Degeneration of rat thalamic reticular neurons following intrathalamic domoic acid injection

Friedberg, Eric B.; Ross, Douglas T.

doi:10.1016/0304-3940(93)90060-x

Cited by 24 publications

(10 citation statements)

References 17 publications

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“…The involvement of the TRN in cognition is highlighted further following directly and indirectly induced neuronal lesions. Lesions of TRN regions usually induce forms of behavioural neglect, suggesting that the TRN is involved in attentional processes [29,39,78,159,271]. Before the Scheibels' discovery of the reticulothalamic projections [225], it was believed that TRN axons project diffusely into the whole cerebral cortex and this led to the proposal that this diencephalic structure was the terminal part of the ascending activating system [36,116,221].…”

Section: Thalamocortical Oscillationsmentioning

confidence: 99%

The thalamic reticular nucleus: structure, function and concept

Pinault

2004

Brain Research Reviews

571

480

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Section: Thalamocortical Oscillationsmentioning

confidence: 99%

The thalamic reticular nucleus: structure, function and concept

Pinault

2004

Brain Research Reviews

571

480

View full text Add to dashboard Cite

“…Several different lines of evidence support this concept of TRN function. First, lesions of the TRN, either experimentally induced or resulting from cardiac arrest or head injuries, seem to impair the ability to attend to stimuli (Friedberg and Ross, 1993;. Second, it has been found that C-FOS expression in the TRN is related to attention.…”

Section: Functional Implicationsmentioning

confidence: 99%

Synaptic targets of thalamic reticular nucleus terminals in the visual thalamus of the cat

Wang

Bickford

Horn

et al. 2001

J of Comparative Neurology

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A major inhibitory input to the dorsal thalamus arises from neurons in the thalamic reticular nucleus (TRN), which use gamma-aminobutyric acid (GABA) as a neurotransmitter. We examined the synaptic targets of TRN terminals in the visual thalamus, including the A lamina of the dorsal lateral geniculate nucleus (LGN), the medial interlaminar nucleus (MIN), the lateral posterior nucleus (LP), and the pulvinar nucleus (PUL). To identify TRN terminals, we injected biocytin into the visual sector of the TRN to label terminals by anterograde transport. We then used postembedding immunocytochemical staining for GABA to distinguish TRN terminals as biocytin-labeled GABA-positive terminals and to distinguish the postsynaptic targets of TRN terminals as GABA-negative thalamocortical cells or GABA-positive interneurons. We found that, in all nuclei, the TRN provides GABAergic input primarily to thalamocortical relay cells (93-100%). Most of this input seems targeted to peripheral dendrites outside of glomeruli. The TRN does not appear to be a significant source of GABAergic input to interneurons in the visual thalamus. We also examined the synaptic targets of the overall population of GABAergic axon terminals (F1 profiles) within these same regions of the visual thalamus and found that the TRN contacts cannot account for all F1 profiles. In addition to F1 contacts on the dendrites of thalamocortical cells, which presumably include TRN terminals, another population of F1 profiles, most likely interneuron axons, provides input to GABAergic interneuron dendrites. Our results suggest that the TRN terminals are ideally situated to modulate thalamocortical transmission by controlling the response mode of thalamocortical cells.

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“…Neuronal dysfunction in the so matosensory thalamus and cortex, manifest as ab normally increased receptive field size, has been found to be the consequence of selective chemical lesions of the rat RT made by intrathalamic injec tion of kainic acid (Lee et aI. , 1992), and the per sisting behavioral consequence of these RT lesions is inattention to tactile, auditory, and visual stimuli (Friedberg and Ross, 1993). Electrolytic lesions of the rat RT have also been reported to adversely affect performance on conditioned avoidance tasks, one type of test used to assess attention in rodents (Klingberg and Klingberg, 1982).…”

Section: T Ross and Dmentioning

confidence: 99%

Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

Ross

Graham

1993

J Cereb Blood Flow Metab

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Summary: Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cor tex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage fol lowing relatively short (:oS5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons oc curred in cases with longer (> lO-min) duration of arrest that was sufficient to produce extensive ischemic neuro nal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticotha-

show abstract

Degeneration of rat thalamic reticular neurons following intrathalamic domoic acid injection

Cited by 24 publications

References 17 publications

The thalamic reticular nucleus: structure, function and concept

The thalamic reticular nucleus: structure, function and concept

Synaptic targets of thalamic reticular nucleus terminals in the visual thalamus of the cat

Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

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