Sustained potential shifts and paroxysmal discharges in hippocampal formation

1985 ◽  
Vol 53 (4) ◽  
pp. 1079-1097 ◽  
Author(s):  
G. G. Somjen ◽  
P. G. Aitken ◽  
J. L. Giacchino ◽  
J. O. McNamara

Paroxysmal firing was provoked by electric stimulation of afferent pathways in hippocampal formation of intact, urethan-anesthetized rats, of freely moving unanesthetized rats, and in hippocampal tissue slices in vitro. The electric responses of fascia dentata and CA3 zone of the hippocampus of urethan-anesthetized rats were recorded with extracellular microelectrodes. Paroxysmal discharges were provoked by stimulating the ipsilateral angular bundle. During repetitive stimulation, intercurrent paroxysmal discharges (IPaD) took the form of compound action potentials (population spikes) of large amplitude, provoked by but not locked in time to the stimulus pulses. IPaD was often but not always followed by paroxysmal after-discharge (PaAD), usually consisting of bursts of population spikes, sometimes superimposed on a slow wave. Stimulus pulses that were not strong enough to evoke population spikes when applied singly could provoke the paroxysmal firing of large amplitude spikes when applied repetitively. The liminal frequency to provoke paroxysmal firing, with 10-s train duration and with pulses evoking 60 to 80% of maximal amplitude focal postsynaptic potential (PSP) waves, varied between 6 and 15 Hz in urethan-anesthetized rats. The outbreak of IPaD was always accompanied by a marked sustained potential (SP) shift. The polarity of the paroxysmal SP shift was the opposite of the polarity of the PSP waves. We conclude that the extracellular paroxysmal SP shifts in fascia dentata are probably generated mainly by current flowing from the dendritic trees toward the cell somata of granule cells. The amplitude of the population spikes fired during paroxysmal discharges could reach 30-40 mV, indicating the precise coincidence of the impulses fired by many neurons. These spikes often arose without a detectable preceding synaptic potential. We conclude that the synchronization of the action potentials fired by granule and pyramidal cells during paroxysmal discharge is probably due to electric interaction among the neurons. In unanesthetized freely moving rats IPaD and PaAD consisting of bursts of population spikes were provoked. These were similar to those observed in urethan-anesthetized rats. Motor seizures provoked in kindled rats were associated with intense and prolonged spike bursts followed by spikeless positive waves recorded in the granule cell layer of fascia dentata. In hippocampal tissue slices maintained in vitro, paroxysmal firing could be provoked in CA1 zone by repetitive stimulation of Schaffer collaterals. IPaD and PaAD could be provoked in some slices exposed to normal (3.5 mM) [K+] and in all slices exposed to elevated (5.5 or 7.0 mM) [K+].(ABSTRACT TRUNCATED AT 400 WORDS)

1982 ◽  
Vol 48 (6) ◽  
pp. 1257-1273 ◽  
Author(s):  
B. A. Vogt ◽  
A. L. Gorman

