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Biomedical subjects

J W Kakolewski

Publications and source records attributed to J W Kakolewski.

At least 19 recordsLinked to original sources

An injury-induced diffuse slow potential from brain.

Three different slow potential (SP) changes resulting from focal brain injury are described. The first is an immediate, high amplitude (in excess of 25 mV)negative shift at the site of injury. The second is a biphasic negative-positive SP wave which spreads throughout the cortex ipsilateral to injury and is similar to spreading depression (SD). The third SP change, called here the injury-induced diffuse slow potential (IDSP)is a prolonged (lasting approx. 2h) negative shift occurring simultaneously in many brain areas, also in those far removed from the injured focus. The SD can be separated from IDSP by the size of focal injury; a 20 mu pucture of the parenchyma will trigger IDSP but not SD. An injury resulting from a larger puncture triggers both, SD and IDSP. IDSPcan not be induced by a re-entry of a previously damaged tissue. The magnitude of IDSP has anatomical specificity in that the largest amplitude occurrs in white as compared to gray of the cortex or of the caudate nucleus. Aso, the magnitude of the hypothalamic IDSP is larger when ipsilateral corpus callosum-commissural regions are injured. Electrical stimulation of the cortex in rats sufficiently strong to result in tonic-clonic convulsions triggers SD and IDSP; these two slow potential changes are similar to those induced by mechanical injury. A transpinnate electrical stimulus strong enough to elicit a grand-mal type of discharge results in a diffuse negative slow potential change similar to IDSP elicited by mechanical damage or direct cortical stimulation.

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Spontaneous whole brain slow potential changes during recovery from experimental neurosurgery.

Prolonged, nonlocalized brain slow potential changes, frequently associated with cortical spreading depression, occur spontaneously during 5 days following brain implant surgery in rats. These potentials are accompanied by reductions in multiple nerve cell activity and reductions in behavioral motility. The method used in this study provides a tool for evaluating recovery from neurosurgical trauma or other brain injuries, and for testing procedures that facilitate or impede this process.

Animals↗

Emotionally induced increases in effective osmotic pressure and subsequent thirst.

Following a brief period of handling or enclosed rotation, rats increased the frequency of drinking relative to eating. Handling also delayed or eliminated eating behavior in hypoosmotic rats. Osmometric analysis revealed a rapid increase in serum osmolality during stress which may account for the emergence of thirst and disruption of eating.

Animals↗

Object-carrying by rats: an approach to the behavior produced by brain stimulation.

Rats were provided with opportunity to turn reinforcing hypothalamic stimulation on and off by traversing back and forth across a chamber. When provided with edible and inedible objects, all animals that self-stimulated carried them from the stimulation to the nonstimulation side. Neither food deprivation nor a history of stimulus-bound eating produced a preference for the edible objects. Equivalent stimulation provided without regard to the animals' location in the chamber did not elicit object-carrying. Results are interpreted in terms of the natural conditions which normally elicit this species-specific unit of behavior. Implications for understanding other behavior patterns elicited by hypothalamic stimulation are suggested.

Animals↗

Short-latency antidiuresis following the initation of food ingestion.

A factor associated with the ingestion of food is shown to produce a short-latency antidiuresis. Animals consuming large quantities of a highly palatable solution during a period of food deprivation exhibit an antidiuresis immediately following the initiation of eating. The rapidity of the response raises the possibility of a signaling factor separate from postingestional influences.

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