Jonathan R. Wolpaw

Scalp distribution of human auditory evoked potentials. II. Evidence for overlapping sources and involvement of auditory cortex

The scalp distributions of human auditory evoked potentials (AEPs) between 20 and 250 msec were investigated using non-cephalic reference recordings. AEPs to binaural click stimuli were recorded simultaneously from 20 scalp locations over the right hemisphere in 11 subjects. Computer-generated isovoltage topographic maps at high temporal resolution were used to assess the stability of AEP scalp distributions over time and relate them to major peaks in the AEP wave forms. For potentials between 20 and 60 msec, the results demonstrate a stable scalp distribution of dipolar form that is consistent with sources in primary auditory cortex on the superior temporal plant near the temporoparietal junction. For potentials between 60 and 250 msec, the results demonstrate changes in AEP morphology across electrode locations and changes in scalp distribution over time that lead to two major conclusions. First, AEPs in this latency period are generated by multiple sources which partially overlap in time. Second, one or more regions of auditory cortex contribute significantly to AEPs in this period. Additional data are needed to determine the relative contribution of auditory cortex sources on the superior temporal plane and the lateral temporal surface and to identify AEP sources outside the temporal lobe.

The complex structure of a simple memory

Operant conditioning of the vertebrate H-reflex, which appears to be closely related to learning that occurs in real life, is accompanied by plasticity at multiple sites. Change occurs in the firing threshold and conduction velocity of the motoneuron, in several different synaptic terminal populations on the motoneuron, and probably in interneurons as well. Change also occurs contralaterally. The corticospinal tract probably has an essential role in producing this plasticity. While certain of these changes, such as that in the firing threshold, are likely to contribute to the rewarded behavior (primary plasticity), others might preserve previously learned behaviors (compensatory plasticity), or are simply activity-driven products of change elsewhere (reactive plasticity). As these data and those from other simple vertebrate and invertebrate models indicate, a complex pattern of plasticity appears to be the necessary and inevitable outcome of even the simplest learning.

Memory traces in spinal cord

The complexity and inaccessibility of the vertebrate CNS impede the localization and description of memory traces and the definition of the processes that create them. Recent work has shown that the spinal stretch reflex (SSR), which is produced by a monosynaptic two-neuron pathway, can be operantly conditioned, and that memory traces responsible for this behavioral change reside in the spinal cord. The probable locations are the terminal of the Ia affernt neuron on the motoneuron and/or the motoneuron itself. Because it modifies a simple well-defined and accessible pathway, SSR conditioning may be a valuable experimental model for studying vertebrate memory.

Spinal cord plasticity in acquisition and maintenance of motor skills

Throughout normal life, activity‐dependent plasticity occurs in the spinal cord as well as in brain. Like other central nervous system (CNS) plasticity, spinal cord plasticity can occur at numerous neuronal and synaptic sites and through a variety of mechanisms. Spinal cord plasticity is prominent early in life and contributes to mastery of standard behaviours like locomotion and rapid withdrawal from pain. Later in life, spinal cord plasticity has a role in acquisition and maintenance of new motor skills, and in compensation for peripheral and central changes accompanying ageing, disease and trauma. Mastery of the simplest behaviours is accompanied by complex spinal and supraspinal plasticity. This complexity is necessary, in order to preserve the complete behavioural repertoire, and is also inevitable, due to the ubiquity of activity‐dependent CNS plasticity. Explorations of spinal cord plasticity are necessary for understanding motor skills. Furthermore, the spinal cords comparative simplicity and accessibility makes it a logical starting point for studying skill acquisition. Induction and guidance of activity‐dependent spinal cord plasticity will probably play an important role in realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy and other motor disorders.

Human middle-latency auditory evoked potentials: vertex and temporal components ☆

We recorded middle-latency (20-70 msec) auditory evoked potentials (MLAEPs) to monaural and binaural clicks in 30 normal adults (ages 20-49 years) at 32 scalp locations all referred to a balanced non-cephalic reference. Our goal was to define the MLAEP components that were present at comparable latencies and comparable locations across the subject population. Group and individual data were evaluated both as topographic maps and as MLAEPs at selected electrode locations. Three major components occurred between 20 and 70 msec, two well-known peaks centered at the vertex, and one previously undefined peak focused over the posterior temporal area. Pa is a 29 msec positive peak centered at the vertex and present with both monaural and binaural stimulation. Pb is a 53 msec positive peak also centered at the vertex but seen consistently only with binaural and right ear stimulation. TP41 is a 41 msec positive peak focused over both temporal areas. TP41 has not been identified in previous MLAEP studies that concentrated on central scalp locations and/or used active reference electrode sites such as ears or mastoids. Available topographic, intracranial, pharmacologic, and lesion studies indicate that Pa, Pb and TP41 are of neural origin. Whether Pa and/or Pb are produced in Heschls gyrus, primary auditory cortex, remains unclear. TP41 is probably produced by auditory cortex on the posterior lateral surface of the temporal lobe. It should prove of considerable value in experimental and clinical evaluation of higher level auditory function in particular and of cortical function in general.

