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Results for “Inhibitory Postsynaptic Potentials”

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PubMed2001

Zinc co-localizes with GABA and glycine in synapses in the lamprey spinal cord.

The presence of zinc in synaptic terminals in the lamprey spinal cord was examined utilizing a modification of the Timm's sulfide silver method and with the fluorescent marker 6-methoxy-8-quinolyl-p-toluenesulfonamide (TSQ). Axons labeled with a Timm's staining method were predominantly located in the lateral region of the dorsal column. This correlated with a maximum of TSQ fluorescence in this region of the spinal cord. Single labeled terminals accumulating Timm reaction product were also found throughout the gray matter and fiber tracts. At the ultrastructural level, zinc was located in a population of synaptic terminals that co-localized gamma-aminobutyric acid (GABA) and glycine. Possible effects of Zn2+ on neuronal activity were examined. In spinobulbar interneurons, which receive GABAergic input in the dorsal column, zinc potentiated responses to GABA application, but it did not affect responses to GABA in motoneurons. Responses in motoneurons to pressure application of glycine were also not affected by Zn2+. Zinc, however, potentiated monosynaptic glycinergic inhibitory postsynaptic potentials (IPSPs) evoked in motoneurons by inhibitory locomotor network interneurons and increased frequency, but not amplitude of spontaneous miniature IPSPs recorded in the presence of tetrodotoxin (TTX), suggesting presynaptic effects. Glutamate responses and the amplitude of monosynaptic excitatory postsynaptic potentials (EPSPs) in motoneurons were reduced by zinc. These effects appeared to be mediated largely postsynaptically through an effect on the N-methyl-D-aspartate (NMDA) component of the glutamatergic input. Our results thus show that free zinc is present in inhibitory synaptic terminals in the lamprey spinal cord, and that it may function as a modulator of inhibitory synaptic transmission.

Aminoquinolines↗

PubMed1999

Synchronization of GABAergic interneuronal networks during seizure-like activity in the rat horizontal hippocampal slice.

We studied the contribution of GABAergic (gamma-aminobutyric acid) neurotransmission to epileptiform activity using the horizontal hippocampal rat brain slice. Seizure-like (ictal) activity was evoked in the CA1 area by applying high-frequency trains (80 Hz for 2 s) to the Schaffer collaterals. Whole-cell recordings from stratum oriens-alveus interneurons revealed burst firing with superimposed high-frequency spiking which was synchronous with field events and pyramidal cell firing during ictal activity. On the other hand, interictal interneuronal bursts were synchronous with large-amplitude inhibitory postsynaptic potentials (IPSPs) in pyramidal cells. Excitatory and inhibitory postsynaptic potentials were simultaneously received by pyramidal neurons during the ictal afterdischarge, and were synchronous with interneuronal bursting and field potential ictal events. The GABAA receptor antagonist bicuculline greatly reduced the duration of the ictal activity in the CA1 layer, and evoked rhythmic interictal synchronous bursting of interneurons and pyramidal cells. With intact GABAergic transmission, interictal field potential events were synchronous with large amplitude IPSPs (9.8 +/- 2.4 mV) in CA1 pyramidal cells, and with interneuronal bursting. Simultaneous dual recordings revealed synchronous IPSPs received by widely separated pyramidal neurons during ictal and interictal periods, indicative of widespread interneuronal firing synchrony throughout the hippocampus. CA3 pyramidal neurons fired in synchrony with interictal field potential events recorded in the CA1 layer, and glutamate receptor antagonists abolished interictal interneuronal firing and synchronous large amplitude IPSPs received by CA1 pyramidal cells. These observations provide evidence that the interneuronal network may be entrained in hyperexcitable states by GABAergic and glutamatergic mechanisms.

2-Amino-5-phosphonovalerate↗

PubMed1978

Synaptic potentials in sympathetic ganglia: are they mediated by cyclic nucleotides?

