The Isodendritic Core of the Brain Stem

Ramon-Moliner, E.; Nauta, Walle J. H.

doi:10.1007/978-1-4684-7920-1_14

Cited by 18 publications

(21 citation statements)

References 41 publications

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“…When stained only for biocytin to reveal fully the dendritic processes of the cells, cholinergic neurones were found to have multiple, though sparsely branched, long radiating dendrites that extend for some distance through the neuropil within the substantia innominata. The considerable dendritic expansion of these cells indicates that, like neurones of the brainstem reticular formation (Ramon-Moliner & Nauta, 1966), the cholinergic neurones extend their dendrites into the path of multiple fibre systems and, thereby, potentially receive input from multiple afferent sources. In ultrastructural studies of identified cholinergic basal forebrain neurones, it has been found that the synaptic input to these cells is greatest on the dendrites and, in fact, of the highest density upon the distal dendrites (Ingham, Bolam, Wainer & Smith, 1985).…”

Section: Discussionmentioning

confidence: 99%

Rhythmical bursts induced by NMDA in guinea‐pig cholinergic nucleus basalis neurones in vitro.

Khateb

Fort

Serafin

et al. 1995

The Journal of Physiology

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1. Intracellular recordings were performed in neurones within the basal forebrain of guinea-pig brain slices. Following injection of biocytin (or biotinamide), a subset of recorded neurones which displayed distinct intrinsic membrane properties were confirmed as being cholinergic by immunohistochemical staining for choline acetyltransferase (ChAT). They were all located within the nucleus basalis magnocellularis. The response of the cholinergic cells to NMDA and to the agonists of the other glutamate receptors was tested by bath application of NMDA, t-ACPD, AMPA and kainate. 2. When depolarized from a hyperpolarized level, cholinergic basalis neurones display the intrinsic ability to discharge in rhythmic bursts that are generated by low-threshold Ca2P spikes. In control solution, these rhythmic bursts were not sustained for more than 5-6 cycles. However, in the presence of NMDA when the membrane was held at a hyperpolarized level, low-threshold bursting activity was sustained for prolonged periods of time. This activity could be reversibly eliminated by D(-)-2-amino-5-phosphonopentanoic acid (D-AP5), showing that it depended upon specific activation of NMDA receptors. 3. NMDA-induced, voltage-dependent, rhythmic depolarizations persisted in the presence of tetrodotoxin (ITX), indicating that they did not depend upon a ITX-sensitive Nae current and were generated postsynaptically. The rhythmic depolarizations were, however, eliminated by the partial replacement of Na+ with choline, demonstrating that they did depend upon Nae, the major carrier of the NMDA current. 4. In the presence of TTX, the NMDA-induced rhythmic depolarizations were also eliminated by removal of Ca2P from or addition of Ni2+ to the bath, indicating that they also depended upon Ca2+, which is carried by both the NMDA current and the low-threshold Ca2+ current. The duration of the rhythmic depolarizations was increased in the presence of apamin, suggesting that the repolarization of the cells depended in part upon a Ca2+-activated K+ (SK) conductance, but that other mechanisms were additionally involved in the repolarization phase of the bursting. 5. In both the absence and presence of TTX, the NMDA-induced rhythmic activity persisted when Mg2+ was removed from the medium, indicating that the sustained rhythmic depolarizations did not hinge upon the Mg2+ block of the NMDA channels during hyperpolarization. The voltage dependence of the NMDA-induced rhythmic depolarizations in the absence of Mg2+ appeared to be determined by the properties of the low-threshold Ca2P spike in the cholinergic basalis neurones.6. These in vitro results show that activation of NMDA channels excites cholinergic basalis neurones and may drive them into tonic firing if allowed to depolarize fully or maintain them in a rhythmic bursting mode if they are simultaneously held at a hyperpolarized level from which intrinsic lowthreshold Ca2P spikes are triggered. Assuming the presence of contingent hyperpolarizing afferent input, these data suggest that brainstem and cortica...

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Section: Discussionmentioning

confidence: 99%

Rhythmical bursts induced by NMDA in guinea‐pig cholinergic nucleus basalis neurones in vitro.

