Journal of Neurophysiology

Lotshaw, D. P.; Levitan, I. B.

doi: N/Apmid: 3694250

Abstract 1. The effect of serotonin (5-HT) and forskolin on an inwardly rectifying K+ conductance (IKR) was studied using voltage-clamp techniques in several identified Aplysia neurons isolated and maintained in primary cell culture. 2. Inward rectification was observed in the current-voltage relationship of the identified neurons R15, R2, B1, and B2 and was predominately due to IKR, as demonstrated by the dependence of inward rectification on the extracellular K+ concentration, instantaneous kinetics of the membrane current response to hyperpolarizing voltage clamp pulses, and voltage-dependent Ba2+ block of the inwardly rectifying current. 3. 5-HT increased IKR conductance between 100 and 400% in the identified neuron R15 in culture and increased IKR conductance approximately 50% in the identified neurons B1, B2, and R2 in culture. The adenylate cyclase activator, forskolin, plus a phosphodiesterase inhibitor, Ro 20-1724, also increased IKR conductance in these neurons. 4. 5-HT and forskolin modulated other ion conductances as well in all of these cultured neurons. Copyright © 1987 the American Physiological Society

Hablitz, J. J.

doi: N/Apmid: 3694244

Abstract 1. Intra- and extracellular recording techniques were used to study epileptogenesis in in vitro slices of immature rat neocortex. Slices of sensorimotor cortex were prepared from animals 5-60 days old. Epileptiform activity was induced by bath application of 50 microM picrotoxin. 2. Convulsant-induced paroxysmal activity was observed only rarely in the youngest age group (5-7 days) and consisted of orthodromically evoked bursts of low-amplitude isolated discharges. This activity was labile and could be evoked only at long interstimulus intervals (greater than 10 s). 3. Extracellular recordings in slices from 8- to 15-day-old rats showed spontaneous epileptiform activity consisting of 10- to 30-s paroxysms of repetitive spike discharges superimposed on a 3- to 5-mV negative steady potential. This steady potential declined slightly during the course of the prolonged discharge and returned quickly to base line following the last spike discharge. 4. Laminar analysis of epileptiform activity in 8- to 15-day-old rats showed that the spike discharges were negative and superimposed on a positive slow wave in superficial cortical layers. At 100 micron below the pial surface, the slow potential reversed polarity and remained negative throughout the remainder of the cortex. Spike discharges reversed polarity 800 micron below the pial surface. 5. In intracellular recordings from slices obtained from 9- to 14-day-old animals, each paroxysm began with a sharply rising membrane depolarization (paroxysmal depolarizing shift, or PDS). A second PDS occurred before the cells repolarized to their resting potential. A series of PDSs then followed, superimposed on a sustained membrane depolarization. This was associated with a 33% decrease in input resistance. Afterhyperpolarizations (AHPs) following termination of the depolarization were low in amplitude or absent. 6. In the 16- to 30-day-old age group, extracellular recordings showed paroxysmal activity consisting of 3-10 initial spikes followed by a sustained, slow, negative-potential shift. This slow potential could be as great as 30 mV in amplitude and could last as long as 180 s. Paroxysmal events recurred spontaneously at intervals of 4-11 min. Spontaneous PDSs and slow, negative-potential shifts were not observed after 30 days of age, although PDSs could still be evoked by orthodromic stimulation. 7. Intracellular recordings in the 16- to 30-day-old group revealed that each paroxysmal event consisted of an initial period of increased synaptic activity and cellular firing, followed by a marked, long-lasting depolarization (LLD), culminating in an AHP.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1987 the American Physiological Society

Schmidt, M.; Humphrey, M. F.; Wassle, H.

