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PubMed1995

Chronic corticosterone treatment maintains synaptic activity of CA1 hippocampal pyramidal cells: acute high corticosterone administration increases action potential number.

The hypothalamic-pituitary-adrenocortical (HPA) axis controls the levels of plasma corticosterone (CT) in the rat and the levels of cortisol in man. CT is important in maintaining homeostasis and regulating energy production. Homeostasis is maintained by basal activation of the hippocampal-HPA axis. In response to stress CT secretion is increased. CT activation of receptors in the hippocampus provides feedback inhibition of the HPA axis to return the system to basal activity. There are two types of CT receptors: the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). CT has a 10-fold higher affinity for MR than GR. Normal basal levels of CT occupy the majority of the MR. During the diurnal surge of CT and following the presentation of a stressful stimulus, the MR and GR are both maximally occupied. To begin to understand how CT influences the hippocampal-HPA axis, intracellular recording techniques in the hippocampal brain slice preparation were used to determine how high concentrations of CT may alter cell characteristics and/or evoked synaptic activity. Two treatment groups were used, i.e., adrenalectomized (ADX) and ADX with CT pellet replacement (ADX+CT) that produced plasma blood levels equal to that seen in a normal rat in the morning. Acute administration of 100 nM CT decreased action potential threshold and the number of action potentials elicited by a depolarizing current pulse in cells from both the ADX and ADX+CT treated rats. The amplitude of the evoked excitatory postsynaptic potentials (EPSP) or inhibitory postsynaptic potentials (IPSP) declined in cells recorded from ADX animals and ADX rats acutely treated with high concentrations of CT (ADX/CT).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1999

Neuronal pathways from low-threshold hindlimb cutaneous afferents to motoneurons innervating trunk muscles in low-spinal cats.

Postsynaptic potentials (PSPs) evoked in motoneurons innervating the back and abdominal muscles in the lumbar part of the body by stimulating hindlimb cutaneous afferents were investigated in unanesthetized decerebate and spinal cats. Various types of PSP: pure excitatory postsynaptic potential (EPSP), pure inhibitory postsynaptic potential (IPSP), and mixed PSP (i.e., EPSP followed by IPSP, EPSP/IPSP; and IPSP followed by EPSP, IPSP/EPSP) were observed. The weak stimulation at 2 times threshold (2T) produced predominantly the EPSP, while at 5T the incidence of IPSP or EPSP followed by IPSP was increased. In about 20-50% of the various groups of motoneurons, PSPs evoked by ipsi- and contralateral nerves were qualitatively and quantitatively similar. For the other motoneurons, PSPs evoked by ipsi- and contralateral nerves were markedly different with respect to magnitude and/or polarity. These findings suggest that, within each motoneuron pool, some neurons act to increase stiffness of the trunk or to move vertically in response to an increased activity of cutaneous afferents, while the other motoneurons act to produce lateral bending of the trunk.

Afferent Pathways↗

PubMed1976

Effect of temperature on postsynaptic potentials of cat spinal motoneurones.

The effect of spinal cord temperature on excitatory postsynaptic potentials (EPSP) and inhibitory postsynaptic potentials (IPSP) were measured by means of intracellular recordings from lumbar motoneurones of 43 cats. While body temperature and oil bath temperature were maintained between 37 and 38 degrees C, the temperature of the spinal segment under investigation was changed separately in the range between 30 and 42 degrees C. Cooling consistently produced an increase in amplitude and duration of both, mono- and poly-synaptic EPSPs and recurrent and direct IPSPs. Warming caused the opposite effect. The input resistance of the motoneurones was inversely related to the spinal cord temperature, while the latency of action potentials produced by intracellular injection of outward current was directly and exponentially related to spinal temperature. Although the data do not provide a quantitative differentiation of pre- versus postsynaptic temperature effects, they are consistent with the notion that temperature dependent changes on postsynaptic membrane properties contribute to the observed PSP changes. It is further suggested that similar postsynaptic temperature effects may be concerned in temperature sensitivity of proposed specific central neurones.