Khateb

Fort

Serafin

et al. 1995

The Journal of Physiology

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“…Its neurons have widespread outputs, heterogeneous inputs, and overlapping dendritic fields that dip into passing fiber tracts. These features have led to the characterization of the nucleus basalis as a telencephalic extention of the brainstem reticular formation (Ramon-Moliner and Nauta 1966). From the vantage point of behavioral neuroanatomy, therefore, the nucleus basalis sits at the confluence of the mediobasal limbic system and the rostral reticular formation.…”

Section: Behavioral Neuroanatomy Of Cortical Cholinergic Innervationmentioning

confidence: 99%

The Cholinergic Lesion of Alzheimer's Disease: Pivotal Factor or Side Show?

Mesulam¹

2004

Learn. Mem.

432

340

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A profound loss of cortical cholinergic innervation is a nearlyinvariant feature of advanced Alzheimer's disease (AD). The temporal course of this lesion and its relationship to other aspects of the disease have not yet been fully clarified. Despite assertions to the contrary, a review of the evidence suggests that a perturbation of cholinergic innervation is likelyto be present even in the veryearlystages of AD. This cholinergic lesion is unlikelyto be a major determinant of the clinical symptoms or of the neuropathological lesions. Nonetheless, it almost certainly contributes to the severityof the cognitive and behavioral deficits, especiallyin the areas of memoryand attention. The cholinergic lesion mayalso influence the progression of the neuropathological process through complex interactions with amyloidogenesis, τ phosphorylation and neuroplasticity.

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“…The patterns of expression of trkA on the one hand and trkB/C on the other show interesting correlations: trkA is primarily expressed in neurons with relatively large, overlapping dendritic fields and functions that have been categorized as 'integrative' [Ramon-Moliner and Nauta, 1966], as opposed to neurons with relatively restricted dendritic and axonal fields and 'analytical' functions that correlate more with trkB and trkC expression ( fig. 2 A, B).…”

Section: Rest Of the Cnsmentioning

confidence: 99%

Comparative Analysis of Neurotrophin Receptors and Ligands in Vertebrate Neurons: Tools for Evolutionary Stability or Changes in Neural Circuits?

Bartheld

Fritzsch

2006

Brain Behav Evol

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To better understand the role of multiple neurotrophin ligands and their receptors in vertebrate brain evolution, we examined the distribution of trk neurotrophin receptors in representatives of several vertebrate classes. Trk receptors are largely expressed in homologous neuronal populations among different species/classes of vertebrates. In many neurons, trkB and trkC receptors are co-expressed. TrkB and trkC receptors are primarily found in neurons with more restricted, specialized dendritic and axonal fields that are thought to be involved in discriminative or ‘analytical’ functions. The neurotrophin receptor trkA is expressed predominantly in neurons with larger, overlapping dendritic fields with more heterogeneous connections (‘integrative’ or ‘modulatory’ systems) such as nociceptive and sympathetic autonomic nervous system, locus coeruleus and cholinergic basal forebrain. Surveys of trk receptor expression and function in the peripheral nervous system of different vertebrate classes reveal trends ranging from dependency on a single neurotrophin to a more complex dependency on increasing numbers of neurotrophins and their receptors, for example, in taste and inner ear innervation. Gene deletion studies in mice provide evidence for a complex regulation of neuronal survival of sensory ganglion cells by different neurotrophins. Although expression of neurotrophins and their receptors is predominantly conserved in most circuits, increasing diversity of neurotrophin ligands and their receptors and a more complex dependency of neurons on neurotrophins might have facilitated the formation of at least some new neuronal entities.

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The Isodendritic Core of the Brain Stem

Cited by 18 publications

References 41 publications

Rhythmical bursts induced by NMDA in guinea‐pig cholinergic nucleus basalis neurones in vitro.

Rhythmical bursts induced by NMDA in guinea‐pig cholinergic nucleus basalis neurones in vitro.

The Cholinergic Lesion of Alzheimer's Disease: Pivotal Factor or Side Show?

Comparative Analysis of Neurotrophin Receptors and Ligands in Vertebrate Neurons: Tools for Evolutionary Stability or Changes in Neural Circuits?

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