The hypothesis that cyclic nucleotides are intracellular second messengers mediating the generation of synaptic potentials was studied in the sympathetic ganglia of the bullfrog. Synaptic potentials and the effect of administering cyclic nucleotides and agents which affect cyclic nucleotide metabolism were recorded by the sucrose gap technique. The administration of adenosine 3',5'-monophosphate (cyclic AMP), guanosine 3',5'-monophosphate (cyclic GMP), or several of their derivatives produced little or no change in membrane potential. Prostaglandin E1 did not block the generation of postsynaptic potentials. Theophylline produced membrane effects that were different from those associated with postsynaptic potential generation; it also reduced the slow excitatory postsynaptic potential (EPSP) and potentiated the slow inhibitory postsynaptic potential (IPSP). The administration of papaverine, however, reduced both the slow EPSP and the slow IPSP. Although synaptic stimulation increases both cyclic GMP and cyclic AMP in these neurons, these results raise the possibility that these cyclic nucleotides may have functionla roles other than mediation of synaptic potentials.

Action Potentials↗

PubMed2001

Activation of inhibitory pathways suppresses the induction of long-term potentiation in neurons of the rat lateral septal nucleus.

Long-term potentiation of the hippocampal-septal pathway was examined by intracellular recording techniques. High frequency stimulation (two 100-Hz 1-s trains with a 20-s interval between them) of the hippocampal CA3 area resulted in a transient depolarization in rat lateral septal nucleus neurons. High frequency stimulation was followed by a facilitation of fast and slow inhibitory postsynaptic potentials, lasting for more than 2 h, but not by a long-lasting increase in the excitatory postsynaptic potential in the normal solution. Long-term potentiation (>2 h) of the excitatory postsynaptic potential did not appear in 74% of neurons tested, even when the fast inhibitory postsynaptic potential was blocked by bicuculline (30 microM), a GABA(A) receptor antagonist. High frequency stimulation produced long-term potentiation of the excitatory postsynaptic potential in the Mg(2+)-free solution containing bicuculline. When the fast and slow inhibitory postsynaptic potentials were blocked by GABA(A) and GABA(B) receptor antagonists (bicuculline and CGP 55845A respectively), high frequency stimulation produced a large and sustained depolarization followed by long-term potentiation of the excitatory postsynaptic potential. However, the excitatory postsynaptic potential was not enhanced by administration of these drugs after termination of high frequency stimulation. Pretreatment with 2-amino-5-phosphonopentanoate, a NMDA receptor antagonist, resulted in loss of long-term potentiation in both sets of experiments. Paired-pulse stimulation of the hippocampal CA3 region with interstimulus intervals between 200 and 800 ms depressed the second excitatory postsynaptic potential in the presence of bicuculline. CGP 35348, a GABA(B) receptor antagonist, reversed the depression of excitatory postsynaptic potentials to facilitation. These data suggest that high frequency stimulation of hippocampal CA3 neurons enhances the efficacy of GABAergic inhibitory circuits which, in turn, depress the ability of lateral septal nucleus neurons to express long-term potentiation.

Animals↗

PubMed1969

Inhibitory miniature potentials in the stretch receptor neurons of crayfish.

Intracellular microelectrodes inserted into the soma of crayfish stretch receptor neurons record frequent fluctuations of the membrane potential. Time course, amplitude, and interval distribution indicate that they are miniature potentials. At the average resting potential the polarity of the miniature potentials depends on the anion used in the microelectrode: KCl electrodes record depolarizing, K citrate or K(2)SO(4) electrodes, hyperpolarizing miniature potentials. The inhibitory postsynaptic potentials (i.p.s.p.'s) show a similar polarity change. The reversal potentials of i.p.s.p.'s and miniature potentials are equal and within 10 mv of the resting potential, more negative with K citrate (or K(2)SO(4)), less negative with KCl electrodes. Reversal can be accomplished by changing the membrane potential by stretching or by current passing. Injection of Cl(-) into the soma or replacement of external Cl by propionate results in an abrupt increase of the amplitude of the miniature potentials lasting for several minutes. The miniature potentials like the i.p.s.p.'s are reversibly abolished by the application of picrotoxin and gamma-aminobutyric acid. They are not affected by tetrodotoxin, nor by acetylocholine, eserine, or atropine. It is concluded that the miniature potentials represent a spontaneous quantal release of transmitter substance from inhibitory nerve terminals, and that the transmitter substance predominantly increases the Cl(-) permeability of the postsynaptic membrane. The effect of the spontaneously released transmitter on the behavior of the receptor neuron is considerable. The membrane conductance is increased by up to 36% and the excitability is correspondingly depressed.

