Activity of cholinergic neurons in the laterodorsal tegmental nucleus during emission of 22kHz vocalization in rats

2011 ◽  
Vol 225 (1) ◽  
pp. 276-283 ◽  
Author(s):  
Stefan M. Brudzynski ◽  
Amaka Iku ◽  
Alison Harness (neé Savoy)
Keyword(s):  
Cholinergic Neurons ◽  
Laterodorsal Tegmental Nucleus ◽  
Tegmental Nucleus

Cholinergic influence of the laterodorsal tegmental nucleus on neuronal activity in the rat lateral geniculate nucleus

1986 ◽  
Vol 56 (5) ◽  
pp. 1297-1309 ◽  
Author(s):  
Y. Kayama ◽  
M. Takagi ◽  
T. Ogawa
Keyword(s):  
Brain Stem ◽  
Lateral Geniculate Nucleus ◽  
Cholinergic Neurons ◽  
Photic Stimulation ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Laterodorsal Tegmental Nucleus ◽  
Tegmental Nucleus ◽  
Lateral Geniculate ◽  
Stimulation Of ◽  
Relay Neurons

The effect of stimulation of the laterodorsal tegmental nucleus (LDT) on the activity of single neurons in the dorsal lateral geniculate nucleus was studied in rats anesthetized with urethan. The LDT is the largest aggregation of cholinergic neurons in the brain stem that project to the thalamus, and in the rat is sufficiently compact to permit its localized stimulation. Position of stimulating electrodes was confirmed on histological sections processed with NADPH-diaphorase histochemistry, which in the rat brain stem selectively stains cholinergic neurons. Repetitive stimulation of the LDT at 200 Hz increased the firing rate of substantially all geniculate relay neurons and weakly depressed the activity of intrinsic interneurons. These effects usually occurred within several hundred milliseconds after the onset of stimulation and began to fade within a few seconds, despite continuing stimulation. The excitatory effects on relay neurons were blocked by scopolamine applied ionophoretically or intravenously, but not by noradrenergic antagonists, suggesting the cholinergic nature of LDT-induced excitation. During LDT stimulation the number of spikes evoked by photic stimulation of the receptive field of relay neurons usually increased, but it remained unchanged in a few cases. The increase was due to simple enhancement of photic responses or due to conversion of phasic type responses to tonic ones. As to the balance of background activity and photic responses, the effects of LDT stimulation varied from neuron to neuron. Even in a given neuron, the effects varied depending on its excitability level or the nature of the photic stimulation. These results show that the cholinergic projection from the LDT may be involved in the ascending reticular activating system, although the functional significance of the activating system in visual information processing in the geniculate nucleus remains to be clarified.

scholarly journals Interleukin-1 Inhibits Putative Cholinergic Neurons in Vitro and REM Sleep when Microinjected into the Rat Laterodorsal Tegmental Nucleus

SLEEP ◽  
2010 ◽  
Vol 33 (7) ◽  
pp. 919-929 ◽  
Author(s):  
Dario Brambilla ◽  
Isabella Barajon ◽  
Susanna Bianchi ◽  
Mark R. Opp ◽  
Luca Imeri
Keyword(s):  
Rem Sleep ◽  
Interleukin 1 ◽  
Cholinergic Neurons ◽  
Laterodorsal Tegmental Nucleus ◽  
Tegmental Nucleus

Cholinergic neurons with monoamine oxidase type B (MAOB)-activity in the laterodorsal tegmental nucleus of the mouse

1999 ◽  
Vol 271 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Keiko Ikemoto ◽  
Kunio Kitahama ◽  
Toshihiro Maeda ◽  
Michel Jouvet ◽  
Ikuko Nagatsu
Keyword(s):  
Monoamine Oxidase ◽  
Cholinergic Neurons ◽  
Type B ◽  
Laterodorsal Tegmental Nucleus ◽  
Tegmental Nucleus ◽  
Monoamine Oxidase Type B

scholarly journals Whole-brain mapping of monosynaptic inputs to midbrain cholinergic neurons

