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PubMed1985

Stereoselectivity of L-baclofen in hippocampal slices of the rat.

Extra- and intracellular recording from hippocampal slices of the rat revealed the following effects when baclofen (BF) (0.1-10 microM) was added to the perfusion fluid: a block of synaptic potentials evoked by stimulation of stratum radiatum; a direct hyperpolarization and a conductance increase (for potassium ions) of CA1 pyramidal cells. All this activity was found in the L- none in the D-enantiomer. D-BF did not antagonize the action of L-BF.

Animals↗

PubMed2001

Synaptic function: dendritic democracy.

Neurons receive synaptic inputs primarily onto their dendrites, which filter synaptic potentials as they spread toward the soma. Recent results indicate that this filtering appears to be compensated by increasing the synaptic conductance at distal synapses, thus normalizing the efficacy of synaptic inputs at the soma.

Dendrites↗

PubMed2006

Dynamical response of the Hodgkin-Huxley model in the high-input regime.

The response of the Hodgkin-Huxley neuronal model subjected to stochastic uncorrelated spike trains originating from a large number of inhibitory and excitatory post-synaptic potentials is analyzed in detail. The model is examined in its three fundamental dynamical regimes: silence, bistability, and repetitive firing. Its response is characterized in terms of statistical indicators (interspike-interval distributions and their first moments) as well as of dynamical indicators (autocorrelation functions and conditional entropies). In the silent regime, the coexistence of two different coherence resonances is revealed: one occurs at quite low noise and is related to the stimulation of subthreshold oscillations around the rest state; the second one (at intermediate noise variance) is associated with the regularization of the sequence of spikes emitted by the neuron. Bistability in the low noise limit can be interpreted in terms of jumping processes across barriers activated by stochastic fluctuations. In the repetitive firing regime a maximization of incoherence is observed at finite noise variance. Finally, the mechanisms responsible for the different features appearing in the interspike-interval distributions (like multimodality and exponential tails) are clearly identified in the various regimes.

Action Potentials↗

PubMed1989

Intracellular recordings of respiratory neurons in the lateral medulla of piglets.

Membrane potentials of respiratory neurons in the ventral respiratory group were recorded using intracellular techniques in the medulla of newborn piglets. Three types of neurons were demonstrated: inspiratory neurons with an augmenting pattern of spike activity during inspiration; postinspiratory neurons with a short decrementing firing pattern that started immediately after inspiration ended; and stage II expiratory neurons with an augmenting spiking pattern that began shortly after inspiratory termination and ended before onset of the next inspiration. When not firing, the membrane potential trajectories of each cell type revealed two complementary patterns of relative inhibition. This latter finding suggests arrival of inhibitory synaptic potentials during these periods. These findings suggest that the respiratory control mechanisms of the newborn piglet are organized in a three-phased manner similar to that of adult cats.

Action Potentials↗

PubMed1986

Partitioning of monosynaptic Ia excitatory postsynaptic potentials in the motor nucleus of the cat lateral gastrocnemius muscle.

Experiments were conducted to test the hypothesis that a partitioning of Ia monosynaptic excitatory postsynaptic potentials (Ia EPSPs) is present in motor nuclei supplying muscles with regions capable of different mechanical actions. Intracellular recordings of synaptic potentials were made in lateral gastrocnemius (LG) motoneurons in anesthetized low-spinal cats. The effects were tested of stimuli (group I range) to the four primary nerve branches of the LG nerve supplying muscle compartments LGm, LG1, LG2, and LG3 (terminology of English, Ref. 26) and the nerve to a heteronymous muscle, soleus. Stimulation of a given LG nerve branch produced monosynaptic Ia EPSPs of greater amplitude in "own-branch" motoneurons than "other-branch" cells. A significant partitioning of mean Ia EPSPs was found in three (LG1, LG2, LG3) out of the four homonymous pathways studied. An EPSP normalization (7) was performed to eliminate potential differences in cell type that might affect the amplitudes of the EPSPs between these four cell groups (e.g., differences in the number of cells supplying FF, FR, and S muscle units). This normalization confirmed that the partitioning of monosynaptic Ia inputs upon stimulation of LG1, LG2, and LG3 could not be attributed to differences in cell type. In addition, the effects of LGm stimulation were found to be significantly greater in the LGm motoneurons compared with the other cell groups. Heteronymous input (from soleus) to the LG motor nucleus showed some partitioned effects. Motoneurons innervating compartment LG2 received larger EPSPs from soleus than did the cells supplying compartments LG1, LG3, and LGm. The contributions of location specificity and species specificity (terminology of Scott and Mendell, Ref. 55) in the establishment of these Ia-afferent-motoneuronal connections were examined. Cell location sites within the spinal cord were consistent with location specificity making some contribution to the observed pattern of homonymous Ia connections. A more prominent role for species specificity was indicated by species-dependent differences in EPSP amplitude in pairs of LG motoneurons (e.g., LGm vs. LG2) at similar rostrocaudal locations upon stimulation of a given homonymous or heteronymous nerve/branch.