doi: N/Apmid: 3694255

Abstract 1. Retinal ganglion cells were recorded extracellularly in the intact eye of anesthetized adult cats. The effects of acetylcholine (ACh), the muscarinic antagonist scopolamine (Sco), the nicotinic antagonist dihydro-beta-erythroidine (DBE), and the acetylcholinesterase inhibitor physostigmine (Phy) on maintained and light-evoked ganglion cell discharge was examined using iontophoresis techniques. 2. A monoclonal antibody directed against the ACh synthesizing enzyme choline acetyltransferase (ChAT) was used to label cholinergic cells in retinal wholemounts. The topographical distribution of these cells was studied. 3. Intracellular filling with the fluorescent dye lucifer yellow (LY) was performed to identify the dendritic morphology of putative cholinergic neurons. 4. ACh increased and Sco decreased neuronal activity of all brisk ganglion cell types under all stimulus conditions tested in this study. The action of ACh was abolished during simultaneous application of Sco. 5. DBE raised the firing rate of ON-center brisk cells and decreased activity of OFF-center brisk cells. Again there was no difference under different stimulus conditions. During DBE application the ACh action on OFF-center cells was completely blocked. The ACh action on ON-center cells was diminished. 6. Phy prolonged and enhanced ACh action on all ganglion cell types. During simultaneous stimulation of the receptive-field center and the surround, Phy caused an activity shift in favor of the center response. 7. Immunocytochemical staining revealed two populations of amacrine cells, one in the inner nuclear layer, and the other in the ganglion cell layer. Their total density increased from 250 cells/mm2 in the periphery to 2,700 cells/mm2 in the central area. Analysis of the distribution pattern indicated a functional independence of the two subpopulations. 8. The dendritic morphology of putative cholinergic amacrine cells in the cat retina resembled that of rabbit and rat "starburst" amacrines, which are known to be cholinergic. 9. The possible function of cholinergic amacrine cells in the cat retina is discussed in view of the present findings and compared with results from other mammalian species. Copyright © 1987 the American Physiological Society

Richardson, T. L.; Turner, R. W.; Miller, J. J.

doi: N/Apmid: 3694254

Abstract 1. The site of origin of evoked action-potential discharge in hippocampal CA1 pyramidal neurons was investigated using the in vitro rat hippocampal slice preparation. 2. Action-potential discharge in pyramidal cells was evoked by stimulation of efferent pyramidal cell fibers in the alveus (antidromic) or afferent synaptic inputs in stratum oriens (SO) or stratum radiatum (SR). Laminar profiles of evoked extracellular field potentials were recorded at 25-micron intervals along the entire dendrosomatic axis of the pyramidal cell and a one-dimensional current source-density analysis was applied. 3. Suprathreshold stimulation of the alveus evoked an antidromic population spike response and current sink with the shortest peak latency in stratum pyramidale or proximal stratum oriens. A biphasic positive/negative potential associated with a current source/sink was recorded in dendritic regions, with both components increasing in peak latency with distance from the border of stratum pyramidale. 4. Suprathreshold stimulation of SO or SR evoked a population spike response superimposed upon the underlying synaptic depolarization at all levels of the dendrosomatic axis. The shortest latency population spike and current sink were recorded in stratum pyramidale or proximal stratum oriens. In dendritic regions, a biphasic positive/negative potential and current source/sink conducted with increasing latency from the border of stratum pyramidale. 5. A direct comparison of alvear- and SR-evoked responses revealed a basic similarity in population spike potentials and associated sink/source relationships at both the somatic and dendritic level and a similar shift in peak latency of spike components along the pyramidal cell axis. 6. It is concluded that the initial site for generation of a spike along the dendrosomatic axis of the pyramidal cell following antidromic or orthodromic stimulation is in the region of the cell body layer (soma or axon hillock). Action-potential discharge in dendritic regions then occurs as the result of a subsequent retrograde spike invasion of basal and apical dendritic arborizations. Copyright © 1987 the American Physiological Society

Suzue, T.; Wu, G. B.; Furukawa, T.

doi: N/Apmid: 2826717

Abstract 1. The effect of hypoxia on synaptic transmission between hair cells and afferent fibers was examined in the sacculus of goldfish. For this, we recorded potentials, intracellularly, from large afferent fibers. Anoxia was introduced by perfusing the gill with water deprived of oxygen or by halting the water flow to the gill. 2. The ear of the goldfish is most sensitive to hypoxia. Sound-evoked afferent activities were profoundly depressed within several minutes after the introduction of hypoxia. 3. The depressed afferent activity was attributed to a reduction in the amplitude of sound-evoked excitatory postsynaptic potentials (EPSPs) generated at afferent fiber terminals, since no significant change was detected in the resting and action potentials of afferent fibers or in intensity of the threshold current required to set up an action potential. Also, there was no marked change in the electrical activity of hair cells, determined by the finding that the amplitude of intramacularly recorded microphonic potentials and that of the coupling potentials was not altered. 4. A statistical analysis of the amplitude of sound-evoked EPSPs revealed that the binomial parameter n decreased during hypoxia, in parallel with a reduction in the amplitude of EPSPs, while the binomial parameter p either remained unaltered or was augmented. No change was found in the quantal size, thereby indicating that the sensitivity of the postsynaptic membrane remained unchanged. These results indicate that presynaptic mechanisms within hair cells, especially those playing a role in transmitter release or in replenishment of the latter, are suppressed during hypoxia. Copyright © 1987 the American Physiological Society

