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W Singer

Publications and source records attributed to W Singer.

At least 217 records · Page 12Linked to original sources
PubMed1985

The cholinergic innervation of the visual thalamus: an EM immunocytochemical study.

In this study we demonstrate at the ultrastructural level that both the dorsal lateral geniculate nucleus (dLGN), the visual relay of the thalamus, and the perigeniculate nucleus (PGN), the visual segment of the thalamic reticular nucleus (TRN), are densely innervated by fibres with Choline-Acetyl-Transferase (ChAT) like immunoreactivity. These axons make synaptic contacts with interneurones considered to be inhibitory, both in the PGN and within the synaptic glomeruli of the dLGN. In addition, Chat positive terminals form intra- and extraglomerular synapses with dendrites thought to arise from relay cells. We interpret these results as evidence for direct cholinergic modulation of both relay cells and inhibitory interneurones.

Animals↗
PubMed1985

Central control of developmental plasticity in the mammalian visual cortex.

Visual experience influences the development of visual cortex functions. By manipulating retinal activity the efficacy of excitatory connections between the eyes and cortical neurones can be modified dramatically. A criterion for the enhancement or impairment of transmission is the temporal contiguity of pre- and postsynaptic activation. For a change to occur it is necessary that the cortical cells respond to retinal activity but this condition is not sufficient. Further permissive gating signals of nonretinal origin are required. It is proposed that these "now print" signals act by controlling the Ca2+-conductance of cortical dendrites. The possible role of these activity dependent modifications is discussed in the context of the development of cooperatively coupled cell assemblies.

Action Potentials↗
PubMed1984

Ultrastructure and synaptic relations of neural elements containing glutamic acid decarboxylase (GAD) in the perigeniculate nucleus of the cat. A light and electron microscopic immunocytochemical study.

The perigeniculate nucleus of the cat (PGN) was examined at light and electron microscopic levels after immunocytochemical labeling for the gamma-aminobutyric acid (GABA) synthesizing enzyme, glutamic acid decarboxylase (GAD). In light microscopic sections, virtually all perikarya were found to be labeled (GAD+), as well as proximal dendrites, fibres and punctiform elements. Cells in the thalamic reticular nucleus (TRN) dorsal to PGN were also labeled. Ultrastructural analysis of PGN showed immunoreactivity in all somata, in dendrites and in the following vesicle containing profiles: 1.) F1 terminals, which are characterized by large size, dark mitochondria, and pleomorphic vesicles. These terminals form symmetrical synaptic contacts with somata, somatic spines and with dendrites of GAD+ PGN cells. 2.) F2 terminals, which are smaller than F1 terminals, contain also pleomorphic vesicles and frequently make serial synapses of the symmetric type with other F2 terminals. Presumably, F1 terminals are formed by collaterals of PGN-cell axons and F2 terminals by vesicle containing dendrites of PGN cells. Terminals devoid of immunoreactivity included: 1.) RLD terminals characterized by large size, round vesicles, dark mitochondria, and by asymmetric synaptic contacts with somata, especially with somatic spines, and with dendrites of GAD+ perigeniculate neurons; 2.) RSD terminals, characterized by small size, round vesicles and dark mitochondria, which make asymmetric synapses with GAD+ dendrites of medium and small size; 3.) Multivesicular (MV) terminals with variably shaped vesicles including dense core vesicles synapsing on GAD+ dendrites. There are reasons to believe that RSD terminals belong to corticofugal axons and RLD terminals to collateral axons of LGN relay cells. The origin of MV terminals remains to be determined. The GABAergic nature of the PGN cells conforms with the presumed function of these cells as mediators of inhibition of LGN relay cells. The complex synaptic relations observed between GAD+ elements in the PGN would allow for reciprocal inhibition between perigeniculate cells.

Animals↗
PubMed1984

A case for hypothalamic acromegaly: a clinicopathological study of six patients with hypothalamic gangliocytomas producing growth hormone-releasing factor.

We report the histological, ultrastructural, and immunocytochemical features of six hypothalamic gangliocytomas associated with pituitary GH cell adenomas and/or acromegaly. In four patients, the gangliocytoma was intrasellar, and no hypothalamic investigation was performed; in two patients, autopsy confirmed hypothalamic involvement. Four patients had a gangliocytoma associated with pituitary GH cell adenoma and acromegaly; electron microscopy demonstrated an intimate association between neurons and adenomatous GH cells. One patient had a gangliocytoma and a GH cell adenoma but no clinical evidence of acromegaly. In the sixth patient, clinical and biochemical acromegaly was manifest, but no pituitary adenoma was demonstrated. Using immunocytochemistry, human pancreatic tumor GRF (hptGRF-40) was localized in the majority of neurons of all six gangliocytomas. The pituitary adenomas and nontumorous adenohypophyses were negative for hptGRF-40. In addition, somatostatin, glucagon, and GnRH were demonstrated within some neurons of several tumors; insulin and gastrin stains were equivocal. These findings confirm previous proposals of production of a GRF by such gangliocytomas. While the significance of other peptides found in some of the tumors is uncertain, the presence of hptGRF-40 in neurons of these gangliocytomas supports the theory that GRF excess is the mechanism responsible for over-production of GH and provides evidence for a syndrome of hypothalamic acromegaly.