Afferent Pathways↗

PubMed1994

Homosynaptic facilitation of transmitter release in crayfish is not affected by mobile calcium chelators: implications for the residual ionized calcium hypothesis from electrophysiological and computational analyses.

1. Evoked neurotransmitter release at the crayfish neuromuscular junction was measured in the presence of the cell-permeant calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetotoxymethyl (BAPTA-AM). Excitatory post-synaptic potentials were greatly diminished after application of the intracellular chelator, an effect resulting from attenuation of the rise in the concentration of cytoplasmic Ca2+ ([Ca]i) that is necessary for neurotransmission. However, short-term homosynaptic facilitation of release, the magnitude and time course of which is thought to depend on the accumulation and removal of residual Ca ions (Ca2+), was not affected. Application of the cell-permeant form of ethylene glycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) gave similar results. 2. To interpret these results we developed a reaction-diffusion model in 3D rectangular coordinates for Ca2+ diffusion in the presence of mobile and immobile buffers. Solutions of the model in response to influx of Ca2+ through one or six channels for different diffusion coefficients and no nondiffusable buffer, predict that 1) the time course of residual Ca2+ is very brief, 2) an unrealistically low Ca2+ diffusion coefficient is required for residual calcium, 3) the spatially distributed Ca2+ signal is attenuated by intracellular BAPTA, 4) the rate at which free Ca2+ returns to resting levels, after entry (residual Ca2+) is faster with more mobile buffer, and 5) when pulse trains of Ca2+ channel current are used as input, computed facilitation is comparable to experimental measurements without buffer, but is abolished in the presence of exogenous buffer. 3. When the diffusion coefficient of Ca2+ in water is used, there is no residual Ca2+; however, when 0.1-1.6 mM nondiffusable buffer is present with a fast binding coefficient comparable to BAPTA, there is a very small residual Ca2+ due to the unbinding from the fixed binding sites. The nondiffusable buffer is saturated next to a Ca2+ channel. For this case of the diffusion coefficient of calcium in H2O and nondiffusable buffer, when a moderate amount of diffusable buffer is added to the system containing nondiffusable buffer, the very small residual Ca2+ is substantially reduced. This is because the product of diffusable buffer and Ca2+ is carried away as diffusable product, in contrast to the nondiffusable product releasing Ca2+, after Ca2+ entry ceases. 4. The model predicts that mobile calcium buffers with appropriate physical properties will attenuate facilitation and hasten its decay by removing residual calcium.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

Subthreshold synaptic activation of voltage-gated Ca2+ channels mediates a localized Ca2+ influx into the dendrites of hippocampal pyramidal neurons.

1. Whole cell recordings and high-speed fluorescence imaging were used to investigate the spatial and temporal characteristics of Ca2+ influx during synaptic activity in hippocampal CA1 pyramidal neurons. Brief, subthreshold trains of synaptic potentials elicited by Schaffer collateral stimulation produced transient increases in [Ca2+]i in the apical dendrites near the site of synaptic input. The rises in [Ca2+]i were not due to Ca2+ entry through N-methyl-D-aspartate (NMDA)-activated or non-NMDA-activated glutamate channels, but were reduced by low concentrations of Ni2+. Hyperpolarizing prepulses caused an increase in the synaptically evoked Ca2+ transients, whereas strong hyperpolarization during the train prevented the rise in [Ca2+]i. The data suggest that subthreshold synaptic activity can open low-voltage-activated (T-type) Ca2+ channels and produce a local increase in intradendritic [Ca2+]. Such local increases in [Ca2+]i may be important for modulating the strength of synaptic connections.

Animals↗

PubMed2005

A molecular window on sleep: changes in gene expression between sleep and wakefulness.

