Fig. 30. Change in form of electrical response of the cerebral cortex surface on direct stimulation at the maximum and minimum of an infraslow wave. (A, B, C, D) level of infraslow potential. (1, 2, 3, 4) corresponding to these levels recordings of the surface response (in recordings 3 and 4 the sign of the stimulation has been reversed). Bottom: superposition of curves recorded at different levels of infraslow potentials. Change of potential in negative direction, upwards. The rabbit was immobilized by diplacin.
the succeeding positive potential 5 msec, and the aiterpotential 20 msec.
Record 2 (Fig. 30) was made at the time when the level of the infra-slow potential between the electrodes (B) changed by 0.5 mV. The initial positive potential in the recording of the response faithfully retains its magnitude and duration. The negative dendrite potential slightly increases in amplitude and lengthens to 20 msec, the succeeding positive potential is absent, and the afterpotential likewise disappears. Record 3 was obtained one second after Record 2, after reversing the sign of the stimulus. Record 4 was the response at an ISPO maximum (D), with a change in amplitude of 1 mV. Comparing this record with record 1, there are several important points to note: the invariability of the positive phase, an almost twofold increase in the amplitude of the dendrite potential and a lengthening of it from 15 to 22 msec. Recordings of the response made at different ISPO levels (designated with letters) are shown in Fig. 30 (bottom).
The above-described changes in amplitude and duration of the dendrite potential at different extrema of the ISPO recurs several times in the same experiment and with the same arrangement of the electrodes, displaying a definite pattern. The pattern is as follows. The dendrite component of the surface response increases at one of the ISPO extrema, while the next phase, which is associated with the manifestation of excitation of neurons in thes deep layers, disappears. The excitability of neurons in the deep layers is evidently decreased and impulses do not reach the layer of the apical dendrites. This agrees with the analysis of the origin of the second positive component of the surface response made by Burns (1951a, b) and Roitbak (1955), and it supports Adrian's hypothesis (1936) that the neurons in the deep layers are the source of this positive potential.
Fig. 31 reveals the relationship between the ISPO level and the negative afterpotential, apparently reflecting the activity of the neurons in the deep layers.
Thus, the amplitude and duration of the electrical response to stimulation of the cortical surface change simultaneously with the infraslow rhythmic change in potential. However, the initial positive potential does not change in time with the ISPO, but the dendrite potential, succeeding positive phase, and negative afterpotential do change.
The initial positive potential is resistant to many factors. For example, the administration of d-tubocurarine (3 mg/kg) reduces the dendrite potential considerably, but the preceding positive potential persists (Purpura and Grundfest, 1956). Only large doses of the drug suppress it. Since d-tubocurarine blocks synaptic transmission, the assumption is that the synapses at the dendrites are more sensitive to its blocking action than the synapses of the internuncial neurons.
The invariability of the initial positive potential at ISPO minima and maxima may likewise reflect the stability of the properties of the neurons in layers III-IV of the cortex.
These facts justify the view that the excitability of some cortical neurons changes with the ISPO, while the excitability of other neurons is independent of this phenomenon. The former includes those neurons whose cell body is localized in the lower layers of the cortex and whose
apical dendrites are in the upper layers. The latter includes the inter-nuncial neurons of the upper layers. The excitability of the apical dendrites seems to be closely linked with the phenomenon of the infra»» slow rhythm.
Rhythmic stimulation of the intralaminar nuclei of the thalamus:
The nuclei of the thalamus are functionally subdivided (Jasper, 1949) into specific and nonspecific. It is assumed that the effect spreads from the nonspecific nuclei to certain cortical areas. Using histological techniques, Adrianov demonstrated several years ago (1958) that the nonspecific nuclei of the thalamus may be associated with a very limited area of the cortex, thus ensuring the localized character of nonspecific influences on the cortex. Local projection to the cortex was found for the dorsomedial and medioventral nuclei of the thalamus; certain nuclei of the midline have no direct connections with the cortex, but are connected with other, specific and nonspecific, thalamic nuclei. Stimulation of the nonspecific nuclei changes the cortical response to stimulation of the specific thalamic nucleus (Narikashvili, 1958). Nonspecific impulses may facilitate discharges of units activated by the specific system, both influencing the dendrites and activating other neurons, and thus result in increased circulation of impulses in closed circuits.
Stimulation of the intralaminar nuclei of the thalamus produces mono-phasic potentials from the surface of the cortex (Fig. 32) consisting of four main components: (1) a negative potential spreading with decrement (Clare and Bishop, 1956; Li et al., 1956b) and regarded as dendrite potential; (2) a positive oscillation reflecting excitation of the subjacent elements and spreading without decrement; (3) a
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