Acetylcholine↗

PubMed1993

Axonal projections and synaptic connections of C5 segment expiratory interneurones in the cat.

1. Respiratory interneurones in the C4-C6 segments of the spinal cord have only recently been described; until now their projections and connections were not known. We investigated expiratory interneurones in the C5 spinal segment, using antidromic mapping to trace their projections and spike-triggered averaging to test their synaptic connections with phrenic motoneurones. 2. A total of seventy expiratory interneurones were recorded in nineteen cats anaesthetized with pentobarbitone, paralysed and ventilated. The interneurones were found scattered dorsomedial to the phrenic motor nucleus, with discharge patterns of a constant (66%), augmenting (24%) or decrementing (10%) type. 3. Interneurone axons were found in the ipsilateral ventrolateral funiculus using antidromic activation at thresholds < 20 microA. The axons of eighteen of thirty-three interneurones tested (55%) were found to extend to the rostral part of the C6 segment, seventeen of thirty-three (52%) to the caudal part of the C6 segment and ten of nineteen (53%) to the rostral part of the C7 segment. 4. Axon collaterals for thirteen of thirty-three interneurones (39%) were found in the ipsilateral half of the C6 segment, with their endings near the phrenic motor nucleus. In three cases two collaterals were found. None of the interneurones had projections in the contralateral halves of the C5 or C6 segments. 5. In a separate group of thirty-four expiratory interneurones, antidromic mapping was used to find an axon collateral in the C6 segment prior to spike-triggered averaging. Eleven of these interneurones had collaterals (32%) and were subsequently tested for synaptic connections to thirty-two phrenic motoneurones. In three separate instances (9%), inhibitory postsynaptic potentials were observed. Amplitudes, fall times and half-amplitude widths of the inhibitory postsynaptic potentials were 6.7, 10.4 and 10.6 microV; 0.3, 0.5 and 0.7 ms and 0.6, 1.6 and 3.3 ms respectively. 6. We conclude: (i) there is a population of expiratory interneurones in the C5 segment, located predominantly dorsomedial to the phrenic motor nucleus; (ii) at least one-half of these interneurones have ipsilateral intersegmental projections to the C6 segment and (iii) although synaptic connections from expiratory interneurones in the C5 segment to phrenic motoneurones in the C6 segment may be rare, the observed inhibitory postsynaptic potentials had fall times and latencies commensurate with monosynaptic connections.

Animals↗

PubMed2006

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus.

The goal of the present study was to determine the effect of activating vagal afferent fibers on the discharge of median preoptic (MnPO) neurons responsive to peripheral angiotensin II (ANG II) and osmotic inputs. Vagal afferents were activated by electrical stimulation of the proximal end of the transected cervical vagus nerve (3 pulses, 100 Hz, 1 ms, 100-500 muA). Of 21 MnPO neurons, 19 were antidromically activated from the hypothalamic paraventricular nucleus (PVH) (latency: 10.3+/-1.3 ms, threshold: 278+/-25 muA). MnPO-PVH cells had an average spontaneous discharge of 2.1+/-0.4 Hz. Injection of ANG II (150 ng) and/or hypertonic NaCl (1.5 Osm/L, 100 mul) through the internal carotid artery significantly (P<0.01) increased the firing rate of most MnPO-PVH neurons (16/19, 84%). Vagus nerve stimulation significantly (P<0.01) decreased discharge (-73+/-9%) in 10 of 16 (63%) neurons with an average onset latency of 108+/-19 ms. Among the remaining 6 MnPO-PVH neurons vagal activation either increased discharge (177+/-100%) with a latency of 115+/-15 ms (n=2) or had no effect (n=4). Pharmacological activation of chemosensitive vagal afferents with phenyl biguanide produced an increase (n=3), decrease (n=2), or no change (n=6) in discharge. These observations indicate that a significant proportion of ANG II- and/or osmo-sensitive MnPO neurons receive convergent vagal input. Although the sensory modalities transmitted by the vagal afferents to MnPO-PVH neurons are not presently known, the presence of inhibitory and excitatory vagal-evoked responses indicates that synaptic processing by these cells integrates humoral and visceral information to subserve potentially important cardiovascular and body fluid homeostatic functions.