Sleep is thought to be "by the brain and for the brain," but despite decades of behavioral and neurophysiologic research, we still do not know why the brain actually needs to sleep. Recently, gene expression studies have allowed researchers to investigate the molecular correlates of sleep and wakefulness and to gain new insights into the benefits that sleep may bring at the cellular level. In the latest series of studies, a genome-wide screening of brain gene expression was performed in rats that had been asleep, spontaneously awake, or sleep deprived for 8 hours. It was found that of approximately 15,000 transcripts expressed in the cerebral cortex, about 5% change their expression levels depending on behavioral state but independently of time of day. Half of the modulated genes increase in wakefulness and half in sleep. Moreover, wakefulness-related and sleep-related transcripts belong to different functional categories. Waking-related transcripts are involved in energy metabolism, excitatory neurotransmission, transcriptional activation, synaptic potentiation and memory acquisition, and the response to cellular stress. Sleep-related transcripts are involved in brain protein synthesis, synaptic consolidation/depression, and membrane trafficking and maintenance, including cholesterol metabolism, myelin formation, and synaptic vesicle turnover.

Animals↗

PubMed1987

Parallel processing of proprioceptive signals by spiking local interneurons and motor neurons in the locust.

The connections made by afferents from a proprioceptor at the femorotibial joint in a hind leg of a locust, the femoral chordotonal organ (FCO), were determined by making intracellular recordings from motor neurons and spiking local interneurons in the central nervous system and from afferent cell bodies in the periphery. Staining the central projections of the afferent neurons with dye introduced into their axons at the receptor, and the intracellular injection of dye into motor neurons and interneurons, shows that the branches of all 3 types of neuron overlap in specific regions of neuropile. Afferents excited by a movement of the receptor apodeme that is equivalent to an imposed extension of the femorotibial joint excite flexor tibiae motor neurons and some spiking local interneurons with cell bodies at the ventral midline of the metathoracic ganglion. The opposite movement excites extensor tibiae motor neurons and a different set of spiking local interneurons. Spikes in afferents that excite flexor motor neurons evoke depolarizing potentials that follow each spike with a consistent central latency of approximately 1.5 msec. The amplitude of the depolarizing potentials is dependent upon the membrane potential of the motor neuron. This evidence points to the connection being direct and to the potentials' being EPSPs. Simultaneous recordings from certain spiking local interneurons and certain flexor motor neurons show that they receive many synaptic potentials in common and are driven in a parallel fashion by movements of the receptor apodeme. Spikes of some afferents evoke EPSPs in both neurons with the same consistency and latency. An afferent can therefore synapse directly upon a motor neuron and a spiking local interneuron. Each afferent synapses on several motor neurons and possibly upon several interneurons. In turn, each motor neuron and each interneuron receives inputs from several afferents.

Animals↗

PubMed1975

An electrophysiological analysis of the effects of reserpine on adrenergic neuromuscular transmission.

1 An electrophysiological study has been made of the effects of depleting synaptic vesicles (i.e. small vesicles less than 60 nm diameter) of their transmitter with reserpine on the quantity of transmitter released by nerve impulses, using the amplitude of the synaptic potential as a measure of transmitter release. 2 Pretreatment of adrenergic nerve terminals with reserpine sufficient to deplete the terminals of 70% of their noradrenaline (NA) did not change the total number of synaptic vesicles in the terminals, but did reduce the number with a large granular core as well as the quantity of NA released by a single nerve impulse by 80%. 3 Pretreatment of adrenergic nerve terminals with reserpine and iproniazid, to decrease vesicular NA but enhance cytoplasmic NA, had the same effect on synaptic vesicles and on the NA released by a single nerve impulse as did reserpine alone. 4 During a short train of impulses at high frequencies in reserpine pretreated terminals, the quantity of NA released by successive impulses increased until a steady-state release was reached comparable to that in untreated preparations. This facilitated release could be quantitatively predicted in terms of the addition of the individual potentiations introduced by each impulse in the train. 5 These results are consistent with the idea that each quantum of transmitter is stored in a synaptic vesicle, and that these may be released by nerve impulses directly from the terminal by a process of exocytosis.

Animals↗

PubMed1983

Associative long-term potentiation in hippocampal slices.

Interactions between two excitatory monosynaptic inputs to hippocampal neurons of the CA1 region were examined in the in vitro slice. By adjusting the strengths of the electrical stimuli delivered to the two input pathways, one was made to generate a weak and the other a strong synaptic response. Simultaneous tetanic stimulation of both input pathways resulted in a subsequent long-term enhanced synaptic efficacy in the weak input under conditions in which the same tetanic stimulation of either input alone failed to have this effect. This form of long-term synaptic potentiation (LTP), known as associative LTP, was shown in some cases to last hours without decrement. The plastic changes were localized within the CA1 region and appear to reside in the pre- or postsynaptic elements of the monosynaptic excitatory input to the pyramidal neurons. The increased synaptic efficacy could not be accounted for by any of several measured postsynaptic passive membrane properties.