Animals↗

PubMed1987

The axon reaction of lamprey spinal interneurons.

Axotomy and partial denervation of giant interneurons (GIs) and lateral cells (LCs) were produced by complete spinal transection in the larval lamprey spinal cord. Both cell types demonstrated a reduction in cytoplasmic basophilia, increase in cell size, nuclear eccentricity, and formation of a chromophilic nuclear cap. This was quantified in the case of cell diameter. During the first 8 weeks of recovery, the GIs with the largest diameters were found progressively further from the scar and this peak change moved at approximately 0.5 mm/day. The increase in size of GIs remained up to 20 weeks post-transection, long after the time required for their axons to regenerate across the scar and form functioning synapses. GIs injected intracellularly with horseradish peroxidase (HRP) also showed this increase in diameter as well as a simplification of their dendritic trees. Intracellular recordings from GIs revealed changes in the frequency and amplitude of spontaneous synaptic input. In the first two weeks after transection, spontaneous excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) were less frequent than in control cells. After 6 weeks of recovery they became more frequent than in control cells. EPSPs predominated in axotomized GIs, while in control cells they constituted only 36% of the total of spontaneous potentials. A reversible increase in the amplitude of these EPSPs occurred at 3-4 weeks of recovery time. The resting membrane potential was significantly reduced by the 6th week after transection and returned to normal after the 22nd week.

Animals↗

PubMed1987

Effects of ethanol on CA1 and CA3 pyramidal cells in the hippocampal slice preparation: an intracellular study.

Superfusion of ethanol (10-350 mM) sometimes caused weak hyperpolarization, but more often elicited weak depolarization or biphasic depolarizing, hyperpolarizing responses in CA1 and CA3 pyramidal neurons of the hippocampal slice. The occasional polarizations were sometimes accompanied by, but not always correlated with, small increases or decreases in input resistance. However, many cells in both areas showed no detectable change in membrane potential (36% of cells) or input resistance (57% of cells), even at very high ethanol concentrations (86-200 mM). Spontaneous spiking, when present, was occasionally accelerated or decelerated, although in CA3 a biphasic speeding-slowing sequence was often seen. The afterhyperpolarizations following bursts of action potentials evoked by current (CA1) or occurring spontaneously (CA3) were most often either slightly reduced in amplitude (CA3) or not affected (CA1) by ethanol superfusion. In contrast, synaptic potentials evoked by stimulation of the hilar mossy fiber pathway (for CA3) or the stratum radiatum (for CA1) were more sensitive to ethanol: excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) were most often reduced in amplitude in both CA1 and CA2, even at low ethanol concentrations (10-50 mM). The action on IPSPs may be exerted presynaptically, because responses to locally applied GABA were little affected. These results suggest that hippocampal evoked synaptic activity may be more sensitive than postsynaptic membrane properties to physiologically relevant ethanol concentrations.

Action Potentials↗

PubMed1996

Electrophysiological actions of hemoglobin on rat hippocampal CA1 pyramidal neurons.

Hemoglobin, the oxygen-carrying component of red blood cells, can be released from erythrocytes in hemorrhagic stroke and intracranial bleeding associated with head injuries. Therefore, neurons may be exposed to this agent. In addition, hemoglobin can chelate nitric oxide (NO) and has been used in studying the role of NO in synaptic plasticity and excitotoxicity. However, the electrophysiological actions of hemoglobin on central neurons are not well characterized. In the present investigation, the electrophysiological actions of hemoglobin on CA1 pyramidal neurons in rat hippocampal slices were studied with conventional intracellular pointed microelectrode- as well as perforated patch-recordings. Superfusion of rat hippocampal slices with hemoglobin (0.05 or 0.1 mM for 10-15 min) induced a depolarization of CA1 neurons and suppressed the stratum radiatum stimulation-induced excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). The hemoglobin-induced depolarization as well as the suppression of the synaptic transients were present in slices pretreated with 0.1 or 0.5 mM of N omega-nitro-L-arginine, a nitric oxide synthase inhibitor, suggesting that hemoglobin has electrophysiological actions on hippocampal CA1 neurons that are independent of its NO scavenging property.

