ISSN:
1432-0568
Keywords:
Key words Retrograde axonal transport
;
Somatosensory system
;
Pedunculopontine nucleus
;
Laterodorsal tegmental nucleus
;
Cholinergic
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Microiontophoretic studies of thalamic neurons suggests that nitric oxide (NO) plays an important role in mediating somatosensory transmission. The thalamus contains few nitric oxide synthase (NOS)-immunoreactive neurons; thus, the major source of thalamic NO is presumably from NOS-positive axons of extrathalamic origin. The cells of origin of these putative NOS-containing pathways to the ventrobasal thalamus were investigated in rats by combining retrograde tracing with immunocytochemistry for NOS. The location and morphology of double-labeled neurons was compared with that of single-labeled neurons. The most significant sources of NOS-containing afferents to the thalamus were found to be the pedunculopontine (PPN) and laterodorsal tegmental (LDT) nuclei. NOS-immunoreactive neurons in these cholinergic nuclei project bilaterally to the thalamus, most strongly ipsilaterally. The thalamus appears to be a major target of PPN, since even selective thalamic injections result in retrograde labeling of at least one third of its NOS-immunoreactive neurons. A significant number of NOS-negative neurons in both the PPN and LDT also project to the thalamus. Minor sources of NOS-containing thalamic afferents include the lateral hypothalamus, the dorsal, median and pontine raphe nuclei, the parabrachial nuclei, and the pontomedullary reticular formation. In all these structures, NOS-negative thalamopetal neurons greatly outnumber the NOS-positive ones. Ascending sensory pathways to the thalamus, including those from the sensory trigeminal nuclei, the dorsal column nuclei, and the spinal cord, as well as the auditory and vestibular centers, arise exclusively from NOS-negative neurons. The major NOS-positive projections are implicated in affective and alerting systems, supporting that NO may act to modulate attentiveness in thalamic relay nuclei.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004290050278
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