1. An in vitro slice preparation of rat cingulate cortex was used to analyze the responses of layer V neurons to electrical stimulation of the corpus callosum (CC). In addition, synaptic termination of callosal afferents with layer V neurons was evaluated electron microscopically to provide a structural basis for interpreting some of the observed response sequences. 2. Layer V neurons had a resting membrane potential (RMP) of 60 +/- 0.68 (SE) mV, an input resistance of 47 +/- 4.74 M omega, a membrane time constant of 4.37 +/- 0.51 ms, an electrotonic length constant of 1.38 +/- 0.25, and produced spontaneous action potentials that were 50 +/- 0.3 mV in amplitude. Intracellular depolarizing current pulses evoked spikes that were sometimes associated with low-amplitude (2-5 mV) depolarizing (5-10 ms in duration) and hyperpolarizing (10-20 ms in duration) afterpotentials. 3. A single stimulus of increasing intensities to the CC produced one of the following response sequences: a) antidromic spike and an excitatory postsynaptic potential (EPSP), which initiated one or more spikes; b) antidromic spike, EPSP-evoked action potentials, and a hyperpolarization, which may have represented an intrinsic cell property or inhibitory synaptic activity; c) EPSP and evoked spikes only; d) high-amplitude EPSP with an all-or-none burst of action potentials. 4. Antidromically activated (AA) neurons always produced EPSPs in response to CC stimulation. When compared with nonantidromically activated neurons, AA cells had a more negative RMP, greater electrotonic length constant (LN), higher ratio of dendritic to somatic conductance (rho), and formed shorter duration, callosal-evoked EPSPs. 5. Neurons in anterior cingulate cortex produced EPSPs of longer duration than did those in posterior cortex (50 +/- 3.57 versus 26 +/- 1.56 ms, respectively). EPSPs in anterior neurons also had a higher maximum amplitude (20.5 +/- 1.0 versus 11.5 +/- 0.79 mV) and longer time to peak (11.6 +/- 2.2 versus 8.2 +/- 0.8 ms). 6. Electron microscopy of Golgi-impregnated neurons following contralateral lesions demonstrated that both pyramidal and nonpyramidal neurons received direct callosal afferents. Synaptic termination of callosal axons with the apical dendritic trees of anterior pyramidal cells was 6 times greater than it was with posterior pyramidal neurons. 7. EPSP shape differences in anterior and posterior neurons may be partially accounted for by the density and distribution of callosal afferents to these two cortices.


1997 ◽  
Vol 77 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Carlota Largo ◽  
Geoffrey C. Tombaugh ◽  
Peter G. Aitken ◽  
Oscar Herreras ◽  
George G. Somjen

Largo, Carlota, Geoffrey C. Tombaugh, Peter G. Aitken, Oscar Herreras, and George G. Somjen. Heptanol but not fluoroacetate prevents the propagation of spreading depression in rat hippocampal slices. J. Neurophysiol. 77: 9–16, 1997. We investigated whether heptanol and other long-chain alcohols that are known to block gap junctions interfere with the generation or the propagation of spreading depression (SD). Waves of SD were triggered by micro-injection of concentrated KCl solution in stratum (s.) radiatum of CA1 of rat hippocampal tissue slices. DC-coupled recordings of extracellular potential ( V o) were made at the injection and at a second site ∼1 mm distant in st. radiatum and sometimes also in st. pyramidale. Extracellular excitatory postsynaptic potentials (fEPSPs) were evoked by stimulation of the Schaffer collateral bundle; in some experiments, antidromic population spikes were evoked by stimulation of the alveus. Bath application of 3 mM heptanol or 5 mM hexanol completely and reversibly prevented the propagation of the SD-related potential shift (Δ V o) without abolishing the Δ V o at the injection site. Octanol (1 mM) had a similar but less reliably reversible effect. fEPSPs were depressed by ∼30% by heptanol and octanol, 65% by hexanol. Antidromic population spikes were depressed by 30%. In isolated, patch-clamped CA1 pyramidal neurons, heptanol partially and reversibly depressed voltage-dependent Na currents possibly explaining the slight depression of antidromic spikes and, by acting on presynaptic action potentials, also the depression of fEPSPs. Fluoroacetate (FAc), a putative selective blocker of glial metabolism, first induced multiple spike firing in response to single afferent volleys and then severely suppressed synaptic transmission (confirming earlier reports) without depressing the antidromic population spike. FAc did not inhibit SD propagation. The effect of alkyl alcohols is compatible with the idea that the opening of normally closed neuronal gap junctions is required for SD propagation. Alternative possible explanations include interference with the lipid phase of neuron membranes. The absence of SD inhibition by FAc confirms that synaptic transmission is not necessary for the propagation of SD, and it suggests that normally functioning glial cells are not essential for SD generation or propagation.


