Learning a motor skill sets in motion neural processes that continue to evolve after practice has ended, a phenomenon known as consolidation. Here we present psychophysical evidence for this, and show that consolidation of a motor skill was disrupted when a second motor task was learned immediately after the first. There was no disruption if four hours elapsed between learning the two motor skills, with consolidation occurring gradually over this period. Previous studies in humans and other primates have found this time-dependent disruption of consolidation only in explicit memory tasks, which rely on brain structures in the medial temporal lobe. Our results indicate that motor memories, which do not depend on the medial temporal lobe, can be transformed by a similar process of consolidation. By extending the phenomenon of consolidation to motor memory, our results indicate that distinct neural systems share similar characteristics when encoding and storing new information.

Consolidation in human motor memory

Previous research has demonstrated that the primate CNS has the ability to learn and store multiple and conflicting visuo-motor maps. Here we studied the ability of human subjects to learn to make reaching movements while interacting with one of two conflicting mechanical environments as produced by a robotic manipulandum. We demonstrate that two motor maps may be learned and retained, but only if the training sessions in the tasks are separated by an interval of ∼5 hr. If the interval is shorter, learning of the second map begins with an internal model appropriate for the first task and performance in the second task is significantly impaired. Analysis of the after-effects suggests that with a short temporal distance, learning of the second task leads to an unlearning of the internal model for the first. With the longer temporal distance, learning of the second task starts with an unbiased internal model, and performance approaches that of naives. Furthermore, the memory of the consolidated skill lasts for at least 5 months after training. These results argue for a distinct change in the state of resistance of motor memory (to disruption) within a few hours after acquisition. We suggest that motor practice results in memories that have at least two functional components: soon after completion of practice, one component fades while another is strengthened. A further experiment suggests that the hypothetical first stage is not merely a gateway to long-term memory, but also temporary storage for items of information, whether new or old, for use in the near-term. Our results raise the possibility that there are distinct neuronal mechanisms for representation of the two functional stages of motor memory.

https://www.jneurosci.org/content/jneuro/17/1/409.full.pdf

Functional Stages in the Formation of Human Long-Term Motor Memory

Recent work has suggested that changes in synapse number as well as changes in the expression of the Fos protein may occur within the motor cortex in association with motor learning. The number of synapses per neuron and the percentage of Fos-positive neurons within layer II/III of the rat motor cortex was measured after training on a complex motor learning task. Adult female rats were allocated randomly to either an acrobatic condition (AC), a motor control condition (MC), or an inactive control condition (IC). AC animals were trained to traverse a complex series of obstacles, and each AC animal was pair matched with an MC animal that traversed an obstacle-free runway. IC animals received no motor training. Animals from each condition were killed at various points during training, and unbiased stereological techniques were used to estimate the number of synapses per neuron and the percentage of Fos-positive cells within layer II/III of the motor cortex. AC animals exhibited an overall increase in the number of synapses per neuron in comparison to MC and IC animals at later stages of training. AC animals also had a significantly higher overall percentage of Fos-positive cells in comparison to both controls, with a trend for the increase to be greater during the acquisition versus the maintenance phase. These data suggest that Fos may be involved in the biochemical processes underlying skill acquisition and that motor learning, as opposed to motor activity, leads to increases in synapse number in the motor cortex.

https://www.jneurosci.org/content/jneuro/16/14/4529.full.pdf

Synaptogenesis and Fos expression in the motor cortex of the adult rat after motor skill learning.