Animals↗

PubMed1981

Differential effects of pentobarbital and ether on the synaptic transmission of the hippocampal CA1 region in the rat.

The effect of ether and sodium pentobarbital on the synaptic transmission of the hippocampal CA1 region was studied in chronically implanted rats. Animal behavior, EEG, and the average evoked potentials (AEPs) following electrical stimulation of the alveus or the stratum radiatum in the CA1 region were recorded. Components of the AEPs, interpreted previously as generated by population excitatory postsynaptic potentials (EPSPs), population inhibitory postsynaptic potentials (IPSPs) (Leung 1979a, b, c) or population postsynaptic spikes (Andersen et al. 1971), were differentially sensitive to ether or pentobarbital. Ether reduced the population EPSPs and population spike evoked at all intensities tested (1-4 X threshold); the population IPSP was slightly enhanced at intermediate stimulus intensities. Pentobarbital suppressed the population EPSP evoked by alvear stimulation but not that by radiatum stimulation, reduced the population spike and greatly enhanced and prolonged the population IPSP evoked at low stimulus intensities. At high stimulus intensities, the IPSP was interpreted to be smaller after pentobarbital but neuronal output from the hippocampal CA1 region, as seen from the evoked population spike, remained attenuated. It is concluded that ether and pentobarbital both suppress hippocampal neuronal excitability but the effect of anesthesia differs for different anesthetics, for different synapses and for different levels of activity in the input fibers.

Animals↗

PubMed1993

Presynaptic inhibition by adenosine A1 receptors on guinea pig small intestinal myenteric neurons.

BACKGROUND: Adenosine acts at A1 receptors to inhibit the release of most neurotransmitters. This study tested the hypothesis that both exogenous adenosine (ADO) and tonic release of endogenous ADO act at presynaptic A1 receptors to suppress excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) in myenteric neurons. METHODS: Intracellular microelectrodes were used to study actions of ADO, the agonists 2-chloro-N6-cyclopentyl ADO, its 1-deaza derivative, 5'-N-ethylcarboxamido ADO, and CGS 21680 or the antagonists 8-cyclopentyl-1,3-dimethylxanthine, its 1,3-dipropyl analog, and 1,3-dipropyl-8-p-sulfophenylxanthine on synaptic behavior in myenteric neurons. RESULTS: Each of the agonists suppressed slow EPSPs in all 35 AH/type 2, 8 of 10 S/type 1, and 7 of 7 nonspiking neurons. ADO also decreased neuronal excitability (n = 63) in AH/type 2 neurons. Agonists suppressed fast nicotinic EPSPs in all 20 S/type 1, 10 nonspiking, and 3 AH/type 2 neurons without having any effect on postsynaptic responses to nicotinic agonists. CCPA was more potent than CGS 21680 in suppressing EPSPs. In 30% of neurons, the only action of antagonists was to block the effect of A1 or A2 agonists on EPSPs. Agonists did not inhibit IPSPs, but unmasked robust slow IPSPs by preventing slow EPSPs. Antagonists acted alone to enhance EPSPs in 70% of neurons. CONCLUSIONS: (1) ADO acts at presynaptic A1 sites to suppress EPSPs in all neurons, (2) IPSPs are revealed by ADO, and (3) ongoing release of endogenous ADO inhibits synaptic transmission.

Adenosine↗

PubMed1994

Influence of temperature on anoxic responses of neocortical pyramidal neurons.