Action Potentials↗

PubMed1997

A subset of ventral tegmental area neurons is inhibited by dopamine, 5-hydroxytryptamine and opioids.

Neurons originating in the ventral tegmental area are thought to play a key role in the formation of addictive behaviors, particularly in response to drugs such as cocaine and opioids. In this study we identified different populations of ventral tegmental area neurons by the pharmacology of their evoked synaptic potentials and their response to dopamine, 5-hydroxytryptamine and opioids. Intracellular recordings were made from ventral tegmental area neurons in horizontal slices of guinea-pig brain and electrical stimulation was used to evoke synaptic potentials. The majority of cells (61.3%) hyperpolarized in response to dopamine, depolarized to 5-hydroxytryptamine, failed to respond to [Met]5enkephalin and exhibited a slow GABAB-mediated inhibitory postsynaptic potential. A smaller proportion of cells (11.3%) hyperpolarized in response to [Met]5enkephalin, depolarized to 5-hydroxytryptamine, failed to respond to dopamine and did not exhibit a slow inhibitory postsynaptic potential. These two groups of cells corresponded to previously described "principal" and "secondary" cells, respectively. A further group of cells (27.4%) was identified that like the principal cells, hyperpolarized to dopamine. However, these "tertiary cells" also hyperpolarized to both 5-hydroxytryptamine and [Met]5enkephalin and exhibited a slow, cocaine-sensitive 5-hydroxytryptamine(1A)-mediated inhibitory postsynaptic potential. When principal and tertiary cells were investigated immunohistochemically, 82% of the principal cells were positive for tyrosine hydroxylase compared with only 29% of the tertiary cells. The 5-hydroxytryptamine innervation of both these cell types was investigated and a similar density of putative contacts was observed near the somata and dendrites in both groups. This latter finding suggests that the existence of a 5-hydroxytryptamine-mediated inhibitory postsynaptic potential in the tertiary cells may be determined by the selective expression of 5-hydroxytryptamine receptors, rather than the distribution or density of the 5-hydroxytryptamine innervation. We conclude that tertiary cells are a distinct subset of ventral tegmental area neurons where cocaine and mu-opioids both mediate inhibition.

Animals↗

PubMed1992

Cholinergic excitation of GABAergic interneurons in the rat hippocampal slice.

1. Intracellular recordings were made from CA1 pyramidal cells in the rat hippocampal slice to study the cholinergic modulation of GABAergic inhibition. The cholinergic receptor agonist, carbamylcholine (carbachol), depressed evoked excitatory postsynaptic potentials (EPSPs) and evoked inhibitory postsynaptic potentials (IPSPs), but enhanced small spontaneously occurring membrane potential fluctuations that resembled IPSPs. Both atropine (1 microM) and picrotoxin (25-60 microM) abolished the small fluctuations. 2. Recording from cells with potassium or caesium chloride (KCl or CsCl)-filled microelectrodes enhanced and inverted spontaneous Cl(-)-dependent GABAA-mediated IPSPs. These events appeared to result from the spontaneous firing of GABAergic interneurons since they could be inhibited by picrotoxin or bicuculline and nearly eliminated by tetrodotoxin. 3. Muscarinic acetylcholine (ACh) receptor activation significantly increased the frequency of spontaneous-activity-dependent IPSPs from 1.7 +/- 0.4 s (mean +/- S.E.M.) in control saline to 7.0 +/- 1.1 s in carbachol (10-50 microM)-containing saline, although evoked IPSPs were inhibited. All effects of carbachol were completely reversed by atropine. 4. The increase in frequency of spontaneous IPSPs observed in carbachol was not secondary to changes in the postsynaptic cell and was not blocked by high doses of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5-10 microM) and 2-amino-5-phosphonovaleric acid (APV, 10-20 microM), which abolished evoked excitatory transmission. Amplitude histograms showed an increase in mean size as well as of frequency of spontaneous IPSCs in carbachol. 5. Stimulation of cholinergic afferents in stratum oriens in the presence of the acetylcholinesterase inhibitor eserine (1 microM) also increased spontaneous IPSP frequency, and the time course of this response was similar to that of the muscarinic slow EPSP. Postsynaptic factors or the activation of glutamatergic excitatory pathways could not account for this effect. 6. Evoked monosynaptic IPSCs in CNQX and APV were diminished by carbachol. 7. We conclude that GABAergic inhibitory interneurons possess muscarinic receptors, that activation of these receptors increases the excitability of the interneurons and that synaptically released ACh increases interneuronal activity. Cholinergic reduction of the monosynaptic IPSC may point to additional complexity in cholinergic regulation of the GABA system.

