Penicillin as an epileptogenic agent: effect on an isolated synapse.

Penicillin enhances the excitatory postsynaptic potential of the squid stellate ganglion. This effect suggests the hypothesis that the epileptic focus created by the topical application of penicillin to the mammalian cerebral cortex is produced by the facilitation of excitatory synaptic coupling within the preexisting positive recurrent feedback system.

Reflex effects of vibration in patients with spinal cord lesions.

The vibration reflex was studied in 49 patients with traumatic spinal cord lesions. It was elicited in all patients, even after presumably complete division of the cord. The vibration relfex consisted of a short-latency, brief outburst of phasic activity of motor units, followed by rapidly decreasing phasic component and a later slowly declining tonic component. When periods of vibration were repeated at short intervals of 2 to 10 seconds, the responses showed an approximately exponential decline, although the beginning of each subsequent response was always larger than the end of the preceding response. A large part of this decline can be characterized as a habituation of the vibration reflex. In comparison with the vibration reflex in normal subjects, the phasic component was increased and the tonic one reduced. The tonic component was especially susceptible to potentiation and dishabituation by voluntary effort to contract the vibrated muscle, even in some patients with no other evidence that the lesion was incomplete. We suggest that the tonic component of the human vibration reflex depends, at least in part, on segmental interneurons and their descending spinal pathways, while the phasic component depends mainly on the excitability level of spinal motoneurons.

Mechanoreceptive submodality channel interactions: single unit analysis of afferent inhibition in the primary somatosensory cortex of the cat.

This study examined whether afferent inhibition generated by activation of one mechanoreceptive submodality influences the response of neurons of the other submodality tested. Response properties of quickly adapting hair and Pacinian neurons in primary somatosensory cortex of the cat were evaluated to assess afferent inhibition generated by single-cycle sinusoidal mechanical stimuli. Animals were lightly anesthetized with sodium thiopental. Stimulation at 20 Hz (low-velocity stimulus) was used to activate hair cells, the receptive fields of which were located in the skin; stimulation at 200 Hz (high-velocity stimulus) was used to activate Pacinian cells, the receptive fields of which were located in the deeper tissues. The skin was partially dissected from the deeper tissue in order to uncouple mechanically the effective receptive surfaces and to achieve greater selectivity. Hair and Pacinian cell test responses were paired with single-cycle 20 and 200 Hz conditioning stimuli. A 20 Hz stimulus, more effective in activating hair cells than Pacinian cells, strongly inhibited the test response of hair cells only and a 200 Hz stimulus, which is more effective in activating Pacinian cells than hair cells, markedly inhibited the test response of Pacinian cells only. Our data indicate that afferent inhibition generated by activation of one submodality channel is largely confined to that submodality channel and is not distributed to the other.

Rebound excitation and the rhythmic activity of the ventrobasal complex of the thalamus.

(1) Membrane potential changes of 18 thalamocortical relay (TCR) cells of the ventrobasal complex of the cat thalamus were recorded intracellularly during rhythmic thalamic activities under moderate barbiturate anesthesia. (2) A single cutaneous stimulus evoked an initial EPSP followed by a longlasting IPSP. On the late declining phase of the IPSP, clustered rapidly rising depolarizations (RDs) were seen to generate a burst of spike potentials. The cluster of depolarizations was often followed by an IPSP, and another cycle of IPSPs and RDs with bursts of spikes was repeated. Similar rhythmic activities of TCR cells and clusters of RDs were also evoked by a single cortical stimulus, Spontaneous occurence of RDs was observed. (3) The temporal correlation between the occurrence of RDs and that of the spike potentials was noted. (4) Chloride ions were injected into the TCR cell through the recording microelectrode to eliminate the membrane hyperpolarization which would initiate the postanodal exaltation. After inversion of the IPSPs, RDs remained in the similar phase of rebound excitation to that before the reversal of the IPSPs. (5) it is concluded that excitatory inputs to TCR cells play an important role for the generation of the rhythmic discharges of TCR cells.

Mechanoreceptive submodality channel interactions: psychophysical observations on differential activation of flutter and vibration.

Psychophysical studies on masking of sensations induced by sinusoidal mechanical stimuli were conducted in human subjects to characterize the interactions within and between the submodalities of flutter and vibration. Using a conditioning-test stimulus paradigm, we found that the threshold of a test stimulus was elevated (masking) when the test stimulus was paired with a twice-threshold conditioning stimulus that activated the same submodality. Detection theory analysis further indicated that the observed elevation in threshold resulted in part from a change in stimulus detectability (i.e.d'). In contrast, when the test stimulus and the twice-threshold conditioning stimulus activated different submodalities, no elevation in test stimulus threshold (no masking) was observed. Thus, for stimuli that activate either flutter or vibration, masking (and the inhibitory operations by which it is presumably mediated) is restricted to a given submodality and not distributed across submodalities. This finding suggests that these submodality channels function independently.

Mechanisms of decubitus ulcer formation--an hypothesis.

Understanding of the etiology of decubitus ulcer formation is fragmentary and the existing literature contains much experimental data that are inconsistent with the idea that pressure sore formation is due extensively to depriving a tissue region of blood. In fact, there is substantial data that illustrate that tissue can remain viable for very extended lengths of time, up to 13 hours, when subjected to externally applied pressures that collapse the blood microvasculature in a region. Based on these observations and on studies done in this laboratory on lymph propulsion and pressure sore prevention, an hypothesis has been formulated that is consistent with the published data and with clinical observations. The hypothesis states that a major contributing factor to pressure sores is the tissue necrosis that is caused by the accumulation of anaerobic metabolic waste products due to occlusion of the lymph vessels.