Cuneate nucleus

Intracellular steroid receptors, which alter gene expression, exist for corticosteroids, oestrogens and progesterone in the brain, as in the periphery but they cannot account for the relatively rapid depression of CNS function induced by some steroids. This was explained when Harrison and Simmonds (1984) discovered that alphaxalone (the steroid anaesthetic) potentiated the duration of GABA-induced currents at the GABAa receptor in slices of rat cuneate nucleus just like the barbiturates (Fig. 13.6). Of the... 

Lan CT, Shieh JY, Wen CY, Tan CK, Ling EA. 1996. Ultrastruc-tural localization of acetylcholinesterase and choline acet-yltransferase in oligodendrocytes, glioblasts and vascular endothelial cells in the external cuneate nucleus of the gerbil. Anat Embryol (Berl) 194 177-185. 

De Biasi S, Vitellaro-Zuccarello I, Bernardi P, Valtschanoff JG, Weinberg RJ (1994a) Ultrastructural and immunocytochemical characterization of primary afferent terminals in the rat cuneate nucleus. J Comp Neurol 547 275-287. 

Abbreviations Al = primary auditory area ac = anterior commissure Acc = accumbens nucleus AON = anterior olfactory nucleus BF = barrel field BLA = basolateral nucleus of the amygdala CAl = cornu ammonis 1 CA3 = cornu ammonis 3 cc = corpus callosum Cg = cingulate area CPu = caudate-putamen DCb = deep cerebellar nuclei DCo = dorsal cochlear nucleus DG = dentate gyrus DMV = dorsal motor nucleus of the vagus nerve ECu = external cuneate nucleus EP = external plexiform layer ER = entorhinal cortex f = fornix Fa = facial nucleus fa = facial nerve fr = fasciculus retroflexus G1 = glomerular layer GPe = (external segment of the)... 

GAD-immunoreactive neurons in the parasolitary and cuneate nuclei could be labelled after injection of retrograde tracers in the inferior olive of the rat (Nelson and Mugnaini, 1989). These nuclei, therefore, provide additional GABAergic projections to the inferior olive. The projection of the ipsilateral parasolitary nucleus was located in the medial subnucleus c of the caudal MAO by these authors. Connections from the parasolitary nucleus (indicated as the lateral solitary nucleus) also were documented in earlier studies by Loewy and Burton (1978) and Molinari (1985) in the cat. The inhibitory connections from the cuneate nucleus in the rat are crossed and terminate in the medial DAO. A similar GABAergic cuneo-olivary pathway appears to be responsible... 

Fig. 201. HRP- and cholineacetyl transferase (ChAT)-labelled neurons in the vestibular complex of rabbit following an HRP injection into the left ventral paraflocculus and immunocytochemistry with an antibody against ChAT. (A) The black and stippled areas correspond to dense and less dense HRP concentrations. The solid arrows delinate borders between the flocculus, ventral and dorsal paraflocculus. (B) 1-5 are rostral-caudal brainstem sections through the left vestibular complex spaced approximately 400 fim apart. The filled circles correspond to HRP- and ChAT-labelled neurons. The open circles correspond to ChAT-labelled neurons only. The filled diamonds correspond to HRP-labelled neurons only. MVN and DVN, medial and descending vestibular nucleus NPH, nucleus prepositus hypoglossi X, nucleus X ICP, inferior cerebellar peduncle N V and tr V, trigeminal nucleus and tract ION, inferior olivary nucleus N VII, facial nucleus VII, facial nerve DMN X, dorsal motor nucleus of the vagus CE, external cuneate nucleus CN, cochlear nucleus Pyr, pyramidal tract FI, flocculus dPf, dorsal paraflocculus vPf, ventral paraflocculus. Barmack et al. (1992b).

Fig. 206. Plots of the distribution of mossy fibers on the dorsal (caudal) surface of lobule IV in the cat. A. Fibers from the central cervical nucleus (Matsushita and Tanami, 1987). B. Fibers from the medial vestibular nucleus (Matsushita and Wang, 1987). C. Fibers from the thoracic cord (Yaginuma and Matsushita, 1987). D. Fibers from the spinal border cells (Yaginuma and Matsushita, 1986). E. Fibers from the external cuneate nucleus (Gerrits, 1985). F. Fibers from the basal pontine nuclei (Gerrits, 1985). G. Localization of AChE in the molecular layer on the dorsal surface of lobule IV. Inset sagittal section of the cerebellum of the cat.

CGRP-containing neurons were double-labelled with HRP from injections in the cerebellum of the cat in the lateral reticular nucleus, the external cuneate nucleus, the descending vestibular nucleus and in the lateral and ventral divisions of the basilar pons (Bishop, 1992). The origin of a major contingent of CGRP-immunoreactive mossy fibers from the pontine nuclei may explain their preferential distribution to the cerebellar hemisphere. 

Grant G (1962) Projection of the external cuneate nucleus onto the cerebellum in the cat. An experimental study using silver methods. Exp. Neurol. 5, 179-195. 

Jasmin L, Courville J (1987a) Distribution of external cuneate nucleus afferents to the cerebellum I. Notes on the projections from the main cuneate and other adjacent nuclei. An experimental study with radioactive tracers in the cat. J. Comp. Neurol, 261, 481-496. 

Barbiturates act throughout the CNS nonanesthetic doses preferentially suppress polysynaptic responses. Facilitation is diminished, and inhibition usually is enhanced. The site of inhibition is either postsynaptic, as at cortical and cerebellar pyramidal cells and in the cuneate nucleus, substantia nigra, and thalamic relay neurons, or presyruq tic, as in the spinal cord. Enhancement of inhibition occurs primarily at synapses where neurotransmission is mediated by GABA acting at GABA receptors. 

SiMMONDS, M. A., and Pickles, H., 1978, Presynaptic action of GABA in isolated slices of cuneate nucleus and olfactory cortex, in Iontophoresis and Transmitter Mechanisms in the Mammalian Central Nervous System (R. W. Ryall and J. S. Kelly, eds.), Elsevier/North-Holland, Amsterdam. 

Similar observations were made in experiments on the cuneate nucleus. When a forelimb nerve was excited, the increase in extracellular aj and the slow tissue potential changes (including the P wave recorded after a single volley) increased with depth and they all reached a maximum at the same depth. The amplitude of these slow potential changes showed a high positive correlation (r = 0.945 n = 45) with changes in recorded simultaneously at various positions in or close to the cuneate nucleus. 

These observations suggested that the slow tissue potentials in the presynaptic terminal regions may be caused by the extracellular accumulation of K" during afferent activity. However, the sensitivity of these terminals to raised levels of extracellular a is not known. Therefore in further experiments we artificially raised a in the cuneate nucleus by micro-injection of KCl or by superfusing the dorsal surface of the medulla with K-enriched solutions. 

Fig, 9, Diagram of stimulating and recording arrangements in eo periments where extracellular aj was artificially increased. Rj - antidromic and E2 - orthodromic responses evoked by stimulation of afferent fibre terminals in the cuneate nucleus via third micro-electrode attached to K electrode. 

A, Potassium activity recorded in cuneate nucleus depth 0.6 mm... 

---