1990 ◽  
Vol 259 (6) ◽  
pp. L403-L409 ◽  
Author(s):  
A. C. Myers ◽  
B. J. Undem ◽  
D. Weinreich

Active and passive membrane membrane properties of parasympathetic neurons were examined in vitro in a newly localized ganglion on the right bronchus of the guinea pig. Neurons could be classified as “tonic” or “phasic” based on their action potential discharge response to suprathreshold depolarizing constant current steps. Tonic neurons (39%) responded with repetitive action potentials sustained throughout the current step, whereas phasic neurons (61%) responded with an initial burst of action potentials at the onset of the step but then accommodated. Tonic and phasic neurons could not be differentiated by other active or passive membrane properties. Electrical stimulation of the vagus nerve elicited one to three temporally distinct fast nicotinic excitatory potentials, and tetanic stimulation of the vagus nerve evoked slow depolarizing (10% of neurons) and hyperpolarizing (25% of neurons) potentials; the latter was mimicked by muscarinic receptor activation. Similar slow and fast postsynaptic potentials were observed in both tonic and phasic neurons. We suggest neurons within the bronchial ganglion possess membrane and synaptic properties capable of integrating presynaptic stimuli.


2020 ◽  
Author(s):  
Zhou Yu ◽  
J. Michael McIntosh ◽  
Soroush Sadeghi ◽  
Elisabeth Glowatzki

ABSTRACTIn the vestibular peripheral organs, type I and type II hair cells (HCs) transmit incoming signals via glutamatergic quantal transmission onto afferent nerve fibers. Additionally, type I HCs transmit via ‘non-quantal’ transmission to calyx afferent fibers, by accumulation of glutamate and potassium in the synaptic cleft. Vestibular efferent inputs originating in the brainstem contact type II HCs and vestibular afferents. Here, we aimed at characterizing the synaptic efferent inputs to type II HCs using electrical and optogenetic stimulation of efferent fibers combined with in vitro whole-cell patch clamp recording from type II HCs in the rodent vestibular crista. Properties of efferent synaptic currents in type II HCs were similar to those found in cochlear hair cells and mediated by activation of α9/α10 nicotinic acetylcholine receptors (AChRs) and SK potassium channels. While efferents showed a low probability of release at low frequencies of stimulation, repetitive stimulation resulted in facilitation and increased probability of release. Notably, the membrane potential of type II HCs measured during optogenetic stimulation of efferents showed a strong hyperpolarization even in response to single pulses and was further enhanced by repetitive stimulation. Such efferent-mediated inhibition of type II HCs can provide a mechanism to adjust the contribution of signals from type I and type II HCs to vestibular nerve fibers. As a result, the relative input of type I hair cells to vestibular afferents will be strengthened, emphasizing the phasic properties of the incoming signal that are transmitted via fast non-quantal transmission.New and NoteworthyType II vestibular hair cells (HCs) receive inputs from efferent fibers originating in the brainstem. We used in vitro optogenetic and electrical stimulation of efferent fibers to study their synaptic inputs to type II HCs. Efferent inputs inhibited type II HCs, similar to cochlear efferent effects. We propose that efferent inputs adjust the contribution of signals from type I and type II HCs that report different components of the incoming signal to vestibular nerve fibers.