Intracellular recordings were made in pyramidal neurons of layers II-III of rat fronto-parietal neocortical slices. The membrane and synaptic properties and effects of brief (4-6 min) anoxia-anoxic depolarization and synaptic depression--were recorded at temperatures between 26 and 37.5 degrees C. In normoxic conditions, both warming (> or = 35 degrees C) and cooling (< or = 32 degrees C) induced a reduction in the amplitude of early and late excitatory postsynaptic potentials and abolished inhibitory postsynaptic potentials. Excitatory postsynaptic potential latency decreased with warming and increased with cooling. Warming also induced spontaneous brief depolarizations, had a general slow depolarizing effect on resting membrane potential, and decreased input resistance. During oxygen deprivation, the steepness of the rising phase of the anoxic depolarization and the duration of the repolarization phase were augmented by warming above 36.5 degrees C (3.7 +/- 0.1 vs 1.9 +/- 0.1 mV/min and 8.75 +/- 0.98 vs 4.16 +/- 0.28 min, respectively). The peak amplitude of the anoxic depolarization increased in only one-third of trials (6.6 +/- 0.6 vs 4.3 +/- 0.4 mV). Warming potentiated the depressant effect of anoxia: at 36.5 degrees C early excitatory postsynaptic potential amplitude decreased to 32.3 +/- 5.2% of control compared with 58.3 +/- 1.2% at 33.5 degrees C, the late excitatory postsynaptic potential was abolished in < 2 min, and the recovery of the compound excitatory postsynaptic potential was prolonged (12.8 +/- 0.8 vs 7.8 +/- 0.3 min). Cooling reduced the amplitude of the anoxic depolarization and increased the input resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1979

Intradendritic recordings from hippocampal neurons.

Dendritic activity in guinea pig hippocampal CA1 and CA3 pyramidal neurons was examined by using an in vitro preparation. Histologically confirmed intradendritic recordings showed that dendrites had an average input resistance of 47.0 M omega and average membrane time constant of 33.3 msec. Active spike responses could be evoked by intracellular injection of outward current or by the activation of synaptic inputs. The predominant activity was burst firing. A typical intracellularly recorded dendritic burst consisted o spikes on a slowly increasing depolarizing potential. The spike components of the burst were of two distinct types: low threshold, fast spikes; and high threshold, slow spikes. Tetrodotoxin (1 microgram/ml) blocked the fast spikes, but slow spikes could still be evoked with direct intracellular stimulation. In contrast to dendritic responses, direct depolarization of CA1 somata did not give rise to burst generation. Orthodromic stimuli evoked large-amplitude excitatory postsynaptic potentials, followed by inhibitory postsynaptic potentials in dendrites of CA1 and CA3 neurons. In two instances, simultaneous recordings were obtained from coupled pairs of elements that were presumed to be soma and dendrite of the same CA3 pyramidal neuron. Depolarization of either element led to burst generation at that site, and the underlying slow depolarization appeared to evoke a burst at the other site. This potential postsynaptic amplifying mecahnism was not ordinarily functional because even suprathreshold orthodromic activation did not normally evoke bursting in dendrites.

Action Potentials↗

PubMed2001

Synaptic and morphological characteristics of temperature-sensitive and -insensitive rat hypothalamic neurones.

1. Intracellular recordings were made from neurones in rat hypothalamic tissue slices, primarily in the preoptic area and anterior hypothalamus, a thermoregulatory region that integrates central and peripheral thermal information. The present study compared morphologies and local synaptic inputs of warm-sensitive and temperature-insensitive neurones. 2. Warm-sensitive neurones oriented their dendrites perpendicular to the third ventricle, with medial dendrites directed toward the periventricular region and lateral dendrites directed toward the medial forebrain bundle. In contrast, temperature-insensitive neurones generally oriented their dendrites parallel to the third ventricle. 3. Both warm-sensitive and temperature-insensitive neurones displayed excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). In most cases, EPSP and IPSP frequencies were not affected by temperature changes, suggesting that temperature-insensitive neurones are responsible for most local synapses within this hypothalamic network. 4. Two additional neuronal groups were identified: silent neurones having no spontaneous firing rates and EPSP-driven neurones having action potentials that are primarily dependent on excitatory synaptic input from nearby neurones. Silent neurones had the most extensive dendritic trees, and these branched in all directions. In contrast, EPSP-driven neurones had the fewest dendrites, and usually the dendrites were oriented in only one direction (either medially or laterally), suggesting that these neurones receive more selective synaptic input.