2-Amino-5-phosphonovalerate↗

PubMed1999

Hippocampal and entorhinal cortex high-frequency oscillations (100--500 Hz) in human epileptic brain and in kainic acid--treated rats with chronic seizures.

PURPOSE: Properties of oscillations with frequencies >100 Hz were studied in kainic acid (KA)-treated rats and compared with those recorded in normal and kindled rats as well as in patients with epilepsy to determine differences associated with epilepsy. METHODS: Prolonged in vivo wideband recordings of electrical activity were made in hippocampus and entorhinal cortex (EC) of (a) normal rats, (b) kindled rats, (c) rats having chronic recurrent spontaneous seizures after intrahippocampal KA injections, and (d) patients with epilepsy undergoing depth electrode evaluation in preparation for surgical treatment. RESULTS: Intermittent oscillatory activity ranging from 100 to 200 Hz in frequency and 50-150 ms in duration was recorded in CA1 and EC of all three animal groups, and in epileptic human hippocampus and EC. This activity had the same characteristics in all groups, resembled previously observed "ripples" described by Buzsáki et al., and appeared to represent field potentials of inhibitory postsynaptic potentials (IPSPs) on principal cells. Unexpectedly, higher frequency intermittent oscillatory activity ranging from 200 to 500 Hz and 10-100 ms in duration was encountered only in KA-treated rats and patients with epilepsy. These oscillations, termed fast ripples (FRs), were found only adjacent to the epileptogenic lesion in hippocampus, EC, and dentate gyrus, and appeared to represent field potential population spikes. Their local origin was indicated by correspondence with the negative phase of burst discharges of putative pyramidal cells. CONCLUSIONS: The persistence of normal-appearing ripples in epileptic brain support the view that inhibitory processes are preserved. FRs appear to be field potentials reflecting hyper-synchronous bursting of excitatory neurons and provide an opportunity to study the role of this pathophysiologic phenomenon in epilepsy and seizure initiation. Furthermore, if FR activity is unique to brain areas capable of generating spontaneous seizures, its identification could be a powerful functional indicator of the epileptic region in patients evaluated for surgical treatment.

Action Potentials↗

PubMed1997

Effects of prenatal cocaine exposure on the developing hippocampus: intrinsic and synaptic physiology.

A variety of neurological complications has been reported in infants exposed to cocaine during gestation. In the present study, intrinsic cell properties of hippocampal neurons from CA1, CA3, and dentate gyrus regions were measured and compared in tissue from neonatal rats exposed to saline or cocaine in utero. Synaptic properties of the CA1 pyramidal cell region were analyzed at postnatal day (P) 20 with the use of extracellular and intracellular recording techniques. In vitro intracellular recordings (n = 223) obtained at P10, P15 and P20 in tissue from cocaine- and saline-exposed animals revealed no differences in standard cell properties such as resting membrane potential, input resistance, time constant, and action potential amplitude or duration. Hippocampal slices from cocaine-exposed animals exhibited a marked reduction of spike frequency adaptation for all three types of principal hippocampal neurons (e.g., CA1, CA3, and granule cells). The amplitudes of afterhyperpolarizations following a spike train were also decreased in CA1 and CA3 cells in tissue from cocaine-exposed animals. Extracellular and intracellular recordings in the CA1 pyramidal cell region at P20 were obtained to assess and compare synaptic function in tissue from cocaine- and saline-exposed animals. In hippocampal slices from cocaine-exposed animals, synaptic responses in the CA1 region were characterized by multiple population spike activity and reduced inhibitory postsynaptic potentials. The reduction in fast inhibitory postsynaptic potential conductance was not associated with a change in reversal potential. These results suggest that gestational cocaine exposure induces significant changes in intrinsic and synaptic electrophysiological properties of hippocampal neurons in the developing animal. The cell and synaptic features are consistent with an increase in hippocampal excitability, which may contribute to the neurobehavioral deficits and epileptogenic predisposition reported in this infant population. As such, this in utero drug exposure model may provide a useful system in which to elucidate and study the basic cellular mechanisms underlying neurological complications associated with maternal cocaine abuse.