1994 ◽  
Vol 71 (1) ◽  
pp. 216-228 ◽  
Author(s):  
S. Jeftinija ◽  
L. Urban

1. The effects of repetitive stimulation of primary afferents in lumbar dorsal roots on synaptic transmission in the dorsal horn (DH) were studied in a rat spinal cord slice-dorsal root ganglion (DRG)-peripheral nerve trunk preparation by the use of intracellular recording from neurons (n = 115) of the spinal dorsal horn (depth 147 +/- 139, mean +/- SD). All DH neurons were excited synaptically by electrical stimulation of the dorsal root or the peripheral nerve trunk. The electrical shocks were calibrated to produce activation either of large fibers (10–20 V, 0.02 ms) or the whole fiber population including unmyelinated afferents (supramaximal stimulus: > 35 V, 0.5 ms). Postsynaptic potentials induced by low intensity repetitive stimulation of primary afferents at frequencies below 5 Hz failed to produce a prolonged change in the resting membrane potential. In 97/115 DH neurons, slow excitatory postsynaptic potentials (EPSP)--evoked by high intensity low-frequency repetitive stimulation (0.1–2 Hz) of primary afferents--summated, producing a prolonged cumulative depolarization. In the remaining 18/115 DH neurons, high intensity low-frequency stimulation produced a cumulative hyperpolarizing response. 2. In 22 of 97 neurons that responded to high intensity repetitive stimulation with a cumulative depolarization, wind-up in the firing of action potentials was recorded. In all but two experiments, neurons that responded with wind-up to stimulation of one root responded with wind-up to stimulation of the adjacent dorsal root. In 14/22 wind-up neurons, the synaptic response to high intensity stimulation of primary afferents was composed of a short latency EPSP, followed by an inhibitory postsynaptic potential (IPSP), followed by a slow EPSP. The decrease of the amplitude and duration of the IPSP obtained during train stimulation did not seem to contribute to facilitation of transmission induced by repetitive stimulation. 3. The wind-up in firing of action potentials was followed by a prolonged potentiation of synaptic transmission in tetanized synapses. A test of other, adjacent primary afferents revealed that these synapses in the neurons in the superficial laminae had not undergone potentiation. This “synaptic specificity” of post-wind-up potentiation suggested that the mechanism for the induction of stimulation-dependent changes in the excitability of the DH neuron is presynaptic to the recorded-from neuron. 4. In a concentration of 0.5 microM and higher, tetrodotoxin (TTX) applied to sensory neurons selectively blocked action potentials in large myelinated primary afferents.(ABSTRACT TRUNCATED AT 400 WORDS)


Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1648-1653 ◽  
Author(s):  
Philippe Zizzari ◽  
Romaine Longchamps ◽  
Jacques Epelbaum ◽  
Marie Thérèse Bluet-Pajot

Administration of ghrelin, an endogenous ligand for the GH secretagogue receptor 1a (GHSR 1a), induces potent stimulating effects on GH secretion and food intake. However, more than 7 yr after its discovery, the role of endogenous ghrelin remains elusive. Recently, a second peptide, obestatin, also generated from proteolytic cleavage of preproghrelin has been identified. This peptide inhibits food intake and gastrointestinal motility but does not modify in vitro GH release from pituitary cells. In this study, we have reinvestigated obestatin functions by measuring plasma ghrelin and obestatin levels in a period of spontaneous feeding in ad libitum-fed and 24-h fasted mice. Whereas fasting resulted in elevated ghrelin levels, obestatin levels were significantly reduced. Exogenous obestatin per se did not modify food intake in fasted and fed mice. However, it inhibited ghrelin orexigenic effect that were evident in fed mice only. The effects of obestatin on GH secretion were monitored in superfused pituitary explants and in freely moving rats. Obestatin was only effective in vivo to inhibit ghrelin stimulation of GH levels. Finally, the relationship between octanoylated ghrelin, obestatin, and GH secretions was evaluated by iterative blood sampling every 20 min during 6 h in freely moving adult male rats. The half-life of exogenous obestatin (10 μg iv) in plasma was about 22 min. Plasma obestatin levels exhibited an ultradian pulsatility with a frequency slightly lower than octanoylated ghrelin and GH. Ghrelin and obestatin levels were not strictly correlated. In conclusion, these results show that obestatin, like ghrelin, is secreted in a pulsatile manner and that in some conditions; obestatin can modulate exogenous ghrelin action. It remains to be determined whether obestatin modulates endogenous ghrelin actions.


2019 ◽  
Author(s):  
Koen Kole ◽  
Yiping Zhang ◽  
Eric J. R. Jansen ◽  
Terence Brouns ◽  
Ate Bijlsma ◽  
...  

Magnetic neuromodulation has outstanding promise for the development of novel neural interfaces without direct physical intervention with the brain. Here we tested the utility of Magneto in the adult somatosensory cortex by performing whole-cell intracellular recordings in vitro and extracellular recordings in freely moving mice. Results show that magnetic stimulation does not alter subthreshold membrane excitability or contribute to the generation of action potentials in virally transduced neurons expressing Magneto.


