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PubMed1995

Modulation of an inhibitory interneuron in the neural circuitry for the tail withdrawal reflex of Aplysia.

1. Serotonin (5-HT), small cardioactive peptide B (SCPB) and FMRFamide have well-established facilitatory and inhibitory effects on sensory neurons and their connections with motor neurons mediating withdrawal reflexes in Aplysia. Little is known, however, about their effects on interneurons contributing to those reflexes. As a first step, we examined the effects of these three transmitters on the identified inhibitory interneuron RP14 in isolated pleural-pedal ganglia. 2. Bath application of 5-HT hyperpolarized RP14, inhibited its spontaneous activity and decreased its excitability. In addition, 5-HT decreased the amplitude of inhibitory postsynaptic potentials produced by RP14 in tail sensory and motor neurons. 3. In contrast, bath application of SCPB increased spontaneous activity in RP14. Subsequent application of 5-HT to the bath, which still contained SCPB, inhibited RP14. Therefore, the effects of SCPB were essentially opposite to those of 5-HT on this inhibitory interneuron. 4. FMRFamide had little effect on RP14. It did not produce an obvious change in its resting membrane potential and produced only a transient increase in its spontaneous activity. 5. These results suggest that various neuromodulators have differential effects on elements of the neuronal circuit underlying the tail-withdrawal reflex of Aplysia. Differential modulation may determine the overall behavioral manifestations associated with sensitization.

Action Potentials↗

PubMed1988

Norepinephrine decreases synaptic inhibition in the rat hippocampus.

The effects of norepinephrine (NE) on inhibitory synaptic potentials were studied on CA1 pyramidal neurons in the hippocampal slice in vitro. Norepinephrine caused the appearance of multiple population spikes in the CA1 region of the hippocampal slice, reminiscent of the actions of gamma-aminobutyric acid (GABA) antagonists. Intracellular recording revealed that NE causes a marked and reversible reduction in inhibitory postsynaptic potentials (IPSPs) recorded in CA1 pyramidal cells. This reduced IPSP results in a larger intracellular excitatory postsynaptic potential (EPSP), which can cause the cell to fire more than one action potential. This disinhibitory effect of NE appears to be mediated by an alpha-receptor, and occurs at a site presynaptic to the pyramidal cell, since NE does not change the reversal potential of the IPSP nor does it affect the amplitude or the reversal potential of iontophoretic GABA responses. In addition to reducing evoked IPSPs, NE causes an increase in the frequency of spontaneous IPSPs, suggesting that inhibition of interneuronal firing may not account for this disinhibitory action of NE.

Action Potentials↗

PubMed1995

Serotoninergic modulation of excitability in area CA1 of the in vitro rat hippocampus.

Intra- and extracellular recordings from the in vitro rat hippocampal slice preparation have been used to investigate the influence of serotoninergic, adrenergic and cholinergic receptor antagonists on the excitability of CA1 pyramidal neurones. The serotonin receptor antagonist 4-amino-N-(1-azabicyclo[2.2.2]oct-3yl)-5-chloro-2- methoxybenzamide(E)-2-butenedioate (zacopride, 100 microM) produced multiple population spikes on the orthodromically evoked field potential, in contrast to the lack of effect of another serotonin antagonist 1 alpha H,3 alpha,5 alpha H-tropan-3-yl-3,5-dichlorobenzoate (MDL 72222, 30 microM), as well as the cholinergic antagonists atropine (10 microM) and hexamethonium (100 microM) and the noradrenergic antagonist atenolol (10 microM). Monosynaptic inhibitory postsynaptic potentials (IPSPs) recorded in the presence of the glutamatergic antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and ketamine (50 microM) were recorded from CA1 pyramidal neurones. Zacopride (100 microM) and MDL 72222 (30 microM) both reduced the isolated IPSP to 54 +/- 9% (n = 8) and 78 +/- 4% (n = 3), respectively. Neither of the cholinergic antagonists had any effect, while atenolol reduced the IPSP to 87 +/- 3% (n = 7) of the control IPSP. We propose that the difference in action of zacopride and MDL 72222 on the field potentials is due to zacopride activating postsynaptic 5HT4 receptors on the pyramidal neurone, thereby reducing a Ca(2+)-activated K(+)-conductance. This, in combination with a 5HT3 receptor-mediated reduction in gamma-aminobutyric acid (GABA)-ergic inhibition, leads to an increase in pyramidal cell excitability evident as epileptic field potentials.