Animals↗

PubMed1992

Synaptic behaviour in the myenteric plexus of the guinea-pig gastric antrum.

1. Intracellular recording methods were used to study the synaptic behaviour of neurones in the myenteric plexus of the guinea-pig gastric antrum. Synaptic potentials occurred spontaneously or were evoked by focal electrical stimulation of interganglionic fibre tracts. Synaptic events consisted of fast and slow excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). 2. Fast EPSPs with durations less than 20 ms were evoked in every antral neurone in a population sample of 370 cells. Most of the ganglion cells received multiple inputs from axons entering the individual ganglia in several different interganglionic fibre tracts. Many of the neurones also received input from multiple axons projecting in individual fibre tracts. The fast EPSPs behaved like nicotinic cholinergic EPSPs. They were evoked at stimulus frequencies up to 60 Hz without evidence of the run-down characteristic of fast EPSPs in the intestine. 3. Slow EPSPs were evoked by repetitive stimulation of the interganglionic connectives. They consisted of a slowly activating depolarization which persisted for several seconds after termination of the stimulus. The depolarizing responses were associated with an increase in the input resistance, with enhanced excitability and with suppression of hyperpolarizing after-potentials in AH/type 2 neurones. They were observed in 14.4% of the neurones of which 89% were AH/type 2 neurones. AH/type 2 neurones, unlike other myenteric neurones, were identified by action potentials with long lasting after-hyperpolarization. 4. IPSPs were hyperpolarizing potentials evoked by repetitive stimulation of interganglionic fibre tracts. The hyperpolarizing responses were associated with decreased input resistance. They occurred in 1.4% of the antral neurones. 5. Application of acetylcholine (ACh) by micro-ejection mimicked the fast EPSPs in all neurones. This fast nicotinic response to ACh was followed by a slowly activating, long-lasting muscarinic depolarization in 32% of the neurones. The slow muscarinic response was associated with increased input resistance, suppression of hyperpolarizing after-potentials and enhanced excitability. 6. Fast EPSPs were not suppressed by accumulation of ACh at presynaptic transmitter release sites. Unlike the intestine, presynaptic muscarinic autoreceptors appeared to be absent from the microcircuits in the antrum. 7. Synaptic behaviour in the local circuits of the gastric antrum differed from the gastric corpus. This may be a reflection of specialization of the circuits for organization of the distinctive patterns of digestive behaviour found in this region of the stomach.

Action Potentials↗

PubMed1978

Pentobarbital: differential postsynaptic actions on sympathetic ganglion cells.

The frog sympathetic ganglion has been used as a model to elucidate the cellular mechanism of barbiturate anesthesia. Anesthetic concentrations of pentobarbital markedly reduced the fast nicotinic excitatory postsynaptic potential while having no effect on the slow excitatory postsynaptic potential or slow inhibitory postsynaptic potential, even though all three synaptic potentials depend on the presynaptic release of acetylcholine. A similar differential effect was seen for nicotinic and muscarinic responses to exogenously applied agonists, while the depolarizing action of gamma-aminobutyric acid (GABA) was enhanced. These results indicate that pentobarbital has remarkably selective actions on the sympathetic ganglion and further indicate that blockade of ganglionic transmission by anesthetic concentrations of pentobarbital can be entirely explained by a postsynaptic action. The present results strengthen the concept that pentobarbital anesthesia results from a postsynaptic blockade of central excitatory synapses which increase sodium conductance coupled with a postsynaptic enhancement of GABA-mediated synaptic inhibition.

