GABA neurons are the major cell type of the nucleus reticularis thalami

116

Immunocytochemical methods were used to identify neurons in the ventral posterior nucleus of the cat and Galago senegalensis that contain glutamic acid decarboxylase (GAD), the synthetic enzyme for the inhibitory neurotransmitter, GABA. In both species GAD-immunoreactive neurons make up about 30% of the total neurons in the ventral posterior nucleus and form a distinct class of small cells. After cortical injections of horseradish peroxidase (HRP), GAD-immunoreactive cells are not labeled with HRP and may, therefore, be GABAergic local circuit neurons. Comparison of the dendritic morphology of GAD-immunoreactive neurons with that of HRP-filled projection neurons reveals that the morphology of the GAD-containing neurons is distinct and, in particular, that the GAD-immunoreactive neurons display fewer primary dendrites. The relay neurons, in turn, can be divided into classes based on dendritic morphology and cell body size.The idea that thalamic neurons could be divided into classes based on morphological criteria has a long history. According to Rambn y Cajal (1909, the most fundamental distinction was between the neurons with long axons that project to the cerebral cortex and neurons with short axons that were thought to be local circuit neurons. Cajal found the neurons with short axons or "cellules 6 cylindre-axe court" to be distributed widely in the nervous system and to be especially numerous in the thalamus and neocortex of higher mammals. The neurons with long axons (or projection neurons) could be further subdivided into classes based on their appearance in Golgi material. T6mb61 recently (1967) identified at least two classes in the case of the somatosensory ventral posterior nucleus of the cat.

Section: Resultssupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Glutamic acid decarboxylase-immunoreactive neurons and horseradish peroxidase-labeled projection neurons in the ventral posterior nucleus of the cat and Galago senegalensis

Penny¹,

Fitzpatrick²,

Schmechel³

et al. 1983

116

“…Nonetheless, our experiments provide substantial evidence that somatosensory transmission in the rat VB thalamus is facilitated directly by an excitatory corticothalamic projection to VB, indirectly by the disinhibition of inhibitory thalamic reticular neurons (Angel, 1983;Houser et al, 1980;Yingling and Skinner, 1976), or by a combination of these mechanisms.…”

Section: Discussionmentioning

confidence: 72%

Corticofugal influences of S1 cortex on ventrobasal thalamic neurons in the awake rat

Yuan¹,

Morrow²,

Casey³

1986

Corticofugal influences on the responses of 39 ventrobasal (VB) thalamic neurons to repetitive stimuli were studied in awake rats by focally suppressing the evoked and spontaneous electrocortical activity of the primary (Sl) somatosensory cortex with magnesium or lidocaine plus magnesium. Suppression of the Sl cortex reduced the number of spikes discharged by 19 (66%) of 29 VB units in response to each of 25 electrical stimuli delivered to the medial lemniscus; 9 units were unaffected and 1 showed an increased response to l-10 Hz stimuli. The responses of 6 (38%) of 16 VB units to electrical somatic stimuli were also reduced following Sl cortical suppression; 9 units were unaffected and 1 showed an increased response to 20-40 Hz stimuli. A comparison of the reduced responsiveness of 5 units studied during medial lemniscal and somatic stimulation did not reveal any additional response attenuation attributable to subthalamic corticofugal influences. We conclude that, in the awake rat, somatosensory transmission to VB thalamic neurons is primarily facilitated by Sl corticothalamic neurons.In previous work (Yuan et al., 1985), we have shown that, in the anesthetized rat, focal suppression of the S 1 cortex decreases the excitability of ventrobasal (VB) thalamic neurons, as tested by their responses to repetitive somatic or medial lemniscal stimuli delivered at various frequencies. A comparison of the effect of cortical suppression on the responses of VB neurons to somatic and medial lemniscal inputs suggested that excitatory corticothalamic neurons mediated a significant fraction of the corticofugal influence.Because general anesthesia affects the activity of neurons in the cerebral cortex, we wished to determine if focal suppression of S 1 corticofugal influences in the awake preparation has effects that are substantially different from those seen in the anesthetized animal. For example, excitatory or inhibitory corticofugal effects on the dorsal column nuclei or the dorsal horn could be increased relative to facilitatory corticothalamic activity. The suppression of Sl cortex would then be expected to have a greater effect when VB neurons were activated cutaneously than when medial lemniscal stimulation was used. In the series of experiments reported here, we present evidence that, in the awake as in the anesthetized rat, Sl corticothalamic neurons facilitate somatosensory transmission in the VB thalamus and that, in the awake rat, corticothalamic facilitation appears to predominate over other inhibitory corticofugal influences.Received Dec. 6, 1985; revised Apr. 14, 1986; accepted Apr. 17, 1986. This work was supported by the Veterans Administration. Materials and MethodsFourteen male albino rats, weighing 350-550 gm, were used in this study. Most of the rats were adapted to a restraining device (see below) for 2-3 d before being selected for surgery. Each rat was anesthetized (chloral hydrate, 40 mg/lOO gm), and a plastic cylinder, 6 mm in diameter and 8 mm in height, was implanted in the skull overlying the i...