Aging↗

PubMed1996

Anoxia blocks the presynaptic control of GABA release at inhibitory terminals in the rat hippocampus.

Field potential and (K+)o recordings were made in rat hippocampal slices during application of 4-aminopyridine (50 microM) and ionotropic excitatory amino acid receptor antagonists, to establish whether anoxia modified the mechanisms that regulate GABA release from inhibitory interneurons. Synchronous, negative-going field potentials (amplitude = 1.41 +/- 0.64 mV, mean +/- S.D.; interval = 40.9 +/- 15.7 s; n = 10) occurred spontaneously in the CA3 stratum radiatum under control conditions. These events were associated with transient elevations in (K+)o (peak values = 5.3 +/- 0.7 mM; duration = 23.4 +/- 3.5 s; n = 5 slices) and were abolished by the GABAA, receptor antagonist bicuculline methiodide (10 microM; n = 5), the GABAB receptor agonist baclofen (100 microM; n = 6) or the mu-opioid receptor agonist (D-Ala2-N-Me-Phe, Gly-ol)enkephalin (10 microM; n = 4). Hence they represented monosynaptic field inhibitory postsynaptic potentials. Brief (4-5 min) episodes of anoxia induced a reversible, slow elevation of the baseline (K+)o to 5.2 +/- 0.3 mM (n = 5), while the rate of the field inhibitory postsynaptic potentials increased by an average of 130.7% (n = 10). Oxygen interruption during application of either baclofen (n = 6) or (D-Ala2-N-Me-Phe,Gly-ol)enkephalin (n = 4) blocked the depressant action of both drugs on the field inhibitory postsynaptic potential. These findings demonstrate that hippocampal monosynaptic field inhibitory postsynaptic potentials are resistant to brief anoxic episodes and that oxygen deprivation readily blocks the presynaptic control of GABA release exerted by GABAB and mu-opioid receptors at inhibitory interneuron terminals.

4-Aminopyridine↗

PubMed2006

Induction of neocortical long-term depression results in smaller movement representations, fewer excitatory perforated synapses, and more inhibitory synapses.

Long-term depression (LTD) is one of the most widely investigated models of the synaptic mechanisms underlying learning and memory. Previous research has shown that induction of LTD in the neocortex decreases measures of pyramidal cell dendritic morphology in both layers III and V. Here, we investigated the effects of LTD induction on 1) the time course of recovery of synaptic efficacy, 2) movement representations, 3) cortical thickness and layer V neuron density, and 4) the density of excitatory and inhibitory synapses in layer V of sensorimotor neocortex. Rats carried a stimulating electrode in the midline corpus callosum and a recording electrode in the right sensorimotor neocortex. Each rat received either low-frequency stimulation composed of 900 pulses at 1 Hz or handling daily for a total of 20-25 days. Callosal-neocortical evoked potentials were recorded in the right hemisphere before and after stimulation or handling. Our results show that LTD induction lasts for 3 weeks and results in smaller motor maps of the caudal forelimb area. We did not observe any reduction in neocortical thickness or neuron density. There was a reduction in the density of excitatory perforated synapses and an increase in the density of inhibitory synapses in layer V of the sensorimotor neocortex, thereby providing a general mechanism for the reduction in motor map size. This study sheds light on the interaction between an artificial model of learning, receptive field characteristics, and synaptic number in the sensorimotor cortex.

Animals↗

PubMed1995

Electrophysiological diversity of pyramidal-shaped neurons at the granule cell layer/hilus border of the rat dentate gyrus recorded in vitro.

