Moschonas EH (2024) Cholinergic neurotransmission during performance of a sustained attention task after traumatic brain injury. Univ Pittsburgh School of Medicine Thesis.
Objective: To elucidate the role of basal forebrain cholinergic neurons (BFCNs) in mediating attentional performance and ACh efflux
Summary: Saporin-induced lesions to the nbM impaired signal detection accuracy during performance of the Sustained Attention Task (SAT). Similarly, in tasks of divided attention that involve both auditory and visual stimuli, cholinergic lesions to the nbM result in prolonged response times during bimodal trials compared to unimodal trials, which involve a single sensory modality.
Related Products: 192-IgG-SAP (Cat. #IT-01)
See Also:
- McGaughy J et al. Sustained attention performance in rats with intracortical infusions of 192 IgG-saporin-induced cortical cholinergic deafferentation: effects of physostigmine and FG 7142. Behav Neurosci 112(6):1519-1525, 1998.
- McGaughy J et al. The role of cortical cholinergic afferent projections in cognition: impact of new selective immunotoxins. Behav Brain Res 115:251-263, 2000.
- Dalley JW et al. Cortical cholinergic function and deficits in visual attentional performance in rats following 192 IgG-Saporin-induced lesions of the medial prefrontal cortex. Cereb Cortex 14(8):922-932, 2004.
- Chudasama Y et al. Cholinergic modulation of visual attention and working memory: Dissociable effects of basal forebrain 192-IgG-saporin lesions and intraprefrontal infusions of scopolamine. Learn Mem 11(1):78-86, 2004.
- Botly LC et al. Cholinergic deafferentation of the neocortex using 192 IgG-saporin impairs feature binding in rats. J Neurosci 29:4120-4130, 2009.
- Butt AE et al. 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, 2002.
- Butt AE et al. 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, 2002.