Afferent Pathways↗

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↗

PubMed1994

Distributed aspects of the response to siphon touch in Aplysia: spread of stimulus information and cross-correlation analysis.

We examined two aspects of the response to siphon stimulation in an attempt to test the hypothesis that the Aplysia CNS functions as a distributed system. First, we estimated the number of central neurons that respond to a light touch to the siphon skin. We made voltage-sensitive dye recordings from the abdominal, pleural, pedal, and cerebral ganglia. From these recordings we estimated that 220 abdominal neurons, 110 pleural neurons, and 650 pedal neurons were affected by the light touch. Thus, the information about this mild and localized stimulus is very widely distributed within the Aplysia CNS. This result allows the possibility that the Aplysia CNS functions as a distributed system. If only a small number of neurons had responded to the touch, it would have supported the conclusion that the gill-withdrawal reflex could be generated by a small, dedicated circuit. Second, we searched for correlations between the spike times of the individual abdominal ganglion neurons. Two time scales were examined: a millisecond time scale corresponding to the duration of a fast synaptic potential and a seconds time scale corresponding to the duration of the gill-withdrawal movement. Neuron pairs with highly correlated spike activity on a millisecond time scale must be connected by (or have a common input that uses) relatively powerful, fast, excitatory synapses. We expected that this kind of synaptic interaction would be relatively rare in nervous systems that functioned in a distributed manner. Indeed, only 0.3% of the neuron pairs had correlation coefficients of 0.15 or greater. These correlations accounted for approximately 2% of the action potentials generated in response to siphon stimulation. Thus, large, fast excitatory synaptic interactions appear to be relatively unimportant. This result is consistent with the hypothesis that the abdominal ganglion functions as a distributed system. When the longer time scale was used for the cross-correlograms, a large fraction of the cell pairs had correlated activity because many neurons are activated by the stimulus. It was not possible to interpret the slow correlations in terms of actual synaptic interactions between individual neurons. Our results are consistent with the possibility that the abdominal ganglion functions in a distributed manner. However, this evaluation is indirect and thus only tentative conclusions can be drawn. Evidence from several sources suggests that the neuronal interactions for generating the Aplysia gill-withdrawal reflex are complex.

Animals↗

PubMed1993

Induction of long-term potentiation at perforant path dentate synapses does not affect place learning or memory.

In two experiments the authors failed to detect an effect of inducing bilateral, long-lasting synaptic potentiation at perforant path dentate synapses on spatial learning by rats in the Morris place navigation task. Daily sessions of high-frequency stimulation of perforant path axons produced large increases to an asymptotic level in population spike and field excitatory postsynaptic potential recorded in ipsilateral dentate gyrus. Place learning proceeded normally 24 hours after the last of 14 high-frequency stimulation sessions in rats that had previously mastered the procedural aspects of place navigation (Experiment 1) and in rats that were naive (Experiment 2).

Animals↗

PubMed1998

3-Alpha-chloro-imperialine, a potent blocker of cholinergic presynaptic modulation of glutamatergic afferents in the rat neostriatum.

Cortico-thalamic glutamatergic afferents control neuronal activity in the neostriatum. Cholinergic interneurons modulate the activity of medium spiny neurons through both pre- and post-synaptic actions via the activation of muscarinic receptors. The muscarinic pre-synaptic modulation was analyzed electrophysiologically. The transmitter release, induced by 4-AP, was studied and the block of paired pulse facilitation (PPF) by different muscarinic receptor antagonists was analyzed. The GABA(A) antagonist bicuculline isolated the glutamatergic transmission. Muscarinic agonists decreased the frequency of random synaptic potentials induced by 4-AP in about 60% of the cases without changes in input resistance (RN) of the post-synaptic neuron or in the mean amplitude of the synaptic events; indicating a presynaptic action. The administration of both 1 microM carbachol or 20 nM muscarine increased PPF. Muscarinic receptor antagonists blocked this action with a potency order: 3-alpha-chloroimperialine > 4-DAMP>>AFDX-116 > or = gallamine >> pirenzepine. The IC50's for the first three antagonists were (nM): 0.65, 1.1, and 3.0. Their respective Hill coefficients were: 1.9, 1.4, and 1.3. 3-alpha-Chloroimperialine reduced the PPF almost completely. The M3 and the M2 muscarinic receptor antagonists 4-DAMP and AFDX-116, given at saturating concentrations, consistently blocked only a part of the PPF but had additive effects when given together. These data are consistent with the existence of both M2 and M3 muscarinic receptors in striatal glutamatergic afferents.