Vestibular evoked myogenic potentials: Past, present and future

Mechanisms of recovery following unilateral labyrinthectomy: a review

We have examined the anticonvulsant properties of propofol in high doses in two experimental models of status epilepticus: generalized pentylenetetrazol (PTZ)-induced seizures and partial, cortically applied penicillin G-induced seizures. Propofol was administered either as a single bolus injection or as a bolus injection followed by an infusion for 1 h. When administered as a single bolus injection, propofol 12 mg kg−1 suppressed electrical and clinical seizures in PTZ generalized epileptic status, and an infusion of 50 mg kg−1 h−1 prevented the reappearance of electrical and clinical signs. In focal epileptic status, the single dose stopped paroxysmal activity and the associated clonic jerks for a few seconds. When the bolus dose was followed by an infusion, the firing bursts were replaced by isolated spikes, and contralateral jerks became sporadic and feeble. The greater efficacy of propofol against PTZ convulsions may be a reflection of the opposite action of the two drugs on neural membrane conductance: PTZ induces paroxysmal neural discharge by enhancing membrane conductance while propofol appears to decrease membrane conductance, thus suppressing paroxysmal discharge. There was no close relationship between blood concentration of the anaesthetic and its clinical effects, at least after a short-term infusion, as used in the present experiments. We suggest that propofol may be a potentially useful drug in status epilepticus in patients in whom benzodiazepines, barbiturates and phenytoin have failed.

Propofol anticonvulsant activity in experimental epileptic status

Introduction: Stimulation of cranial nerves modulates central nervous system (CNS) activity via the extensive connections of their brainstem nuclei to higher-order structures. Clinical exp...

Anatomo-Physiologic Basis for Auricular Stimulation.

The potential for cardiac arrhythmia was studied in an experimental focal epilepsy induced in hemispherectomized rats by topical application of buffered penicillin G onto the thalamus. The epileptic burst triggered cardiac and hemodynamic responses, as simultaneously monitored by arterial pressure, and hypothalamic and heart activity. During interictal epileptic activity, the single burst triggered a short-latency cardiac arrhythmia, characterized by sinus bradyarrhythmia and junctional rhythm, and lengthening of intervals between sphygmic waves with significant reduction of diastolic pressure. When the epileptic burst stopped, the cardiac activity resumed normal rhythm, and diastolic pressure returned to basal value. During ictal epileptic activity, the sinus and junctional bradyarrhythmic episodes lasted longer, and supraventricular extrasystoles, sinus arrest, and bigeminal ventricular extrasystoles were observed. Both systolic and diastolic pressures decreased from 120/85 to 100/65 mm Hg. The end of the ictal episode always marked resumption of normal cardiac rhythm and systemic pressure. Considering the absence of metabolic complications (blood-gas analytic parameters and acid-base balance being controlled) and the short latency of the cardiac and hemodynamic responses, it is suggested that during paroxysmal hypothalamic activity the observed cardiac arrhythmias and the hemodynamic modifications were neurogenic in origin. A role for cardiovascular alterations in sudden unexplained epileptic death is postulated.

Neurogenic myocardial arrhythmias in experimental focal epilepsy.

In the present study the possible derangement of the autonomic system and its influence in life threatening arrhythmias were analysed during paroxysmal activity. In hemispherectomized rats a paroxysmal activation of the hypothalamic and mesencephalic cardioarrhythmogenic triggers was performed by topical application of penicillin-G. Blood gas parameters and electrical activity of the thalamus, hypothalamus, vagal nerve fibre, ECG and arterial blood pressure were simultaneously monitored in basal conditions and repeated after the appearance of paroxysmal activity. Temporal correlation analysis was carried out. Results showed that during activation of these triggers, the spontaneous vagal nerve fibre activity significantly increased and triggered the appearance of cardiac arrhythmias which could become life threatening and induce animal death when blood gas and electrolytic parameters were simultaneously impaired. These experiments suggest that fatal evolution of the heart impairment is related not only to an autonomic cardiac trigger, but also to a concomitant metabolic derangement, which most likely shares the same autonomic origin.

F. Melis

Papers

Propofol anticonvulsant activity in experimental epileptic status

Anatomo-Physiologic Basis for Auricular Stimulation.

Neurogenic myocardial arrhythmias in experimental focal epilepsy.

Autonomic nervous system activity and life threatening arrhythmias in experimental epilepsy

The brainstem cardioarrhythmogenic triggers and their possible role in sudden epileptic death.