Animals↗

PubMed1991

Synaptic potentials evoked in spiny neurons in rat neostriatal grafts by cortical and thalamic stimulation.

1. Fetal rat striatal primordia were implanted into the neostriatum of adult rats 2 days after kainic acid lesion. Two to 6 mo after transplantation, in vivo intracellular recording and staining were performed to study the responses of spiny neurons in the grafts to the cortical and thalamic stimuli. The physiological characteristics and synaptic responses of 27 cells recorded in the grafts were compared with a sample of 23 neurons recorded from the surrounding host neostriatum in the same animals. Nineteen of the graft neurons and 19 of the host neurons were identified as spiny neurons by intracellular staining with biocytin. The responses of the remaining neurons were the same as those of identified spiny cells. 2. The spontaneous synaptically driven membrane potential shifts and long-lasting responses to afferent stimulation that are characteristic of neostriatal cells in normal animals were greatly reduced or absent in graft neurons. Presumably this reflects the reduction in synaptic input to the grafts and the lack of convergence of inputs from diverse sources. 3. Short-latency synaptic responses to cortical and thalamic stimulation were present and could consist of either excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs). The IPSPs were accompanied by a membrane conductance increase, and their reversal potentials could be altered by injection of chloride ions. Several minutes after impaling the cell, the IPSPs gradually disappeared, and the same stimuli could then evoke EPSPs. The disappearance of the IPSPs was independent of the presence of chloride in the electrodes. Most of the EPSP responses appeared to be monosynaptic but occurred at longer latencies than those seen in host neurons of the same type. 4. In cells not exhibiting IPSPs, or after the IPSP responses disappeared, cortical or thalamic stimulation could evoke slow depolarizing potentials and bursts of action potentials. These could not be evoked by current injection. They could be prevented or delayed by an exaggerated action potential after hyperpolarization that developed in neurons maintained in a depolarized state for several seconds, but could not be prevented by passage of hyperpolarizing current from the recording electrode. 5. The input resistance of graft spiny neurons was higher than that of the host cells, and time constants were longer. Both of these properties appeared to be due to the absence of the strong inward rectification that is usually present at resting membrane potentials in neostriatal neurons.

Animals↗

PubMed1993

Electrophysiology of cat association cortical cells in vivo: intrinsic properties and synaptic responses.

1. The intrinsic properties and synaptic responses of association cortical neurons (n = 179) recorded from cat's areas 5 and 7 were studied in vivo. Intracellular recordings were performed under urethane anesthesia. Resting membrane potential (Vm) was -71.7 +/- 1.2 (SE) mV, amplitude of action potential was 83.7 +/- 2.3 mV, and input resistance was 18.4 +/- 1.8 M omega. Cells were identified ortho- and antidromically from lateroposterior and centrolateral thalamic nuclei and from homotopic foci in the contralateral cortex. Physiologically identified neurons were intracellularly stained with Lucifer yellow (LY) and found to be pyramidal-shaped elements (n = 21). 2. We classified the neurons as regular-spiking and intrinsically bursting cells. Regular-spiking cells were further classified as slow- and fast-adapting according to the adaptation of spike frequency during long-lasting depolarizing current pulses. 3. Regular-spiking, slow-adapting neurons had a monophasic afterhyperpolarization (AHP) or a biphasic AHP with fast and medium components (FAHP, mAHP). Slow-adapting behavior was observed in 84% (n = 119) of the regular-spiking cells. 4. Regular-spiking, fast-adapting cells only fired a train of spikes at the beginning of the pulse. Thereafter, the Vm remained as a depolarizing plateau, occasionally triggering some spikes. These neurons had a monophasic AHP and represented 16% (n = 23) of the regular-spiking neurons. 5. Intrinsically bursting neurons (n = 37) were observed in 20% of neocortical cells at depolarized Vm. Their action potential was followed by a marked depolarizing afterpotential (DAP). Rhythmic (4-10 Hz) bursts occurred during long-lasting depolarizing current pulses. 6. Small (3-10 mV), fast (1.5-4 ms), all-or-none depolarizing potentials were triggered by depolarizing current pulses. They are tentatively regarded as dendritic spikes recorded from the soma because their rate of occurrence changed as a function of the Vm and they were eventually blocked by hyperpolarization. 7. Synaptic stimulation of either thalamic or homotopic contralateral cortical areas elicited a sequence of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Two components of the EPSP were revealed. At a hyperpolarized Vm, the initial component of the EPSP increased in amplitude, whereas the secondary component was blocked. Repetitive (10 Hz) stimulation of the thalamus or contralateral cortex elicited incremental responses. The augmentation phenomenon was due to an increase in the secondary component of the EPSP. The cortically elicited augmenting responses survived extensive thalamic lesions. A short IPSP and a long-lasting IPSP were evoked by thalamic or cortical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

