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J M Horowitz

Publications and source records attributed to J M Horowitz.

126 records · Page 7Linked to original sources
PubMed1975

Dispersion along fiber tracts and in the coupling between tracts and a cortical network.

Dispersion in a neuronal coritcal network was modeled using CSMP, a Continuous Systems Modeling Program. The signal dispersion over pathways was simulated by use of a serial product approximating the convolution integral. The program was written in a sufficiently general format to be applied to a variety of biological signals. Calculated signals from a fiber tract and activation of a cortical network were compared with experimental data from cats. The network consists of excitatory cells in a forward limb which send collaterals to interneurons that, once excited, feed back to inhibit the excitatory cells. The model was consistent with data from neuronal assemblies in the prepyriform cortex and fibers in the lateral olfactory tract.

Action Potentials↗
PubMed1975

Sorting of signals from thermosensitive areas.

Of the several models proposed for the neural regulation of temperature in cold-exposed animals, two have been previously restated in dynamic form using CSMP. Subsequently, computer simulations have led to the design and execution of experiments for selection of the more appropriate model for cold-exposed rats. These experiments, as described in the present paper, have been interpreted as being consistent with the model which sorts signals from thermosensitive areas and channels the selected signals over separate neural pathways to independently control each mode of heat production. Since this model requires multiplication of neural signals, possible neuronal mechanisms which may underline such multiplication are discussed. In addition, parameter variation to account for febril responses and rate sensitivity have been evaluated.

Animals↗
PubMed1975

Shivering and nonshivering thermogenic responses of cold-exposed rats to hypothalamic warming.

The concurrent neural control of two thermoregulatory responses, shivering thermogenesis (ST) and nonshivering thermogenesis (NST), was investigated in chronically implanted cold-exposed rats. The effects of heating the preoptic/anterior hypothalamus (POAH) on shivering and on the rate of oxygen consumption (Vo2) were measured in these unanesthetized animals. With ambient temperature maintained constant (at some value between 10 and 16 degrees C), warming the hypothalamus 2-3 degrees C resulted in a significant decrease in Vo2 (Psmaller than 0.001) and an increase in shivering (Psmaller than .01), these responses being reversed on cessation of hypothalamic warming. These results are consistent with the proposal that, in the cold-exposed animal, elevated POAH temperatures directly inhibit NST even though shivering may increase (possibly as a compensation for the decrease in nonshivering heat production). They also rule out the possibility that, in the rat, signals from cutaneous and hypothalamic thermoreceptors are integrated in an indentical manner by the neural controllers for ST and NST.

Animals↗
PubMed1969

Norepinephrine-induced depolarization of brown fat cells.

Intracellular potentials of brown fat cells in lightly anesthetized cold-acclimated rats were measured in vivo. The effects of adrenergic agonists and antagonists on these potentials were examined in an attempt to relate the electrical activity of the cells to the adrenergic-induced stimulation of brown fat thermogenesis.Norepinephrine, the physiological mediator of brown fat heat production, significantly depolarized the membrane of these cells in vivo. This was effected either upon norepinephrine administration (3-100 mug/kg body wt) or excitation of the transsected nerve trunk to the interscapular fat pad and appreciably inhibited (55%) by doses of propranolol (1 mg/kg) sufficient to abolish the temperature increase of the tissue. Since theophylline (325 mum/kg) did not depolarize the cells, although it stimulated thermogenesis in the tissue, the depolarizing effect of norepinephrine is interpreted as being at least partially associated with biochemical events terminating in the activation of adenylate cyclase. However, the norepinephrine-induced electrical changes and the ensuing increase in brown fat thermogenesis appear to be causally independent and experimentally separable. On the other hand, our data do not preclude the speculation that the membrane phenomenon, if accompanied by increased Na(+), may serve partially to regulate the metabolic rate of brown fat during long-term physiological stimulation (e.g., cold stress) by increasing the rate of ATP utilization via the Na(+)/K(+) pump.

Acclimatization↗
PubMedDate not supplied

Drugs of abuse and brain gene expression.

Addictive drugs like cocaine, ethanol, and morphine activate signal transduction pathways that regulate brain gene expression. Such regulation is modulated by the presence of certain transcription factor proteins present in a given neuron. This article summarizes the effects of several addictive drugs on transcriptional processes contributing to the development of a drug-dependent state. The characterization of drug-induced changes in gene expression shows promise for improving our understanding of drug-addiction phenomena and cellular modes of cocaine, ethanol, and morphine action.

Animals↗