4-Aminopyridine↗

PubMed1998

Activation of muscarinic receptors during blockade of GABA(A)-mediated inhibition induces synchronous epileptiform activity in immature rat hippocampus.

We investigated the effects of the cholinergic agonist carbachol (25 microM) on the synaptic potentials recorded extracellularly and intracellularly from the CA3 area of immature hippocampal slices of the rat (postnatal days 10-20). In control conditions, carbachol reduced the amplitude of evoked synaptic responses (n=8) and did not induce any spontaneous synchronous activity (n=12); the depressant effect of carbachol was mimicked by acetylcholine (100 microM, in eserine 10 microM, n=5) and was reversed by the muscarinic antagonist atropine (1 microM, n=2). The GABA(A)-receptor antagonist bicuculline (10 microM) enhanced the amplitude and duration of the evoked synaptic responses and induced infrequent (0.016-0.045 Hz) spontaneous synchronous discharges in 23/37 of the slices. Application of carbachol in the presence of bicuculline reduced the amplitude of the evoked synaptic responses (n=21) and in addition induced synchronous discharges with rates of occurrence 0.075-0.225 Hz, in 64/68 slices. Both effects were mimicked by acetylcholine and eserine, and antagonized by atropine. The specific muscarinic antagonists pirenzepine (M1-type), tripitramine (M2-type), 4-diphenylacetoxy-N-methylpiperidine methiodide (M3-type) and tropicamide (M4-type) (all tested at 0.1-1 microM) reversibly reduced the frequency of synchronous carbachol-induced discharges. In addition, these discharges were reversibly blocked by high Ca2+ perfusion medium (7 mM CaCl2, n=4) and by the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM, n=7). Synchronous epileptiform discharges were recorded from both CA1 and CA3 areas in intact slices (n=3), but only from CA3 following disruption of the CA1-CA3 synaptic connections (n=3). These experiments suggest that activation of muscarinic receptors during blockade of GABA(A)-mediated potentials, may enhance synchronous epileptiform activity in immature (postnatal days 10-20) hippocampus, through activation of local excitatory circuits and that endogenous acetylcholine may be sufficient to play this role.

Animals↗

PubMed1993

Effects of axotomy or target atrophy on membrane properties of rat sympathetic ganglion cells.

1. The electrical properties of rat superior cervical ganglion cells were examined in vitro with intracellular microelectrodes after axotomy or atrophy of the submandibular salivary gland. 2. Membrane time constant, input resistance and excitatory synaptic potentials (EPSPs) were decreased to about 50% of their control values 7-10 days after axotomy. 3. Axotomized ganglion cells also showed reduced action potentials and after-hyperpolarizations (AHPs). The AHP duration was reduced to 40% of the control value. 4. In 25% of the axotomized cells, the action potential was followed by an after-depolarization (ADP) instead of the AHP that was always present in control cells. In eleven out of seventeen axotomized cells with ADP, preganglionic stimulation failed to evoke an EPSP, whereas the failure of the synaptic response was never observed in control cells and occurred only in two of fifty-three axotomized cells with AHP. 5. In some axotomized cells with AHP, a depolarizing potential developed after a train of action potentials. This was never observed in control cells. 6. Sympathetic neurones innervating the submandibular gland in control animals had membrane properties similar to those observed in other ganglion cells. 7. The properties of neurones innervating the submandibular gland remained unaltered after the experimentally induced atrophy of the gland. 8. It is concluded that the marked effects of short-term axotomy on membrane properties of sympathetic ganglion cells are not reproduced by long-term atrophy of the target tissue.

Action Potentials↗

PubMed1988

Blockade of a late inhibitory postsynaptic potential in hippocampal CA3 neurons in vitro reveals a late depolarizing potential that is augmented by pentobarbital.

These experiments show that blockade of a late inhibitory postsynaptic potential (IPSP) in rat hippocampus by injection of GTP gamma s into a single monitored neuron, or by injection of pertussis toxin into the hippocampus, exposed a synaptic potential that was depolarizing relative to the early, GABAA mediated IPSP. The reversal potential of this late depolarizing potential (LDP) was 10-12 mV positive to that of the early IPSP. The response was augmented by 40-60 microM pentobarbital, and the augmented response appeared to be sensitive to picrotoxin, an antagonist of GABAA action. The LDP is comparable to a depolarizing GABAA synaptic response that had been previously observed only when synaptic behavior of slices was grossly altered by exposure to pentobarbital or 4-aminopyridine.

Animals↗