Electrical stimulation of the brain stem and subsequent sleep.
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Animals↗
Biomedical subjects
C J Frederickson
Publications and source records attributed to C J Frederickson.
The effect of lateral geniculate lesions on phasic electrical activity of the cortex during desynchronized sleep in the cat.
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Animals↗
Movement-dependent and movement-independent changes in hippocampal RSA in cats.
EEG was recorded from the dorsal hippocampus of cats during walking in situations intended to elicit a minimum of orienting or attentional behavior. The situations included walking in an alley for food after prolonged overtraining, and ad lib walking in an observation chamber after 24 hours habituation. In virtually all (82-100%) cases of sustained walking RSA was present in the dorsal hippocampus; however, the amplitude of the RSA during walking was quite variable and in many cases quite small. The results suggest that in the cat motoric factors may influence the occurrence of RSA and non-motoric factors may influence the amplitude of RSA.
Animals↗
Distribution of histochemically reactive zinc in the forebrain of the rat.
The major cytoarchitectonic regions of the rat brain that stain with the Timm-Danscher metal stain were tested with the fluorescent probe for zinc, 6-methoxy 8-para toluene sulfonamide quinoline (TSQ). Throughout most of the striatum, cerebral cortex and limbic system, the diffuse, even neuropil staining produced by the Timm-Danscher method was mirrored by comparable fluorescence in TSQ-stained sections. Blockade of the TSQ fluorescence by prior treatment with sulphide indicated that the Timm-Danscher and the TSQ procedures both labeled the same pool of endogenous metal, which is inferred to be the zinc that is in axonal boutons. It is concluded that the Timm-Danscher staining generally indicates zinc-containing axonal boutons. The distribution of the zinc-containing axonal boutons throughout the forebrain is described.
Aminoquinolines↗
Synaptically released zinc: physiological functions and pathological effects.
In addition to its familiar role as a component of metalloproteins, zinc is also sequestered in the presynaptic vesicles of a specialized type of neurons called 'zinc-containing' neurons. Here we review the physiological and pathological effects of the release of zinc from these zinc-containing synaptic terminals. The best-established physiological role of synaptically released zinc is the tonic modulation of brain excitability through modulation of amino acid receptors; prominent pathological effects include acceleration of plaque deposition in Alzheimer's disease and exacerbation of excitotoxic neuron injury. Synaptically released zinc functions as a conventional synaptic neurotransmitter or neuromodulator, being released into the cleft, then recycled into the presynaptic terminal. Beyond this, zinc also has the highly unconventional property that it passes into postsynaptic neurons during synaptic events, functioning analogously to calcium in this regard, as a transmembrane neural signal. To stimulate comparisons of zinc signals with calcium signals, we have compiled a list of the important parameters of calcium signals and zinc signals. More speculatively, we hypothesize that zinc signals may loosely mimic phosphate 'signals' in the sense that signal zinc ions may commonly bind to proteins in a lasting manner (i.e., 'zincylating' the proteins) with consequential changes in protein structure and function.
Alzheimer Disease↗
Stimulation-induced uptake and release of zinc in hippocampal slices.
The mossy-fibre axons of the hippocampus form a dense plexus, uniquely rich in chelatable zinc. Because the metal is apparently concentrated within the terminal bags of the axons, it has been hypothesized that the zinc is involved in mossy-fibre synaptic transmission. Although some electrophysiological findings have favoured the hypothesis, neither preferential uptake of zinc into the hippocampus nor depolarization-induced release of zinc from hippocampal tissue has previously been found. Using the hippocampal slice preparation, we now report that the mossy-fibre neuropil and cells of origin (dentate granule cells) take up zinc preferentially, and that electrical stimulation selectively facilitates both uptake of exogenous zinc into mossy-fibre neuropil and release of previously incorporated 65Zn from the tissue. The results suggest that the role of zinc in mossy-fibre axons is dynamically linked to neural signalling processes.
Animals↗
Effects of subcutaneous injections of zinc chloride on seizures induced by noise and by kainic acid.
Several lines of evidence implicate zinc in the pathogenesis of epileptic seizures, and administration of zinc salts has been shown to affect seizure susceptibility. In the present work, we studied the effects of subcutaneous (s.c.) injections of ZnCl2 on seizures induced by intraperitoneal (i.p.) kainic acid (10 mg/kg) in rats and by noise (80-120 dB) in the DBA/2J mouse. Previous administration of zinc salt (20-200 mg/kg) substantially reduced the frequency of noise-induced running fits, clonic and tonic seizures, and deaths in mice, but had no significant effect on the incidence or severity of kainic acid-induced seizures in rats. Together with findings in the literature, our results suggest that zinc plays multiple, sometimes antagonistic roles in seizure development.
Animals↗
Zinc-containing neurons.
Zinc-containing neurons are cells that sequester zinc in their presynaptic vesicles and release it in a calcium- and impulse-dependent manner. The zinc-containing neurons are a subclass of the glutaminergic neurons: all known zinc-containing pathways are also glutaminergic pathways. With a few exceptions, zinc-containing neurons are located only in the telencephalon. The major glutaminergic systems of the brain stem, thalamus, and cerebellum, for example, all lack vesicular zinc, whereas many cerebrocortical systems are zinc containing. Within the telencephalon, the zinc-containing fiber systems form a vast associational network that reciprocally interconnects isocortical, allocortical and 'limbic' structures. Because the hippocampal, amygdalar, and perirhinal regions are prominent nodes in this network, it is presumed that vesicular zinc is involved in epileptic phenomena (in pathology) and (in normal function) in the synaptic plasticity of developmental and experiential learning. Zinc ions are potent modulators of amino acid receptors [especially the N-methyl-D-aspartate (NMDA) receptor] and corelease of zinc along with glutamate would provide a mechanism for modulating postsynaptic excitability levels. One useful hypothesis is that synaptically released zinc controls a 'window' of postsynaptic excitability, having little or no effect at physiological firing rates, but selectively depressing excitability (by NMDA receptor depression) when firing rates reach dangerous, paroxysmal levels.
Animals↗