In vitro brain slice studies of the rat's dorsal nucleus of the lateral lemniscus. I. Membrane and synaptic response properties.

1. We examined the physiological properties of neurons in the dorsal nucleus of the lateral lemniscus (DNLL) of the rat in a 400-microns tissue slice taken in the frontal plane through the auditory midbrain. The brain slice was placed in a small chamber and was perfused fully submerged in a warm, continuously circulating oxygenated saline solution. We made intracellular recordings with glass pipettes filled with 4 M potassium acetate. Synaptic potentials were evoked by electrical stimulation of either the lateral lemniscus or the commissure of Probst. 2. We tested the membrane characteristics of DNLL neurons by recording the electrical potentials produced by intracellular injection of positive or negative current. Typically, DNLL neurons had nearly linear current-voltage curves and responded to depolarizing currents with a sustained train of action potentials. Injection of intense or prolonged depolarizing currents frequently resulted in a pronounced afterhyperpolarization of the cell membrane. Intense hyperpolarizing currents were often followed by a large rebound depolarization. 3. The action potentials of most DNLL neurons were characterized by a double undershoot, i.e., the initial hyperpolarization after a spike was followed by a second, longer-latency hyperpolarization. Seventy-nine percent of the cells recorded had this type of double undershoot. The remaining cells had a single undershoot in which the postspike hyperpolarization was followed by a steady return to resting potential without any indication of a second phase of hyperpolarization. 4. Electrical stimulation of the lateral lemniscus evoked both excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) in DNLL. The EPSPs were evoked alone without any evidence of an IPSP in 67% of neurons and IPSPs were evoked alone in 6% of the neurons from which recordings were made. In 27% of the recordings both EPSPs and IPSPs were elicited in the same neuron by stimulation of a single location on the lateral lemniscus. 5. The combined EPSPs and IPSPs produced by lemniscal stimulation could often be dissociated by their different thresholds and/or different response latencies. For 35% of the neurons in which both an EPSP and IPSP were present, the IPSP had a lower threshold; for 23% of the cells, the EPSP had a lower threshold. For the remaining cells the thresholds for producing an EPSP and IPSP were the same. 6. DNLL neurons were capable of responding with great fidelity to a single pulse of stimulation delivered to the lateral lemniscus, i.e., an action potential was evoked after every stimulus.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1995

Dynamics of sensory afferent synaptic transmission in aortic baroreceptor regions on nucleus tractus solitarius.