Altmann, L.; Luhmann, H. J.; Greuel, J. M.; Singer, W.

doi: N/Apmid: 3694253

Abstract 1. In order to determine the degree of synchrony of binocular activation required for the development of binocularity we reared 11 kittens with rapidly alternating monocular occlusion. Alternating occlusion was achieved with microprocessor-controlled electrooptic solid-state shutters, which were fitted to individually moulded goggles. The intervals of alternating occlusion were varied from 50 to 1,000 ms. Two normally reared kittens and three kittens that were reared with the shutters operating synchronously with open/close intervals of 50/50 ms, 200/200 ms, and 400/100 ms, respectively, were used as controls. Toward the end of the critical period we examined the kittens' ability for binocular depth discrimination and tested binocular luminance summation of the pupillary light reflex. Single-cell recordings were made from the visual cortex in order to determine the percentages of binocularly excitable neurons. 2. There was a good correlation between the degree of asynchrony of binocular experience, the impairment of depth discrimination, and the percentage of binocular neurons. Kittens reared with alternation rates of 200, 330, and 400 ms, respectively, had developed normal binocularity and were indistinguishable from the controls. Alternation rates of 500 ms or longer prevented the development of normal depth discrimination and luminance summation and resulted in reduced cortical binocularity. 3. A linear relationship between depth discrimination, binocular luminance summation, and percentages of binocular neurons was found. 4. Our findings indicate that an asynchrony of binocular activation of several hundred milliseconds is compatible with the development of normal binocularity in the kitten visual system. Copyright © 1987 the American Physiological Society

Lotshaw, D. P.; Levitan, I. B.

doi: N/Apmid: 3694251

Abstract 1. The effect of serotonin (5-HT) and forskolin on a hyperpolarization activated Cl- conductance (gCl-) was studied using voltage-clamp techniques in identified Aplysia neurons maintained in primary cell culture. 2. The hyperpolarization-activated conductance induced by intracellular Cl- loading was carried by Cl- as determined by the following criteria: the extrapolated reversal potential of the current closely approximated the reversal potential of a cholinergic Cl- conductance, the current was not affected by extracellular ion substitutions other than Cl-, extracellular thiocyanate ions reversibly inhibited the current and the current exhibited slow voltage-dependent exponential kinetics similar to those described for the hyperpolarization-activated Cl- current in Aplysia neurons in situ. 3. In the identified neurons B1, B2, R15, and R2, 5-HT or forskolin reversibly inhibited gCl-, suggesting that 5-HT acted via an adenosine 3',5'-cyclic monophosphate-dependent mechanism. 4. Serotonergic inhibition resulted from a change in the voltage dependence of Cl- channel gating. Copyright © 1987 the American Physiological Society

Sawaguchi, T.

doi: N/Apmid: 3694245

Abstract 1. Quantitative properties of neuronal activity related to a visual reaction time task were studied in the monkey prefrontal cortex. The task consisted of an initial waiting phase (3.0-s period), a warning phase (green lamp, a variable period of 1.5-3.5 s), a go phase (red lamp), and a reward phase. 2. A total of 189 task-related neurons showed 233 changes in discharge rates during the warning (n = 86), GO (n = 103), and reward (n = 44) phases of the task. Most of the task-related neurons (145/189, 77%) showed changes during only one of the task phases, and were designated W (warning phase)-type (n = 42), GO (go phase)-type (n = 59), and RE (reward phase)-type (n = 44) neurons. The remainder (n = 44, 23%) showed changes during both the warning and the go phases, and were designated WG (warning and go phase)-type neurons. In each phase, onset latencies, peak latencies, and decay times of each change were measured and compared. 3. The changes during the warning phase (n = 86) were separated into three groups based on decay time; that is, phasic changes (n = 31), phasic-tonic changes (n = 23), and tonic changes (n = 32). Onset latencies and peak latencies were homogeneously distributed, and there were no clear groupings, although phasic and phasic-tonic changes tended to show shorter latencies than tonic changes. 4. The changes during the go phase (n = 103) did not show distinct differences, either in terms of decay time or of latency. The changes during the go phase showed various degrees of coupling to both the visual go signal (GS) and lever-release hand movement. To quantitate the coupling, a value to indicate the degrees of coupling (coupling index) was calculated. The changes coupled more strongly to the GS (cue coupled), those coupled more closely to the lever release (movement coupled), and intermediate changes could be distinguished from each other. The cue-coupled changes showed shorter latencies from the time onset of the GS than the movement-coupled changes, and the intermediate changes showed intermediate latencies. The decay time and the duration of the intermediate changes were longer than those of the cue-coupled changes and the movement-coupled changes. 5. The properties of WG-type neurons were compared with those of W-type and GO-type neurons.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1987 the American Physiological Society