Acromegaly↗
PubMed1984

Immunohistochemical localization of neuron-specific enolase in the human hypophysis and pituitary adenomas.

Neuron-specific enolase (NSE) was localized, using the immunoperoxidase technique, in the cytoplasm of the five adenohypophyseal hormone-secreting cell types, and in nerve fibers of the pars nervosa of the human pituitary. Crooke's hyaline material was negative. Neuron-specific enolase was found in all pituitary adenoma types; there was no correlation between degree of granularity or differentiation of tumor cells and intensity of NSE immunopositivity. One hypothalamic hamartoma was positive for NSE; a craniopharyngioma and a neurohypophyseal granular cell tumor were not. Neuron-specific enolase was present in peptide hormone-producing endocrine cells outside the pituitary and in their tumors; the majority of other tumors were negative for NSE, although one breast carcinoma, one ovarian cystadenocarcinoma, and one lymphoma were positive for NSE. In control studies, absorption of NSE antisera with growth hormone abolished immunoreactivity; there was no immunologic cross-reaction demonstrable by radioimmunoassay.

Adenoma↗
PubMed1983

Pituitary and hypothalamic dysfunction in a patient with a basal encephalocele.

A 31 year old Chinese man was found to have a large basal encephalocele extending into the nasopharynx associated with a cleft palate and chiasmal damage producing visual field defects. He was found to have marked hypothalamic-pituitary dysfunction including deficiencies of growth hormone, thyrotropin, adrenocorticotropic hormone and gonadotropins, diabetes insipidus, adipsia with essential hypernatremia and poikilothermia. This man illustrates the importance of careful assessment of patients with craniofacial anomalies and outlines a simple investigational protocol.

Adult↗
PubMed1983

Direct and indirect visual inputs to superficial layers of cat superior colliculus: a current source-density analysis of electrically evoked potentials.

1. The spatiotemporal pattern of visual inputs to the stratum griseum superficiale (SGS) and stratum opticum (SO) of the cat superior colliculus (SC) has been determined by an analysis of the current sinks occurring during postsynaptic activity following stimulation of each optic nerve (ON) and the optic chiasm (OX). Electrolytic lesions were used to determine the locations of the five major current sinks. 2. Direct SC afferents from the contralateral ON induced three current sinks whose maxima were located a) in the upper part of the SGS, b) in the middle part of the SGS, and c) in the lower part of the SGS and upper part of the SO. These three sinks were generated by three afferent fiber groups conducting in the optic nerve with modal and maximum velocities, respectively, of a) 4 and 5 m/s (slow W-group), b) 7 and 10 m/s (fast W-group), and c) 32 and 43 m/s (Y-group). 3. Indirect SC inputs from the contralateral ON via the ipsilateral visual cortex were identified by comparing the pattern of current sinks generated by OX stimulation before and after cortical ablation. The most prominent and fastest indirect sink (Y-group) was found in ;the lower half of the SGS and uppermost part of the SO. Low-amplitude, long-latency indirect current sinks were also found in the upper and lower thirds of the SGS. 4. The principal conclusions of this report are first, that the SGS is divisible into three physiologic regions according to the spatiotemporal pattern of excitatory synaptic activity generated by the afferent inputs and second, that there is a spatiotemporal matching of the direct collicular afferents from the contralateral retina and the indirect retinal afferents relaying through the ipsilateral visual cortex.

Animals↗
PubMed1983

Mechanisms of experience dependent self-organization of neuronal assemblies in the mammalian visual system.

Neuronal activity and hence sensory signals serve as a shaping factor in the development of the structural and functional organization of the mammalian visual cortex. The electrical responses of cortical neurons control the consolidation and repression of interneuronal connections. The algorithms of this activity dependent selection process closely resemble those proposed by Hebb for adaptative synaptic connections. These local modifications depend in addition on internally generated gating signals. The latter exert a "now print" function by controlling Hebbian modifications as a function of the animal's central state. These permissive gating signals are related to mechanisms which control arousal and visual attention. Evidence as available which suggests that the activation of voltage dependent Ca++ -channels in the dendrites of cortical neurones is the trigger signal for a Hebbian modification. The permissive gating signals appear to control the probability of Ca++ -channel activation. It is concluded that these activity-dependent modifications of neuronal connectivity have an function. They are capable of developing assemblies of cooperating neurones by specifying according to functional criteria which neurones should interact with each other.

Adaptation, Physiological↗
PubMed1982

Central core control of developmental plasticity in the kitten visual cortex: I. Diencephalic lesions.