1966 ◽  
Vol 45 (2) ◽  
pp. 305-319
Author(s):  
ROBERT K. JOSEPHSON

1. Brief electrical potentials can be recorded from a suction electrode over the marginal sphincter or over a tentacle of the anemone Calliactis polypus following appropriate stimulation of the anemone. These potentials are thought to be muscle action potentials because they precede contraction by about 12 msec. (29-31° C.) and their size is smoothly graded with the size of the contraction. 2. The tentacles and sphincter are activated by a through-conducting system in the oral disk and column. As with other anemones studied, two stimuli are required to evoke sphincter contraction. The maximum interval between an effective pair of stimuli is about 600 msec, and the sphincter potential and contraction increase with decreasing intervals to a minimum interval (as short as 15 msec.) below which there is no response to the second shock. Tentacles behave similarly except that they often produce small potentials and sometimes tiny contractions to single stimuli. 3. During repetitive stimulation the muscle potentials facilitate and the individual contractions both facilitate and sum. The tentacle musculature becomes maximally active earlier in a stimulus burst than does the sphincter.


1981 ◽  
Vol 90 (2) ◽  
pp. 255-265 ◽  
Author(s):  
A. J. S. SUMMERLEE ◽  
D. W. LINCOLN

A method is described for making extracellular recordings of the spontaneous activity of single hypothalamic neurones in unanaesthetized, freely moving, lactating rats using chronically implanted micro-wire electrodes. Extracellular recordings taken from individual neurones were maintained for periods of between 1 and 12 days. These records were not affected by any normal movement of the animal. As several micro-wires were implanted into each animal it was possible to make simultaneous recordings from several different hypothalamic sites in the same animal. Some recordings were identified as those from magnocellular neurones in the paraventricular nucleus on the basis of antidromic invasion after electrical stimulation of the neurohypophysis. Milk ejection in response to the prolonged sucking of ten or more pups was intermittent, and individual milk ejections recurred at intervals of 2–10 min throughout each period of nursing. The rise in intramammary pressure at milk ejection was associated with a vigorous extensor response from the pups. This was monitored by radar to provide an index of milk ejection in the unanaesthetized rat. Eleven antidromically identified neurones were recorded through 321 milk ejections. Eight of these neurones displayed a transient (2–6 s) and very substantial acceleration in discharge at the time predicted for oxytocin release, i.e. 10–12 s before milk ejection. The background discharge of these cells was 0·1–2·6 action potentials/s; this increased to 16–50 action potentials/s during the brief period of accelerated activity. Twenty-five neurones were studied during 365 milk ejections in rats which did not have a stimulating electrode implanted in the neurohypophysis. Thirteen of these neurones displayed a burst of high frequency discharge before each milk ejection, similar to that described for the antidromically identified neurones. Two of the non-responsive cells displayed a phasic pattern of discharge, characteristic of vasopressinergic neurone discharge recorded in anaesthetized rats. These observations of putative oxytocinergic neurones in unanaesthetized, freely moving rats are identical with those previously made on anaesthetized rats, and establish that the high frequency burst of electrical activity displayed by magnocellular neurones some 10–12 s before milk ejection is responsible for oxytocin release under normal physiological circumstances.


2020 ◽  
Author(s):  
Kristen L. Kozielski ◽  
Ali Jahanshahi ◽  
Hunter B. Gilbert ◽  
Yan Yu ◽  
Önder Erin ◽  
...  

AbstractDevices that electrically modulate the central nervous system have enabled important breakthroughs in the management of neurological and psychiatric disorders. Such devices typically have centimeter-scale dimensions, requiring surgical implantation and wired-in powering. Using smaller, remotely powered materials could lead to less invasive neuromodulation. Herein, we present injectable magnetoelectric nanoelectrodes that wirelessly transmit electrical signals to the brain in response to an external magnetic field. Importantly, this mechanism of modulation requires no genetic modification of the brain, and allows animals to freely move during stimulation. Using these nanoelectrodes, we demonstrate neuronal modulation in vitro and in deep brain targets in vivo. We also show that local thalamic modulation promotes modulation in other regions connected via basal ganglia circuitry, leading to behavioral changes in mice. Magnetoelectric materials present a versatile platform technology for less invasive, deep brain neuromodulation.


Sign in / Sign up

Export Citation Format

Share Document