotrophic factors rescue basal forebrain cholinergic neurons and improve performance on a spatial learning test

Lee

Danandeh

Baratta

et al. 2013

Experimental Neurology

View full text Add to dashboard Cite

This study investigated whether animals sustaining experimental damage to the basal forebrain cholinergic system would benefit from treatment with exogenous neurotrophic factors. Specifically, we set out to determine whether neurotrophic factors would rescue damaged cholinergic neurons and improve behavioral performance on a spatial learning and memory task. Adult rats received bilateral injections of either saline (controls) or 192 IgG-saporin to damage basal forebrain cholinergic neurons (BFCNs). Two weeks later, animals received implants of an Alzet mini-pump connected to cannulae implanted bilaterally in the lateral ventricles. Animals received infusions of nerve growth factor (NGF), neurotrophin 3 (NT3), a combination of NGF and NT3, or a saline control over a 4-week period. Compared to saline-treated controls, animals sustaining saporin-induced damage to BFCNs took significantly more trials to learn a delayed match to position task and also performed more poorly on subsequent tests, with increasing delays between test runs. In contrast, animals infused with neurotrophins after saporin treatment performed significantly better than animals receiving saline infusions; no differences were detected for performance scores among animals infused with NGF, NT3, or a combination of NGF and NT3. Studies of ChAT immunnocytochemical labeling of BFCNs revealed a reduction in the numbers of ChAT-positive neurons in septum, nucleus of diagonal band, and nucleus basalis in animals treated with saporin followed by saline infusions, whereas animals treated with infusions of NGF, NT3 or a combination of NGF and NT3 showed only modest reductions in ChAT-positive neurons. Together, these data support the notion that administration of neurotrophic factors can rescue basal forebrain cholinergic neurons and improve learning and memory performance in rats.

show abstract

Section: Resultssupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Neurotrophic factors rescue basal forebrain cholinergic neurons and improve performance on a spatial learning test

Lee

Danandeh

Baratta

et al. 2013

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…For this purpose, we used a selective method to permanently lesion the cholinergic neurons of all BFn. In contrast to electrolytic or excitatory acid-induced lesions (Höhmann and Coyle, 1988), with an inherent lack of sensitivity, immunolesion using SAP led to exclusive destruction of cholinergic neurons in the BFn by recognizing the expressed p75 receptor (Wiley et al, 1991;Book et al, 1992;Robertson et al, 1998;Pappas and Sherren, 2003).…”

Section: Activation Of Cholinergic Projections Differentially Modulatmentioning

confidence: 99%

Cholinergic Control in Developing Prefrontal–Hippocampal Networks

Janiesch¹,

Krüger²,

Poschel³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

The cholinergic drive enhances input processing in attentional and mnemonic context by interacting with the activity of prefrontalhippocampal networks. During development, acetylcholine modulates neuronal proliferation, differentiation, and synaptic plasticity, yet its contribution to the maturation of cognitive processing resulting from early entrainment of neuronal networks in oscillatory rhythms remains widely unknown. Here we show that cholinergic projections growing into the rat prefrontal cortex (PFC) toward the end of the first postnatal week boost the generation of nested gamma oscillations superimposed on discontinuous spindle bursts by acting on functional muscarinic but not nicotinic receptors. Although electrical stimulation of cholinergic nuclei increased the occurrence of nested gamma spindle bursts by 41%, diminishment of the cholinergic input by either blockade of the receptors or chronic immunotoxic lesion had the opposite effect. This activation of locally generated gamma episodes by direct cholinergic projections to the PFC was accompanied by indirect modulation of underlying spindle bursts via cholinergic control of hippocampal theta activity. With ongoing maturation and switch of network activity from discontinuous bursts to continuous theta-gamma rhythms, accumulating cholinergic projections acting on both muscarinic and nicotinic receptors mediated the transition from high-amplitude slow to low-amplitude fast rhythms in the PFC. By exerting multiple actions on the oscillatory entrainment of developing prefrontal-hippocampal networks, the cholinergic input may refine them for later gating processing in executive and mnemonic tasks.

show abstract

“…For this purpose, we used a selective method to permanently impair the basal forebrain cholinergic neurons. In contrast to the electrolytic and excitatory amino acid-induced lesions (Hohmann and Coyle, 1988), with an inherent lack of selectivity, the immunolesion technique using 192 IgG-saporin leads to exclusive destruction of the cholinergic neurons in the basal forebrain (Wiley et al, 1991;Book et al, 1992;Robertson et al, 1998;Pappas and Sherren, 2003). The immunotoxin termed Figure 5.…”

Section: Immunotoxic Lesion Of Cholinergic Basal Forebrain Nuclei Dramentioning

confidence: 99%

Cholinergic Modulation of Spindle Bursts in the Neonatal Rat Visual CortexIn Vivo

Hanganu¹,

Staiger²,

Ben-Ari³

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

Acetylcholine (ACh) is known to shape the adult neocortical activity related to behavioral states and processing of sensory information. However, the impact of cholinergic input on the neonatal neuronal activity remains widely unknown. Early during development, the principal activity pattern in the primary visual (V1) cortex is the intermittent self-organized spindle burst oscillation that can be driven by the retinal waves. Here, we assessed the relationship between this early activity pattern and the cholinergic drive by either blocking or augmenting the cholinergic input and investigating the resultant effects on the activity of the rat visual cortex during the first postnatal week in vivo. Blockade of the muscarinic receptors by intracerebroventricular, intracortical, or supracortical atropine application decreased the occurrence of V1 spindle bursts by 50%, both the retina-independent and the optic nerve-mediated spindle bursts being affected. In contrast, blockade of acetylcholine esterase with physostigmine augmented the occurrence, amplitude, and duration of V1 spindle bursts. Whereas direct stimulation of the cholinergic basal forebrain nuclei increased the occurrence probability of V1 spindle bursts, their chronic immunotoxic lesion using 192 IgG-saporin decreased the occurrence of neonatal V1 oscillatory activity by 87%. Thus, the cholinergic input facilitates the neonatal V1 spindle bursts and may prime the developing cortex to operate specifically on relevant early (retinal waves) and later (visual input) stimuli.

show abstract

Neonatal 192 IgG-saporin lesion of forebrain cholinergic neurons: focus on the life span?

Cited by 13 publications

References 81 publications

Neurotrophic factors rescue basal forebrain cholinergic neurons and improve performance on a spatial learning test

Neurotrophic factors rescue basal forebrain cholinergic neurons and improve performance on a spatial learning test

Cholinergic Control in Developing Prefrontal–Hippocampal Networks

Cholinergic Modulation of Spindle Bursts in the Neonatal Rat Visual CortexIn Vivo

Contact Info

Product

Resources

About