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Neurotrophic Factors
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
In the septohippocampal system, cholinergic neurons of the medial septum and vertical limb of the nucleus of the diagonal band of Broca project their axons predominantly to the ipsilateral dorsal hippocampal formation through the fimbria-fornix and supracallosal stria (Figure 9.2, A).53 In the 1970s and 1980s, evidence from animal studies established that NGF has a physiological role for the cholinergic neurons of the basal forebrain. The septal cholinergic neurons have Trk and p75NGFRreceptors.54–57 NGF is produced in the hippocampal formation and in the basal forebrain58–61 and the cholinergic neurons retrogradely transport NGF.15 Exogenous NGF causes an increase in levels of the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT) in vivo.62,63 Evidence for an endogenous role of NGF was also provided by the finding that NGF-antibodies decrease levels of ChAT in vivo.64,65 Nonetheless, the neurons appear not to be dependent for their survival on NGF or other neurotrophic factors from the hippocampus, because hippocampal removal leads to their atrophy but not to their death.66 Subsequent axotomy of such cholinergic neurons (with a removed hippocampal formation) does induce their apparent loss, suggesting that other endogenous sources of neurotrophic factors (e.g., basal forebrain) cannot protect the cells against the more severe insult.
Neuroanatomy of basic cognitive function
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Mark J. Ashley, Jessica G. Ashley, Matthew J. Ashley
Cholinergic neurons (Figure 6.15) project from the mesopontine tegmentum and the basal forebrain. The neurons of the pontine region provide a descending projectional pathway to the nuclei of the pontine and medullary reticular formation. They also project in a major ascending pathway to the thalamus. The ascending pathway to the thalamus exerts an arousal effect that is mediated indirectly by excitatory projections from the thalamus to the cortex.177 Projections arising in the basal forebrain provide indirect cholinergic input to the cortex. By contrast, cholinergic projections arising from the nucleus basalis neurons project entirely to nearly all the cerebral cortex. The hippocampal formation is fed by projections from the medial septal nuclei and the nucleus of the diagonal band of Broca. Cholinergic neurons of the descending pathway are thought to impact the sleep–wake cycle via these projections. Cholinergic blockade of central cholinergic transmission results in delirium, and blockade of the striatal neurons results in movement disorders.177 The primary function of acetylcholine is found in attention, memory, and learning.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
The diagonal band of Broca collects AXON fibres from the BASAL FOREBRAIN and the AMYGDALA, courses towards the midline as the horizontal limb, and ascends dorsally into the medial septum as the vertical limb. Mixed with the fibres of the diagonal band of Broca are cell bodies of neurons, referred to as the nuclei of the horizontal and the vertical limbs of the diagonal band of Broca. These nuclei contain numerous CHOLINERGIC neurons that are part of the magnocellular cholinergic cell group in the basal forebrain.
Combination Effects of Forced Mild Exercise and GABAB Receptor Agonist on Spatial Learning, Memory, and Motor Activity in Striatum Lesion Rats
Published in Journal of Motor Behavior, 2019
Shaghayegh Modaberi, Soomaayeh Heysieattalab, Mehdi Shahbazi, Nasser Naghdi
The results of MWM test showed that distance and escape latency to find hidden platform significantly decreased in all groups in four training days. Comparison of MWM and probe tests showed that there was no significant difference between Str (IA) and Str (IA) + T groups. Therefore, mild forced treadmill exercise could not significantly improve spatial learning and memory impairment in striatum lesion groups. This result is inconsistent with previous studies for the duration of exercise. It has been reported that forced running paradigm for 5 weeks is effective in enhancing spatial learning and memory by increasing in the number of cholinergic neurons in the horizontal diagonal band of Broca in the septum (Ang, Dawe, Wong, Moochhala, & Ng, 2006). De Senna et al. has shown that exercise for 12 weeks improves short-term memory retention, enhances motor performance in diabetic rats, and affects important structural components of the striatal blood-brain barrier (de Senna et al., 2015). Overall, our findings suggest that exercise program could not improve impairment induced in striatum lesion by IA injection. However, further research is needed to consider various intensity and period of treadmill exercise and another types of exercise in this field, because this kind of exercise has a forced potential and animals may exposure stress during running. Results of open field test demonstrated a significant difference between Str (IA) and Str (IA) +T groups. So, mild forced treadmill exercise could improve motor activity consistent with previous studies (Loprinzi, Herod, Cardinal, & Noakes, 2013).