“…Four of these subjects were nonenucleated rats, two of which received cerebroventricular injections of colchicine 48 hr before sacrifice by a procedure described previously (Houser et al, 1980). This treatment was performed to enhance GAD-positive product within cell bodies and dendrites , and both of the colchicine-treated rats were used exclusively for light microscopic preparations.…”

Section: Animalsmentioning

confidence: 99%

Immunocytochemical localization of glutamic acid decarboxylase in normal and deafferented superior colliculus: evidence for reorganization of gamma-aminobutyric acid synapses

Cr¹,

Lee²,

Vaughn³

1983

There is circumstantial evidence that GABAergic synaptic terminals in the superior colliculus might become reorganized in response to a loss of the retinal innervation of this brain region. The present investigation tests this possibility by identifying y-aminobutyric acid (GABA) neurons and their synaptic relationships with an immunocytochemical localization of the GABA-synthesizing enzyme, glutamic acid decarboxylase (GAD), and by comparing these synaptic relationships in normal superior colliculus with those present 6 and 16 weeks after unilateral eye removal. In normal superior colliculus, light microscopy revealed a much denser concentration of GAD-positive reaction product in the superficial layers than in the intermediate and deep collicular layers. Most of this reaction product was contained within small, punctate structures, but GAD-positive somata and proximal dendrites also were observed. Electron microscopy showed that GAD was localized in numerous synaptic terminals, including those that were the presynaptic elements of dendrodendritic synapses. The vast majority of GAD-positive presynaptic elements formed symmetric synaptic junctions. In addition, GAD-positive profiles frequently were postsynaptic to unstained retinal terminals as well as presynaptic to unstained dendritic profiles and thus participated in serial synaptic relationships. Furthermore, both retinal and GAD-positive elements commonly were presynaptic to the same postsynaptic dendrite, and often these synaptic contacts were adjacent to each other. In deafferented specimens, profiles with the characteristics of retinal axon terminals were not observed, whereas there appeared to be no reduction of GAD-positive synaptic profiles. However, there was a marked and statistically significant increase in the proportion of GADpositive presynaptic terminals that formed asymmetric synaptic contacts in superior colliculus deprived of retinal input. This change indicates that partial deafferentation induces a reorganization of GAD-positive synapses. The long-term presence of the GABA-synthesizing enzyme within reorganized synaptic terminals also suggests that such presynaptic elements could produce and, presumably, release neurotransmitter.Previous investigations have sought evidence in a number of different brain regions for lesion-induced synaptic reorganization of neurons that use y-aminobutyric acid (GABA) as a neurotransmitter, but such alterations still remain to be demonstrated unequivocally.