In the rat dentate gyrus, pyramidal-shaped cells located on the border of the granule cell layer and the hilus are one of the most common types of gamma-aminobutyric acid (GABA)-immunoreactive neurons. This study describes their electrophysiological characteristics. Membrane properties, patterns of discharge, and synaptic responses were recorded intracellularly from these cells in hippocampal slices. Each cell was identified as pyramidal-shaped by injecting the marker Neurobiotin intracellularly (n = 17). In several respects the membrane properties of the sampled cells were similar to "fast-spiking" cells (putative inhibitory interneurons) that have been described in other areas of the hippocampus. For example, input resistance was high (mean 91.3 megohms), the membrane time constant was short (mean 7.7 ms), and there was a large afterhyperpolarization following a single action potential (mean 10.5 mV at resting potential). However, the action potentials of most pyramidal-shaped cells were not as brief (mean 1.2 ms total duration) as those of most previously described fast-spiking cells. Many pyramidal-shaped neurons had strong spike frequency adaptation relative to other fast-spiking cells. Although these latter two characteristics were apparent in the majority of the sampled cells, there were exceptional pyramidal-shaped neurons with fast action potentials and weak adaptation, demonstrating the electrophysiological variability of pyramidal-shaped cells. Responses to outer molecular layer stimulation were composed primarily of excitatory postsynaptic potentials (EPSPs) rather than inhibitory postsynaptic potentials (IPSPs), and were usually small (EPSPs evoked at threshold were often less than 2 mV), and brief (less than 30 ms). There was variability, because in a few cells EPSPs evoked at threshold were much larger. However, regardless of EPSP amplitude, suprathreshold stimulation (up to 4 times the threshold stimulus strength) rarely evoked more than one action potential in any cell. The results suggest that stimulation of perforant path axons produces limited excitatory synaptic responses in pyramidal-shaped neurons. This may be one of the reasons why they are relatively resistant to prolonged perforant path stimulation. The pyramidal-shaped neurons located at the base of the granule cell layer have been associated historically with a basket plexus around granule cell somata, and have been called pyramidal "basket" cells. However, basket-like endings were rare and axon collaterals outside the granule cell layer as the outer molecular layer and the central hilus, and antidromic action potentials could be recorded in some cells in response to weak stimulation of these areas. Taken together with the electrophysiological variability, the results indicate that these cells are physiologically heterogeneous.

Animals↗

PubMed1985

Neuronal mechanisms of the interaction of Deiters' nucleus with some brainstem structures.

The effects of stimulation of the interstitial nucleus of Ramón y Cajal, as well as the nucleus of Darkschewitsch, inferior olive and nucleus reticularis tegmenti pontis on the neuronal activity of the lateral vestibular nucleus of Deiters were studied by means of an intracellular recording technique. Stimulation of these structures is shown to lead to antidromic and orthodromic activation of Deiters' neurons. Collaterals of vestibulospinal neurons entering these structures are revealed electrophysiologically. It was shown that stimulation of the rostral part of the inferior olive evoked in Deiters' neurons predominantly antidromic responses, whereas stimulation of the caudal part of the inferior olive leads mostly to synaptic activation. Stimulation of Ramón y Cajal's and Darkschewitsch's nuclei evokes mono- and/or polysynaptic excitatory and inhibitory postsynaptic potentials in Deiters' neurons. Mono-, oligo- and/or polysynaptic inhibitory postsynaptic potentials were also evoked by stimulation of nucleus reticularis tegmenti pontis, as well as the rostral and particularly, caudal parts of the inferior olive. Stimulation of the caudal part of the inferior olive evoked mono-, oligo- and/or polysynaptic excitatory postsynaptic potentials in Deiters' neurons. Convergence of influences from the stimulated structures on the vestibular neurons under study was shown. A topical correlation between Deiters' nucleus and the brainstem nuclei mentioned above was found. The presence of inhibitory and excitatory interaction of these structures with Deiters' nucleus was established.

Animals↗

PubMed1993

Modulation by serotonin of the neurons in rat nucleus raphe magnus in vitro.