Effects of amylin on food intake and body weight via sympathetic innervation of the interscapular brown adipose tissue
Published in Nutritional Neuroscience, 2022
Kuikui Fan, Qiang Li, Deng Pan, Haodong Liu, Penghui Li, Rihan Hai, Chenguang Du
Neuronal nitric oxide synthase (nNOS) is a well-established neuronal messenger in the NTS [7] and controls synapse formation. nNOS regulates other neurotransmitters through the secretion of nitric oxide (NO) in the rat LDT [8] and human LC [9]. Moreover, studies have demonstrated that nNOS can regulate gluconeogenic neuroendocrine function in rats [7]. Extracellular signal-regulated kinase (ERK) is another transcription modulator [10] that is widely expressed in the CNS, especially in the LC [11] and is an effector of both metabotropic (slow) and ionotropic (fast) neurotransmission that have been implicated in normal brain function and CNS diseases [10]. Amylin time – and dose-dependently induces ERK phosphorylation in the AP, which shows that the ERK cascade can be activated in amylin-sensitive AP neurons [12]. Choline acetyl transferase (ChAT) is a definitive marker of cholinergic neuronal cells and plays a role in neurotransmission in the CNS [13]. The human amylin receptor and nicotinic acetylcholine receptors on the diagonal band of Broca (DBB) neurons act co-operatively to influence the excitability of DBB, which can result in human Alzheimer’s disease [14]. ChAT and GABA immunoreactivity were found to co-exist in the hypoglossal nuclei of rats [15]. Furthermore, studies have demonstrated that in rats, the LDT mainly consists of neurons that express both nNOS and ChAT [16] and that the ghrelin receptor was found to co-localise with ChAT in the LDT to regulate ghrelin- and fasting-induced food intake [17], which implies that activities associated with these play a role in the LDT. Therefore, these neurotrophic and signalling factors are also involved in the metabolic regulation process; the LDT and LC innervated nuclei may be involved in the modulation of amylin-induced food suppression and activation of thermogenesis.
Therapeutic approaches to cholinergic deficiency in Lewy body diseases
Published in Expert Review of Neurotherapeutics, 2020
Matthew J. Barrett, Leslie J. Cloud, Harsh Shah, Kathryn L. Holloway
In addition to a shared proteinopathy, Lewy body diseases demonstrate neurodegeneration in the same vulnerable regions. Neurotransmitter systems are especially vulnerable and there is degeneration of noradrenergic, dopaminergic, serotonergic, and cholinergic neurons across these diseases. This review will focus on degeneration of the cholinergic basal forebrain in Lewy body diseases. There are three main sources of cholinergic innervation in the central nervous system: cholinergic neurons in the basal forebrain, cholinergic neurons in the pedunculopontine nucleus (PPN) and lateral tegmental area, and cholinergic interneurons in the striatum. In addition to cholinergic innervation from the PPN, the cerebellum also receives cholinergic afferents from the medial vestibular nucleus and other brainstem nuclei [6]. Cholinergic neurons in the basal forebrain are divided into four nuclei based on their location and primary projections. Cholinergic neurons in the medial septal area (cholinergic nucleus 1; Ch1) and vertical limb of the diagonal band of Broca (cholinergic nucleus 2; Ch2) project to the hippocampus. Cholinergic neurons in the horizontal limb of the diagonal band of Broca project to the olfactory bulb (cholinergic nucleus 3; Ch3), and cholinergic neurons in the nucleus basalis of Meynert (NBM) project to the neocortex and amygdala (cholinergic nucleus 4; Ch4). Not all cholinergic neurons in these nuclei correspond to these primary target regions. For example, the visual cortex and posterior cingulate receive cholinergic inputs from Ch2 and Ch3 in addition to Ch4 [7]. Following this naming scheme, cholinergic neurons in the PPN comprise cholinergic nucleus 5 and cholinergic neurons in the lateral tegmental area comprise cholinergic nucleus 6 [8,9]. Degeneration of Ch4 is of greatest interest because its degeneration results in cortical (and amygdalar) cholinergic denervation, and this is associated with some of the more disabling neuropsychiatric symptoms observed in Lewy body diseases. For this reason, cortical cholinergic denervation resulting from Ch4 degeneration is an important target for symptomatic therapies in Lewy body diseases.