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2022, Nanobioanalytical Approaches to Medical DiagnosticsImpaired hippocampal and thalamic acetylcholine release in P301L tau-transgenic mice
2019, Brain Research BulletinCitation Excerpt :The major source of cholinergic innervation to the hippocampus is provided by the medial septal nucleus (Ch1), a group of cholinergic neurons in the basal forebrain (Frotscher and Léránth, 1985). Thalamic cholinergic fibres also receive input from the basal forebrain (Sofroniew et al., 1985), while cholinergic neurons innervating the red nucleus are exclusively located in the brain stem (Mesulam et al., 1992). This pattern of cholinergic dysfunction resembles the human situation.
Visual hallucinations, thalamocortical physiology and Lewy body disease: A review
2019, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Collectively, these data suggest that dopamine may play less of a role in DLB-associated hallucinations than hallucinations seen in other conditions, and point to a key role for acetylcholine. Cholinergic inputs to the thalamus are derived from the pedunculopontine and laterodorsal tegmental nuclei ((Mesulam et al., 1983; Sofroniew et al., 1985), and reviewed in (Varela, 2014; Yeomans, 2012)). In addition, the TRN receives dense cholinergic input mostly from the basal forebrain with a minority of cholinergic input from the pedunculopontine/laterodorsal tegmental nuclei (Hallanger et al., 1987).
Modulation of Neuronal Activity in the Motor Thalamus during GPi-DBS in the MPTP Nonhuman Primate Model of Parkinson's Disease
2017, Brain StimulationCitation Excerpt :An unanticipated finding was that the predominant effect of GPi DBS on the cerebellar receiving area of the motor thalamus (VPLo) was also inhibition; despite the absence, insofar as is currently known, of direct projections from the GPi to the VPLo. One possible mechanism for this observation may relate to a secondary reduction in cholinergic excitatory inputs from the pedunculopontine tegmental nucleus [21] or other brainstem, cerebellar or spinal areas [22,23] due to chronic activation of GPi GABAergic output to these regions [24]. Interestingly, a small subset of neurons within each subnucleus increased their mean discharge rate during DBS, likely as a further reflection of the multiple pathways impacted by GPi DBS whose delays in effect likely produce the poly-phasic responses observed in both subnuclei.
Ascending Projections of the RAS
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