Nucleus raphe magnus contains a large population of raphe-spinal serotonergic neurons that are thought to be involved in descending control of pain transmission and the modulation of opioid analgesia. Intracellular recordings were made from nucleus raphe magnus neurons in the slice preparation. Cells were divided into two groups, primary and secondary cells, based on the action potential waveform and response to opioids, as reported previously. In some experiments, cells were filled with biocytin and 5-hydroxytryptamine-containing cells were identified immunohistochemically. Of the primary cells that were filled with biocytin, 93% stained for 5-hydroxytryptamine; 90% of biocytin-filled secondary cells were unlabeled for 5-hydroxytryptamine. Previous studies have shown that primary cells are disinhibited by opioids; the finding that most primary cells are serotonergic suggests that at least some 5-hydroxytryptamine-containing neurons in the nucleus raphe magnus are excited by opioid analgesics. 5-Hydroxytryptamine hyperpolarized cells in both primary and secondary cell groups. The 5-hydroxytryptamine agonists (+/-)-2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronaphthalene hydrobromide and 5-carboxamidotryptamine mimicked this action of 5-hydroxytryptamine, indicating that the 5-hydroxytryptamine 1A-subtype mediated this hyperpolarization. The hyperpolarization was mediated by an increase in potassium conductance that rectified inwardly. Local electrical stimulation of afferents evoked an inhibitory postsynaptic potential in primary cells. The inhibitory postsynaptic potential reversed polarity at the potassium equilibrium potential and was blocked by 5-hydroxytryptamine 1A receptor antagonists. It is proposed that the 5-hydroxytrypamine1A receptor on serotonergic primary cells may function as an autoreceptor to regulate the activity.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1993

Giant cells of the dorsal cochlear nucleus of mice: intracellular recordings in slices.

1. In slices of the murine cochlear nuclear complex, intracellular recordings were made from five giant cells that were identified by intracellular labeling with biocytin. Giant cells form one of the two output pathways of the dorsal cochlear nucleus (DCN). Understanding how neuronal circuits and intrinsic electrical properties interact to control the firing of giant cells is a step toward understanding what acoustic information is conveyed through these cells. 2. Cell bodies of the labeled giant cells lay in the deep layer of the DCN. Dendrites, widespread both along the isofrequency axis and along the tonotopic axis, occupied mainly the deep layer, but some distal ends strayed into the molecular layer. Axons of giant cells were large, varying between 1 and 2 microns diam, and left through the dorsal acoustic stria. They were not observed to branch in the cochlear nuclei. 3. Giant cells fired large, overshooting action potentials that were followed by two afterhyperpolarizations. The first brought the membrane potential below rest, independent of the strength of injected current. The more variable second one produced either an undershoot or an inflection in the membrane potential between action potentials. 4. In each of the five labeled giant cells, shocks to the nerve root or to the anteroventral cochlear nucleus (AVCN) evoked a monosynaptic excitatory postsynaptic potential and two tandem inhibitory postsynaptic potentials (IPSPs) in the first 10 ms. Later IPSPs followed after latencies of between 10 and 50 ms. Monosynaptic excitation was usually cut short by the inhibition. 5. Strychnine, at 1 microM, blocked all IPSPs in the one giant cell tested, indicating that inhibitory input to this giant cell from circuits intrinsic to the cochlear nuclear complex was glycinergic. 6. The location of afferents was mapped for two giant cells. Both excitatory and inhibitory inputs to giant cells could be driven by the local application of glutamate to many loci in the AVCN and posteroventral cochlear nucleus, indicating that the ventral cochlear nucleus VCN contains interneurons that are monosynaptically or polysynaptically connected to giant cells. 7. An interpretation consistent with the results is that giant cells are excited by auditory nerve fibers and are inhibited by tuberculoventral cells. Giant cells may also be excited by granule or T stellate cells.

Animals↗

PubMed1984

Ethanol-induced modulation of the membrane potential and synaptic activity of trigeminal motoneurons during sleep and wakefulness.

In the present study we investigated the direct actions of ethanol on the membrane properties and excitatory and inhibitory postsynaptic potentials of trigeminal motoneurons in chronic cats. During states of sleep and wakefulness, extracellular and intracellular recordings were carried out together with juxtacellular (somatic and dendritic) and intracellular pressure injections of 0.05-2.5 M ethanol solutions in femtoliter quantities. Juxtacellularly applied ethanol induced: a sequence of excitatory-inhibitory alterations in firing activity which were accompanied by depolarizing-hyperpolarizing shifts in the resting membrane potential; a decrease in the amplitude of action potentials; and a depression in excitatory and inhibitory postsynaptic potentials. Intracellular ethanol injections resulted in depolarization of the membrane potential and a decrease in the amplitude of action potentials as well as a reduction in the amplitude of excitatory and inhibitory postsynaptic potentials. Both juxtacellularly and intracellularly applied ethanol affected the membrane potential and synaptic activity in a fashion that was not dependent upon the animal's behavioral state of sleep or wakefulness.

Action Potentials↗