Electrophysiology of the undergraduate neuroscience student: a laboratory exercise in human electromyography.

A laboratory exercise is described in which students in a neuroscience, psychobiology, or similar laboratory course record the electromyogram (EMG) from themselves, using surface electrodes (placed on the skin). This exercise is intended to give students a firsthand demonstration that electrical activity is produced within them and to allow the students to use this activity to study biological and psychological concepts. The students study the nature of the EMG (changes with tension and the temporal relationship with limb movement) and the concepts of flexion and extension, reaction time, and patellar ("knee jerk") reflex. In postlaboratory evaluations, undergraduate introductory neuroscience students indicated that they appreciated the opportunity to record electrical activity from their own bodies. The students found the exercise enjoyable, believed that they had learned from it, and indicated that it should be a regular part of the course. If electrophysiology in animal preparations is already part of the course, this exercise requires minimal additional equipment, some of which is easily constructed and the reminder of which is available inexpensively.

Inhibitory avoidance impairments induced by intra-amygdala propranolol are reversed by glutamate but not glucose.

Both systemic and central injections of glucose can enhance memory. For example, glucose reverses impairments on inhibitory avoidance resulting from intra-amygdala injections of morphine. The present experiment investigated the ability of glucose to reverse memory impairments resulting from intra-amygdala injections of propranolol, a beta-noradrenergic antagonist. Pretraining administration of 10 microg propranolol significantly reduced inhibitory avoidance retention latencies but had no effect on performance in a spontaneous alternation task. Coadministration of glucose into the amygdala at 3 doses (1.5, 3.0, and 6.0 microg) did not reverse the propranolol-induced inhibitory avoidance deficits. However, coadministration of 2.5 microg of glutamate with the propranolol did reverse these deficits. The ability of glucose to reverse impairments following intra-amygdala injections of morphine but not propranolol may reflect the neurotransmitter system or systems through which glucose exerts its effects.

Pyruvate infusions into the septal area attenuate spontaneous alternation impairments induced by intraseptal morphine injections.

Glucose infusions into the medial septal area attenuate memory impairments produced by concurrent intraseptal morphine injections. One possible explanation for these effects of glucose on memory is that the treatment modulates regional energy metabolism. As a test of this hypothesis, the present experiment determined whether intraseptal pyruvate injections could attenuate a spontaneous alternation impairment seen after intraseptal morphine injections. Intraseptal injections of morphine (4.0 nmol) 30 min prior to testing produced spontaneous alternation scores significantly lower than those in control groups. Morphine injections near, but outside, the septal region did not impair spontaneous alternation performance. The morphine-induced impairment was similarly reversed by coadministration of either glucose (18 nmol) or pyruvate (18 nmol) into the septum. These findings suggest that glucose may act through the tricarboxylic acid cycle by increasing the availability of ATP, augmenting the synthesis of certain neurotransmitters, or both.

Glucose does not reverse impairments on spontaneous alternation induced by the noncompetitive NMDA antagonist MK-801.

N-Methyl-D-aspartate (NMDA) antagonists have been demonstrated to impair acquisition in a variety of tasks, including maze learning. It was previously reported from this laboratory that glucose can reverse the deficits on spontaneous alternation resulting from administration of the competitive NMDA antagonist NPC 12626 in mice. The present study tested the ability of glucose to reverse deficits induced by the noncompetitive NMDA antagonist MK-801. Although subcutaneous administration of 0.10 mg/kg of MK-801 resulted in a deficit on spontaneous alternation, glucose (100 and 250 mg/kg) did not reverse the impairment. This difference in the ability of glucose to reverse the impairment caused by the two NMDA antagonists may reflect their different modes of actions at the NMDA receptor complex.

Frequency selectivity is related to temporal processing in parallel thalamocortical auditory pathways.

Lemniscal and non-lemniscal parallel thalamocortical auditory pathways have been identified with the ventral medial geniculate body (MGB) vs. the dorsal and medial MGB, respectively. Lemniscal neurons have narrow frequency tuning and provide highly specific frequency information to the auditory cortex whereas non-lemniscal neurons generally have broader tuning and greater response lability, including plasticity of frequency receptive fields during learning. To determine if frequency selectivity is related to temporal fidelity of response, we measured both the breadth of tuning and neuronal excitability in a paired tone paradigm for single neurons throughout the MGB. Excitability to the second tone of a pair was directly correlated with frequency selectivity: the narrower the frequency tuning, the greater the excitability. Cells with broad tuning based on multiple-peak response areas also were less excitable than cells with single-peak RAs. Cells in the ventral MGB showed greater temporal fidelity of response (greater excitability) than cells in the dorsal and medial MGB. These findings show that high degrees of both frequency selectivity and temporal response fidelity are characteristic of the lemniscal, but not the non-lemniscal, thalamocortical auditory system.

Frequency-specific receptive field plasticity in the medial geniculate body induced by pavlovian fear conditioning is expressed in the anesthetized brain.

Fear conditioning modifies the processing of frequency information; receptive fields (RF) in the auditory cortex and the medial geniculate body (MGB) are altered to favor processing the frequency of the conditioned stimulus (CS) over the pretraining best frequency (BF) and other frequencies. This experiment was designed to determine whether brief conditioning in the waking state produces RF plasticity that is expressed under general anesthesia. Guinea pigs bearing electrodes in the MGB received 20 trials of tone-shock pairing in a single training session. RFs were determined with animals under ketamine anesthesia before conditioning and 1-3 hr and 24 hr after conditioning. Frequency-specific RF plasticity was evident for both postconditioning periods: The BF shifted toward or to the CS frequency, responses to the BF decreased, and responses to the CS increased. Broadly tuned cells developed greater RF plasticity than narrowly tuned neurons. The results demonstrate that the specific neuronal results of brief learning experiences can be expressed in the anesthetized brain.