1. Synaptic responses of medial nucleus tractus solitarius (mNTS) neurons to solitary tract (ST) activation were studied in a horizontal brain slice preparation of the rat medulla. Slices included sections of ST sufficiently long that the ST could be electrically activated several millimeters from the recording site of cell bodies in mNTS. 2. Three types of synaptic events were evoked in response to ST stimulation: simple excitatory postsynaptic potentials (EPSPs), simple inhibitory postsynaptic potentials (IPSPs), and complex EPSP-IPSP sequences. Simple EPSPs had substantially shorter latencies than IPSPs (3.39 +/- 0.65 ms, mean +/- SE, n = 42, vs. 5.86 +/- 0.71 ms, n = 6, respectively). 3. EPSP amplitude increased linearly with increasing hyperpolarization, with an extrapolated reversal potential near 0 mV. 4. EPSPs were maximal at < 0.5 Hz of sustained, constant-frequency ST stimulation (n = 14). EPSP amplitude declined to an average of 57.5% of control at 10 Hz after 2 s of sustained stimulation. With 1 min of sustained, 100-Hz stimulation, EPSP amplitude declined to near zero. 5. With stimuli intermittently delivered as 100-ms bursts every 300 ms, generally comparable average EPSPs were evoked during constant and burst patterns of ST stimulation. The amplitude of the initial EPSP in each burst was very well maintained even at intraburst stimulation rates of 100 Hz. 6. At resting membrane potentials, low constant frequencies of ST stimulation (< 5 Hz) reliably elicited action potentials and suppressed spontaneous spiking, but higher frequencies led to spike failures (> 85% at 100 Hz). Between 5 and 10 Hz, this periodic stimulation-suppression cycle clearly entrained action potential activity to the ST stimuli. Similar patterns of current pulses (5 ms) reliably evoked action potentials with each pulse to higher frequencies (50 Hz) without failures, and entrainment was similar to ST stimulation. 7. In a subset of nucleus tractus solitarius (NTS) neurons (3 of 9 studied), bursts of ST stimuli were as much as 50% more effective at transmitting high frequencies (> 10 Hz) of ST stimulation than the equivalent constant frequencies (P < 0.0001). 8. The long-latency simple IPSPs with no preceding EPSPs reversed to become depolarizing at potentials more negative than -62.9 +/- 7.0 mV (n = 5) and were blocked by the non-N-methyl-D-aspartate antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (n = 3). The ST stimulation frequency-response relation of these IPSPs was similar to that for the short-latency EPSP response excited by ST synapses. Thus these IPSPs appear to be activated polysynaptically via a glutamatergic-GABAergic sequence in response to ST activation. 9. The results suggest that sensory afferent synapses in mNTS have limited transmission of high-frequency inputs. Both synaptic transmission and the characteristics of the postsynaptic neuron importantly contribute to the action potential transmission from afferent to NTS neuron and beyond. This overall frequency response limitation may contribute to the accommodation of reflex responses from sensory afferent inputs such as arterial baroreceptors within their physiological discharge frequency range.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1989

Physiological and anatomical studies of the interactions between Purkinje cells and basket cells in the cat's cerebellar cortex: evidence for a unitary relationship.

Intracellular recordings have been obtained from neurons in lobule V of the cat's vermis, which were identified as basket cells following intracellular injections of HRP. Stimulation of the inferior cerebellar peduncle or peripheral nerves elicited an initial depolarizing and subsequent hyperpolarizing response. Neither potential could be graded with changes in stimulus intensity; both displayed all-or-none properties at threshold levels of stimulation. The depolarization and hyperpolarization were confirmed as an excitatory postsynaptic potential and an inhibitory postsynaptic potential (IPSP), respectively, on the basis of their response to intracellular injections of hyperpolarizing and depolarizing currents into the cell body. A possible source of the unitary IPSP is the Purkinje cell, via its recurrent axonal collaterals. To test this hypothesis, an electron microscopic analysis was carried out to define the synaptic relationships between the recurrent collaterals of an HRP-filled Purkinje cell and 3 basket cells. Serial section analysis reveals that collaterals from a single Purkinje cell contact several basket cells, but each basket cell received somatic input from only one Purkinje cell. These data provide an anatomical substrate for the unitary IPSP observed during intracellular recording from basket cells. The unitary nature of the Purkinje cell-basket cell interaction indicates that a very limited population of cortical neurons may be involved in local circuits that integrate afferent information in the cerebellar cortex.

Animals↗