Cerebellar posterior interpositus neurons were recorded in cats during delayed and trace conditioning of eyeblinks. Type A neurons increased their firing in the time interval between conditioned and unconditioned stimulus presentations for both paradigms, while type B neurons decreased it. The discharge of different type A neurons recorded across successive conditioning sessions increased, with slopes of 0.061-0.078 spikes/s/trial. Both types of neurons modified their firing several trials in advance of the appearance of eyelid conditioned responses, but for each conditioned stimulus presentation their response started after conditioned response onset. Interpositus microstimulation evoked eyelid responses similar in amplitude and profiles to conditioned responses, and microinjection of muscimol decreased conditioned response amplitude. It is proposed that the interpositus nucleus is an enhancer, but not the initiator, of eyelid conditioned responses.

We have recorded the firing activities of hippocampal pyramidal cells throughout the classical conditioning of eyelid responses in alert cats. Pyramidal cells (n = 220) were identified by their antidromic activation from the ipsilateral fornix and according to their spike properties. Upper eyelid movements were recorded with the search coil in a magnetic field technique. Latencies and firing profiles of recorded pyramidal cells following the paired presentation of conditioned (CS) and unconditioned (US) stimuli were similar, regardless of the different sensory modalities used as CS (tones, air puffs), the different conditioning paradigms (trace, delay), or the different latency and topography of the evoked eyelid conditioned responses. However, for the three paradigms used here, evoked neuronal firing to CS presentation increased across conditioning, but remained unchanged for US presentation. Contrarily, pyramidal cell firing was not modified when the same stimuli used here as CS and US were presented unpaired, during pseudoconditioning sessions. Pyramidal cell firing did not seem to encode eyelid position, velocity, or acceleration for either reflex or conditioned eyelid responses. Evoked pyramidal cell responses were always in coincidence with a beta oscillatory activity in hippocampal extracellular field potentials. In this regard, the beta rhythm represents a facilitation, or permissive time window, for timed pyramidal cell firing. It is concluded that pyramidal cells encode CS-US associative strength or CS predictive value.

Summary: Purpose:To analyze the effect of prolonged (daily) electrical vagus nerve stimulation (VNS) on daily amygdaloid kindling (AK) in freely moving cats.Methods: Fifteen adult male cats were implanted in both temporal lobe amygdalae, both lateral geniculate bodies, and prefrontal cortices. A bipolar hook (5-mrn separation) stainless steel electrode also was implanted in the unsectioned left vagus nerve. AK only was performed on five of the cats as a control. The remaining 10 cats were recorded under the following experimental conditions: VNS (1.2-2.0 mA, 0.5-ms pulses, 30 Hz) for 1 min along with AK (I-s train, 1 -ms pulses, 60 Hz, 300-600 PA), followed by VNS alone for 1 min, four times between I1:OO a.m. and 2 p.m. At different times, VNS was arrested, and AK was continued until stage VI kindling was reached.Results: The behavioral changes evoked by VNS were as follows: left miosis, blinking, licking, abdominal contractions, swallowing, and eventually yawning, meowing, upward gaze, and short head movements. Compulsive eating also was present with a variable latency. Outstanding polygraphic changes consisted of augmentation of eye movements and visual evoked potentials while the animal was awake and quiet, with immobility and upward gaze. An increase of the pontogeniculooccipital (PGO) wave density in rapid eye movement (REM) sleep also was noticeable. AK was completed (to stage VI) in the control animals without a vagus nerve implantation in 23.4 & 3.7 trials. In animals with VNS, the AK was significantly delayed, remaining for a long time in the behavioral stages and showing a reduction of afterdischarge duration and frequency. Stage VI was never reached despite 50 AK trials, except when the vagus nerve electrodes were accidentally broken or vagal stimulation was intentioilally arrested. Under these circumstances, 24.4 8.16 AK trials alone were necessary to reach stage VI of kindling.Conclusions: Our results indicate that left, electrical VNS interferes with AK epileptogenesis. This anticonvulsant effect could be related to the increase of REM sleep.

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Summary:Purpose: This work analyzed the effect of electrical stimulation of the nucleus of the solitary tract (NTS) on the development of electrical amygdaloid kindling (AK) in freely moving cats.Methods: Nine male adult cats with implanted electrodes in both amygdalae (basolateral nucleus), both lateral geniculate bodies, left NTS, and both prefrontal cortices were used. Electromyogram and electrooculogram also were recorded. The AK was performed every 24 h (1-s train, 1-ms pulses, 60 Hz, 300-600 A). The NTS was stimulated previously for 1 min (0.5-ms pulses, 30 Hz, 150-300 A), just before the AK at 10:00 a.m., and then every 60 min, 4 times, from 11:00 a.m. to 2:00 p.m. On different days, all NTS stimulation was suspended, and AK was continued until stage VI kindling was reached.Results: Behavioral changes produced by the stimulation of the NTS were blinking, immobility periods with upward sight, licking, and swallowing. Animals with simultaneous stimulation of NTS and AK did not reach stage VI, remaining in behavioral stages I-III. Stage VI was reached after NTS stimulation was intentionally suspended. The amplitude, duration, and the propagation of the amygdaloid afterdischarge did not exhibit progressive evolution during NTS stimulation. A regression analysis was performed between the number of days with only AK stimulation and days with simultaneous NTS stimulation, which showed a positive correlation (values of r ‫ס‬ 0.84).Conclusions: Our results suggest that NTS stimulation interferes with the development of convulsive evolution and secondary generalization. This delay effect may be due to the activation of the locus ceruleus and some areas of the midbrain reticular formation, among other structures, which has been demonstrated to inhibit experimental convulsive seizures.