Sixteen male hooded rats were trained to reach into a narrow feeding tube for small food pellets. The paw movements were photoelectrically detected. An epileptic focus established by local application of 1% picrotoxin on the exposed motor cortex increased the frequency of reaching with the ipsilateral paw and impaired reaching with the contralateral paw. Interictal discharge rate of all ipsilateral foci was increased by reaching in the same way as the slow activity (less than 0.5/sec) of contralateral foci. On the other hand, fast activity (greater than 0.5/sec) of contralateral foci was decreased by reaching. Computer analysis of interictal discharge indicence during 512 msec before and after reaching onset showed that the brief facilitation of discharge (50 msec) during the actual movement was often preceded and followed by more prolonged inhibition (200 msec). The inhibition was better expressed in the contralateral hemisphere. The results are interpreted as due to changes of cortical excitability associated with reaching and to interference of the epileptic focus with the cortical elaboration of the skilled movement.

Action Potentials↗

PubMed1975

Facilitation of Leao's spreading depression by a pyrrolopyrimidine derivative.

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Animals↗

PubMed1975

Functional decortication by cortical spreading depression does not prevent forced extinction of conditioned saccharin aversion in rats.

Conditioned taste aversion established in rats by association of saccharin drinking with subsequent lithium chloride intoxication decreased saccharin intake to 22% of normal consumption. Force-feeding saccharin to intact and functionally decorticate trained rats returned saccharin consumption on the next day to 62% (n equals 18) and 77% (n equals 19), respectively. Over-trained conditioned saccharin aversion was affected by forced extinction in a similar way (saccharin intake increased from 28% to 50% and 63%, respectively). Intact brain rats refused to swallow saccharin during forced feeding. while functionally decorticate animals showed no signs of aversion; but extinction was almost equal in both cases. Application of lithium chloride after forced feeding of saccharin in functionally decorticate rats neither prevented extinction of conditioned taste aversion nor reestablished the aversion habit extinguished earlier with intact brain. It is concluded that acquisition of the conditioned taste aversion requires cortical input to a short-term memory file, whereas decorticate extinction can be induced by subcortical gustatory processing analogous to the mechanism controlling feeding behavior during the preweaning period.

Animals↗

PubMed1975

Interhemispheric transfer of extinction of the active avoidance reaction in rats.

Cortical spreading depression (CSD) was employed in rats to study the lateralization of extinction of a jumping avoidance reaction. Under unilateral CSD, 181 nonreinforced trials were needed to extinguish the avoidance reaction acquired in three 100-trial sessions of intact-brain training. During a second extinction session, either with the same or with the contralateral hemisphere depressed, the mean number of trials to the extinction criterion (9/10) was 39 (n = 12) or 186 (n = 15), respectively. Five extinction trials performed with the brain intact 1 hr before extinction with contralateral CSD decreased the number of trials to extinction of 98 (n = 11). Thus, extinction of active avoidance can be lateralized and interhemispherically transferred in the same way as acquisition of this habit.

Animals↗

PubMed1975

Blockage of cortical spreading depression by picrotoxin foci of paroxysmal activity.

1 per cent Picrotoxin placed on cortex of rat caused paroxysmal ECoG discharges with concomitant increase in [Ke"] from 3 to 6.7 mM with oscillations corresponding to ictal (maximum) and interictal (minimum) spiking. Invasion of the epileptogenic focus by spreading depression was blocked when the amplitude of oscillations of [Ke+] reached 2.6 mM. Epileptogenic activity induced by topical 10 per cent pentazol caused a less marked increase in [Ke+] (4.6 mM) and did not prevent depression from invading the focal area, but did diminish [Ke+] from the normal of 60 to 70 mM to 39 mM. It is concluded that seizure-induced depolarization of neural elements in deep cortical layers, though inadequate to trigger spreading depression, does prevent it from spreading, in part by activating the sodium pump.

Animals↗

PubMed1975

Techniques for termination of reverberating spreading depression in rats.

Reverberation of cortical spreading depression (CSD) around a circular obstacle (thermocoagulation lesion) in the frontal cortex of anesthetized rats was elicited by appropriately timed and spaced applications of KCl. The probability of continued reverberation was increased by a pyrrolopyrimidine drug BW 58-271 (10 mg/kg) from 0.93 to 0.98. Three methods of reverberation arrest were tested: a) CSD propagation was blocked by an interfering CSD wave which was initiated in the rear of the reverberating wave, passing through a narrow segment of the circular pathway, and collided with the reverberating wave on the opposite side of the obstacle; b) CSD propagation through a part of the circular pathway was blocked by a 10-min application of 10% MgCl2 on the exposed cortical surface; c) 1-min asphyxia stopped RCSD by increasing the overall refractoriness of cortical tissue. Least reliable was the interference method which stopped reverberation, even with optimum timing, only in 42% of the trials. The magnesium blockade was reliable but slow, the reverberation stopping only 30 min after MgCl2 application. Asphyxia evoked in any phase of the reverberation cycle stopped RCSD reliably and immediately. The results obtained with the interference method confirm the predictions of the mathematical model of impulse reverberation in sheets of excitable tissue. Anoxia seems best suited for practical control of CSD reverberation in functional decortication studies.

Animals↗

PubMed1975

Electrophysiological investigation of discrete skilled movements in rats.

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Animals↗

PubMed1975

Eelectrophysiological correlates of pecking.

Electrophysiological correlates of pecking were studied in 50 freely moving pigeons. With the backward averaging technique average motor potentials (AMPs) were found in all subdivisions of the striatum. The AMPs appeared significantly earlier (40 msec before pecking) in the Wulst than in the neostriatum, ectostriatum, and archistriatum (18 to 28 msec before pecking). Their amplitude could be reduced by monocular occlusion. Average visual responses (AVRs) in the optic tectum were decreased at brief peck-flash intervals, reached maximum with 100 to 200 msec peck-flash delays and then again decreased at intervals corresponding to the occurrence of the next peck (300 msec). A head-mounted microdive system and a miniature FET probe were employed to record unit activity with glass microelectrodes. Out of 280 examined neurones, 83% were activated and 6% inhibited by pecking. The pre- and post-pecking histograms indicated that hyperstriatal neurones are activated earlier and for a longer time than the neostriatal units. It is concluded that rostral parts of striatum play an important role in the functional organisation of pecking.

Animals↗

PubMed1974