What Can the Spinal Cord Teach Us about Learning and Memory

The work of recent decades has shown that the nervous system changes continually throughout life. Activity-dependent central nervous system (CNS) plasticity has many different mechanisms and involves essentially every region, from the cortex to the spinal cord. This new knowledge radically changes the challenge of explaining learning and memory and greatly increases the relevance of the spinal cord. The challenge is now to explain how continual and ubiquitous plasticity accounts for the initial acquisition and subsequent stability of many different learned behaviors. The spinal cord has a key role because it is the final common pathway for all behavior and is a site of substantial plasticity. Furthermore, because it is simple, accessible, distant from the rest of the CNS, and directly connected to behavior, the spinal cord is uniquely suited for identifying sites and mechanisms of plasticity and for determining how they account for behavioral change. Experimental models based on spinal cord reflexes facilitate study of the gradual plasticity that makes possible most rapid learning phenomena. These models reveal principles and generate concepts that are likely to apply to learning and memory throughout the CNS. In addition, they offer new approaches to guiding activity-dependent plasticity so as to restore functions lost to injury or disease.

Adaptive plasticity in the primate spinal stretch reflex: reversal and re-development

Monkeys can gradually increase or decrease the amplitude of the segmentally mediated spinal stretch reflex (SSR) without change in initial muscle length or background EMG activity. Both increase (under the SSR increases mode) and decrease (under the SSR decreases mode) occur slowly, progressing steadily over weeks. The present study investigated reversal and re-development of SSR amplitude change. Over a period of months, following collection of control data, monkeys were exposed to one mode, then to the other, and then to the first mode again. Development, reversal, and re-development of change all took place over weeks, following very similar courses. These data are consistent with the hypothesis that persistent segmental alteration underlies SSR amplitude change. Such persistent segmental alteration would constitute a technically accessible substrate of memory.

Jendrassik maneuver facilitates soleus H-reflex without change in average soleus motoneuron pool membrane potential

Facilitation of spinal reflex amplitude by remote muscle contraction, otherwise known as the Jendrassik maneuver (JM), was first shown over 100 years ago, yet the mechanism by which this facilitation operates remains undetermined. Earlier work has eliminated participation of the muscle spindle in JM-induced spinal reflex facilitation, leaving changes in postsynaptic (e.g., change in average soleus motoneuron membrane potential) and presynaptic (e.g., inhibition of presynaptic inhibition) mechanisms as viable candidates. We recorded background EMG in the soleus muscle during JM-induced soleus H-reflex facilitation in humans. The JM in this experiment consisted of wrist muscle contraction. Soleus background EMG was maintained by the subject at either a zero level (e.g., relaxed) or a specified moderate level prior to and during the JM. The JM increased H-reflex amplitude by comparable amounts in both situations, but had no effect on soleus background EMG. Given the well-known relationship between the average motoneuron pool membrane potential and background EMG, we conclude that JM facilitation of the soleus H-reflex is not caused by an increase in background excitatory input to the soleus motoneuron pool. Remaining candidates for mediation of JM induced H-reflex facilitation include change in stimulus-evoked afferent input at some point proximal to the muscle spindle, such as reduction in presynaptic inhibition, or a change in motoneuron input resistance.

Operant conditioning of H-reflex in freely moving monkeys

The H-reflex, the electrical analog of the stretch reflex or tendon jerk, is the simplest behavior of the primate CNS. It is subserved by a wholly spinal two-neuron reflex arc. Recent studies show that this reflex can be increased or decreased by operant conditioning, and that such conditioning causes plastic changes in the spinal cord itself. Thus, H-reflex conditioning provides a powerful new model for investigating primate memory traces. The key feature of this model, the conditioning task, originally required animal restraint. This report describes a new tether-based design that allows H-reflex measurement and conditioning without restraint. This design integrates the conditioning task into the life of the freely moving animal.

Time course of H-reflex conditioning in the rat

This study sought to define the course of operantly conditioned change in the rat soleus H-reflex and to determine whether, like H-reflex conditioning and spinal stretch reflex conditioning in the monkey, it develops in distinct phases. Data from 33 rats in which the right soleus H-reflex was trained up (i.e. HRup mode) and 38 in which it was trained down (i.e. HRdown mode) were averaged to define the courses of H-reflex increase and decrease. In HRup rats, the H-reflex showed a large phase I increase within the first 2 days followed by gradual phase II increase that continued for weeks. In HRdown rats, the H-reflex appeared to show a small phase I decrease and then showed a gradual phase II decrease over weeks. In combination with other recent work, the data suggest that H-reflex conditioning begins with a rapid mode-appropriate alteration in corticospinal tract influence over the spinal arc of the H-reflex, which causes phase I change, and that the continuation of this altered influence induces gradual spinal cord plasticity that is responsible for phase II change. The results further establish the similarity of H-reflex conditioning in primates and rats. Thus, they encourage efforts to produce a single coherent model of the phenomenon based on data from the two species and indicate the potential clinical relevance of the rat data.