In five, dark-reared, 4-week-old kittens the posterior two thirds of the corpus callosum were split, and a lesion comprising the intralaminar nuclei was made of the left medial thalamic complex. In addition, the right eye was closed by suture. Post-operatively, the kittens showed abnormal orienting responses, neglecting visual stimuli presented in the hemifield contralateral to the side of the lesion. Sudden changes in light, sound, or somatosensory stimulation elicited orienting responses that all tended toward the side of the lesion. These massive symptoms faded within a few weeks but the kittens continued to neglect visual stimuli in the hemifield contralateral to the lesion when a second stimulus was presented simultaneously in the other hemifield. Electrophysiologic analysis of the visual cortex, performed after the end of the critical period, revealed marked interhemispheric differences. In the visual cortex of the normal hemisphere most neurons were monocular and responded exclusively to stimulation of the open eye, but otherwise had normal receptive field properties. In the visual cortex of the hemisphere containing the thalamic lesion, the majority of the neurons remained binocular. In addition, the selectivity for stimulus orientation and the vigor of responses to optimally aligned stimuli were subnormal on this side. Thus, the same retinal signals, which in the control hemisphere suppressed the pathways from the deprived eye and supported the development of normal receptive fields, failed to do either in the hemisphere containing the thalamic lesion. Apparently, experience-dependent changes in the visual cortex require both retinal stimulation and the functioning of diencephalic structures which modulate cortical excitability and control selective attention.

Animals↗
PubMed1982

Central core control of developmental plasticity in the kitten visual cortex: II. Electrical activation of mesencephalic and diencephalic projections.

Fifteen dark-reared, 4- to 5-week-old kittens were stimulated monocularly with patterned light while they were anesthetized and paralyzed. Six of these kittens were exposed to the light stimuli only, in four kittens the light stimuli were paired with electric stimulation of the mesencephalic reticular formation and in five kittens with electric activation of the medial thalamic nuclei. Throughout the conditioning period, the ocular dominance of neurons in the visual cortex was determined from evoked potentials that were elicited either with electric stimulation of the optic nerves or with phase reversing gratings of variable spatial frequencies. In two kittens, ocular dominance changes were assessed after the end of the conditioning period by analyzing single unit receptive fields. Monocular stimulation with patterned light induced a marked shift of ocular dominance toward the stimulated eye, when the light stimulus was paired with electric activation of either the mesencephalic reticular formation or of the medial thalamus. Moreover, a substantial fraction of cells acquired mature receptive fields. No such changes occurred with light or electric stimulation alone. It is concluded that central core projections which modulate cortical excitability gate experience-dependent modifications of connections in the kitten visual cortex.

Animals↗
PubMed1982

Binocular deprivation can erase the effects of preceding monocular or binocular vision in kitten cortex.

Kittens were given visual experience through one or both eyes for two weeks around the peak of the sensitive period. Subsequently they were binocularly deprived for at least one year. This period of pattern deprivation erased completely the effects of the preceding temporary experience. Ocular dominance distribution, orientation selectivity and response quality of the cortical units resembled those obtained from kittens which are contour-deprived throughout their early postnatal development. This suggests that the effect of visual experience is not to engrave irreversibly certain features of the early visual world, but to adapt the cortex continuously and in an integrative fashion to features which are prominent throughout the sensitive period.

Animals↗
PubMed1982

Central gating of developmental plasticity in kitten visual cortex.

1. In nine 4-week-old, dark-reared kittens we sutured one eye closed and rotated the other surgically. The kittens then grew up in a normally lighted animal colony with adequate room to play.2. For about two weeks after surgery their visual-motor co-ordination did not differ from that of kittens with conventional monocular deprivation; then severe disturbance of visually guided behaviour became progressively more apparent until, after another two to three weeks, all the kittens stopped responding to most visual stimuli entirely. At that point their behaviour in an unfamiliar environment closely resembled that of binocularly deprived cats exposed to light for the first time.3. Four weeks (n = 3) and 6 months (n = 6) after surgery, we examined the visual cortex with single-unit recordings, and with evoked potentials elicited by electrical stimuli and patterned lights. We obtained the single-unit recordings from 586 neurones of the striate cortex in both hemispheres, both ipsi- and contralateral to the deprived eye.4. The single-unit recordings and the evoked potentials showed a clear relation between the kitten's abnormal visual behaviour and the functioning of the striate cortex. Only about half the normal percentage of cells responded to light, and most of those which did react had abnormal receptive field properties: they responded only sluggishly even when the light stimuli were aligned optimally.5. We also evoked cortical potentials with phase alternating square wave gratings of variable contrast and spatial frequency. The amplitude of the potentials indicated that contrast-sensitivity was reduced at all spatial frequencies.6. In the kittens tested 4 weeks after surgery, ocular dominance had shifted toward the open rotated eye but this shift was considerably less pronounced than in control kittens monocularly deprived for a comparable period of time.7. In the kittens tested 6 months after surgery fewer cells than normal were binocular; ocular dominance had not shifted towards the open eye.8. Numerous control experiments indicated that these abnormalities did not result from transitory immobilization of the eye alone nor from lesions of the retina or of the optic nerve.We infer that a central mechanism prevents the inappropriate signals from the rotated eye from influencing the consolidation of central pathways.

Animals↗