Sawaguchi, T.

doi: N/Apmid: 3694246

Abstract 1. Using microiontophoretic techniques and conscious monkeys, sensitivities to noradrenaline (NA) and dopamine (DA) of neurons of the prefrontal cortex (PFC), which showed changes in activity during a visual reaction time task, were investigated. The visual reaction time task was initiated by the pressing of a lever and consisted of four phases: an initial waiting phase of 3.0 s, a warning phase (green light of variable duration of 1.5-3.5 s), a lever release go phase (red light), and a final reward phase. 2. A total of 153 neurons, which showed changes in activity during one or two phase(s) of the task, were sampled. Of these neurons, 39 changed their activity during the warning phase, 48 changed their activity during the go phase, 38 changed their activity during both the warning and the go phases, and 28 changed their activity during the reward phase. 3. Iontophoretically applied NA and DA (with a current of 30-70 nA, but usually with a current of 50 nA) induced excitatory and/or inhibitory responses in 141 of the 153 task-related neurons. NA induced responses in 99 neurons, and these responses were predominantly inhibitory (n = 90). DA induced excitatory (n = 62) and inhibitory (n = 30) responses in 92 neurons. Fifty neurons were sensitive to both NA and DA. 4. The neurons showing changes in activity during different phases of the task showed different sensitivities to NA and DA applied with 50 nA. The warning phase-related neurons were primarily sensitive to NA (36/39), the go phase-related neurons were primarily sensitive to DA (44/48), neurons related to both the warning and go phases were sensitive to both NA and DA (33/38), and the reward phase-related neurons were primarily sensitive to NA (23/28). 5. In the neurons that showed increased changes in activity during the warning phase, NA reduced the background activity to a greater extent than the activity during the warning phase and increased the ratio of the warning phase-related activity to the background activity. In the neurons that showed decreased changes during the warning phase, NA reduced the activity during the warning phase to a great extent than the background activity, and increased ratio of the background activity to the warning phase-related activity. Furthermore, the latency of onset of the change in activity tended to become shorter by application of NA. Thus, NA enhanced the change in activity during the warning phase, irrespective of whether the direction of the change was toward an increase or a decrease.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1987 the American Physiological Society

Calancie, B.; Nordin, M.; Wallin, U.; Hagbarth, K. E.

doi: N/Apmid: 3694249

Abstract 1. Transcranial cortical stimuli (TCCS) were used to elicit motor responses in contralateral wrist flexor and extensor muscles of healthy adult subjects. The motor responses were assessed by surface EMG recordings, by needle recordings of single motor-unit discharges, and by measurements of wrist twitch force. Our main aim was to analyze the single-unit events underlying those changes in latency, amplitude, and duration of the compound EMG responses, which could be induced by voluntary preactivation of target muscles and by changes in stimulation strength. 2. Different stimulus strengths were tested with and without background contractions in the flexor or extensor muscles. For each test (consisting of a series of 20 stimuli) the compound EMG responses were averaged and displayed together with the averaged wrist force signals. Responses of individual flexor and extensor motor units were displayed in raster diagrams and peristimulus time histograms. For units exhibiting a background firing, the mean background interdischarge interval was calculated and compared with the subsequent poststimulus intervals. 3. In relaxed muscles, a shortening of onset latency of evoked compound EMG responses was observed when raising stimulation strength. A similar latency reduction was not seen in any of the single-unit recordings. This would be consistent with the size principle of motoneuron recruitment. 4. A shortening of onset latency of evoked EMG potentials was observed also as a result of a voluntary preactivation. Such latency shifts, which were seen also in single-unit recordings, might be attributed to variations in the time required for D and I wave temporal summation at the anterior horn cell. 5. When raising stimulation strength or when adding voluntary background contraction, the evoked compound EMG potential grew not only in amplitude but also in duration, as later peaks of activity were added to the initial ones. Under optimal conditions (strong stimulus + background contraction), the period of excitation (termed E1) had an onset latency of approximately 15 ms and a duration of approximately 35 ms and was similar for wrist flexor and extensor muscles. 6. We never saw the same flexor or extensor unit fire more than once during the E1 period. For units preactivated by a background contraction, the stimulus-triggered impulse exhibited latency shifts, which, to a large extent, depended on the timing of the stimulus in relation to a preceding background discharge and which could be influenced by a change in stimulation strength.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1987 the American Physiological Society