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Icnelia Huerta-Ocampo ◽  
Daniel Dautan ◽  
Nadine K. Gut ◽  
Bakhtawer Khan ◽  
Juan Mena-Segovia
Keyword(s):  
Basal Ganglia ◽  
Cholinergic Neurons ◽  
Female Rats ◽  
Functional Domains ◽  
Laterodorsal Tegmental Nucleus ◽  
Whole Brain ◽  
Tegmental Nucleus ◽  
Male And Female Rats ◽  
Wide Range ◽  
Basal Ganglia Structures

AbstractThe cholinergic midbrain is involved in a wide range of motor and cognitive processes. Cholinergic neurons of the pedunculopontine (PPN) and laterodorsal tegmental nucleus (LDT) send long-ranging axonal projections that target sensorimotor and limbic areas in the thalamus, the dopaminergic midbrain and the striatal complex following a topographical gradient, where they influence a range of functions including attention, reinforcement learning and action-selection. Nevertheless, a comprehensive examination of the afferents to PPN and LDT cholinergic neurons is still lacking, partly due to the neurochemical heterogeneity of this region. Here we characterize the whole-brain input connectome to cholinergic neurons across distinct functional domains (i.e. PPN vs LDT) using conditional transsynaptic retrograde labeling in ChAT::Cre male and female rats. We reveal that input neurons are widely distributed throughout the brain but segregated into specific functional domains. Motor related areas innervate preferentially the PPN, whereas limbic related areas preferentially innervate the LDT. The quantification of input neurons revealed that both PPN and LDT receive similar substantial inputs from the superior colliculus and the output of the basal ganglia (i.e. substantia nigra pars reticulata). Notably, we found that PPN cholinergic neurons receive preferential inputs from basal ganglia structures, whereas LDT cholinergic neurons receive preferential inputs from limbic cortical areas. Our results provide the first characterization of inputs to PPN and LDT cholinergic neurons and highlight critical differences in the connectome among brain cholinergic systems thus supporting their differential roles in behavior.

Does the ascending cholinergic projection inhibit or excite neurons in the rat thalamic reticular nucleus?

1986 ◽  
Vol 56 (5) ◽  
pp. 1310-1320 ◽  
Author(s):  
Y. Kayama ◽  
I. Sumitomo ◽  
T. Ogawa
Keyword(s):  
Cholinergic Neurons ◽  
Sensory Stimulation ◽  
Thalamic Reticular Nucleus ◽  
Resting Potential ◽  
Reticular Nucleus ◽  
Laterodorsal Tegmental Nucleus ◽  
Unit Recording ◽  
Tonic Firing ◽  
Tegmental Nucleus ◽  
Low Threshold

In rats anesthetized with urethan, neuronal activity was recorded in those portions of the thalamic reticular nucleus (TR) excitable by visual, somatosensory, or auditory input. Observations were made on changes in rate and pattern of discharge of these neurons during repetitive stimulation of the laterodorsal tegmental nucleus (LDT), which is composed of cholinergic neurons projecting to the thalamus. In general, TR neurons showed spontaneous activity consisting of sporadic bursts of several spikes and responded to sensory stimulation with bursts of spikes which repeated several times. Weak LDT stimulation depressed or eliminated the occurrence of both spontaneous and evoked burst discharges. When LDT stimulation was sufficiently strong, however, the majority of TR neurons resumed their tonic discharges. In some animals the cortical EEG was recorded simultaneously with unit recording in TR. Suppression of burst discharges in TR was obtained even with LDT stimulation weaker than the threshold for desynchronizing the EEG. The induction of tonic discharge, on the other hand, required stimulation strong enough to produce desynchronization. The effects of LDT stimulation, such as the suppression of bursts and the induction of tonic discharge, were mimicked by acetylcholine and were antagonized by scopolamine, both drugs being applied ionophoretically. Cooling of the visual cortex abolished LDT-induced tonic discharges of visual TR neurons. A recent report and our preliminary observation show that, when the resting potential is relatively hyperpolarized, TR neurons generated a burst of spikes superposed on a low-threshold broad spike, which is inactivated and replaced with tonic firing by depolarization. Supported by these facts, the present results suggest that cholinergic input depolarizes TR neurons directly and that further depolarization occurs indirectly via activated cortex when the LDT stimulation is sufficiently strong to desynchronize EEG.

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