Acetylcholine↗

PubMed1976

Characteristics of the output from the dentate nucleus to spinal neurons via pathways which do not involve the primary sensorimotor cortex.

Experiments were performed to determine the action of the dentate output on neurons in the spinal cord mediated by pathways which do not involve the primary sensorimotor and premotor cortices. The dentate nucleus was electrically stimulated by stereotaxically placed electrodes in Rhesus monkeys whose contralateral sensorimotor and premotor cortices were ablated. The resultant changes in excitability of lumbar alpha motorneurons activated by Ia afferents from nerves innervating femoral, hamstring, gastrocnemius-soleus and peroneal muscles were measured by intracellular recordings and by determining the percent change in the amplitude of the monosynaptic reflex recorded from ventral roots. The effect of stimulation of the dentate nucleus on proprioceptive reflexes was determined by recording the changes in postsynaptic potentials evoked by selective stimulation of Ia and Ib afferent fibers. The results demonstrated that dentate nucleus exerts a significant action on the excitability of spinal neurons via pathways which do not include the sensorimotor and premotor cortices. Whether the dentate stimulus produced an increase or decrease in the excitability of these neurons was dependent upon the site within the dentate nucleus at which the stimulus was applied, demonstrating that, in the decorticate preparation, the output from this nucleus is quite heterogeneous. In addition, stimulation of the dentate nucleus in these monkeys did not affect the Ia reflex pathway but significantly changed the amplitude of the inhibitory postsynaptic potential evoked by Ib afferents in lumbar alpha motorneurons.

Animals↗

PubMed1999

The anticonvulsant BW534U87 depresses epileptiform activity in rat hippocampal slices by an adenosine-dependent mechanism and through inhibition of voltage-gated Na+ channels.

1. The cellular and molecular actions of BW534U87 were studied using intracellular and extracellular recordings from the CA1 region of rat hippocampal slices and whole-cell voltage-clamp recordings of recombinant human brain type IIA Na+ channels expressed in Chinese hamster ovary (CHO) cells. 2. Normal excitatory and inhibitory postsynaptic potentials evoked in hippocampal slices were unaffected by BW534U87 or the adenosine deaminase inhibitor EHNA. However, epileptiform activity was depressed by BW534U87 (50 micronM) and this inhibition was reversed by the adenosine receptor antagonist 8-phenyl theophylline (8-PT, 30 micronM). EHNA (10 micronM) mimicked the effects of BW534U87. Furthermore, BW534U87 enhanced the inhibitory effects of exogenous adenosine on evoked synaptic potentials. BW534U87 (50 micronM) also voltage- and use-dependently inhibited action potentials elicited by current injection, independent of the adenosine system, since it was not affected by 8-PT. 3. In CHO cells expressing the recombinant human brain Na+ channel, BW534U87 produced a concentration- and voltage-dependent inhibition of Na+ currents with a half-maximal inhibitory concentration of 10 micronM at a Vh of -60 mV. Use-dependent inhibition was evident at high-frequencies (20x20 ms pulse train at 10 Hz). 4 In conclusion, BW534U87 blocks hippocampal epileptiform activity by a dual mechanism. The first action is similar to that produced by EHNA and is dependent on endogenous adenosine probably by inhibition of adenosine deaminase. Secondly, BW534U87 directly inhibits voltage-gated Na+ channels in a voltage- and frequency-dependent manner. Both actions of BW534U87 are activity-dependent and may synergistically contribute to its overall anticonvulsant effects in animal models of epilepsy.

Action Potentials↗

PubMed1993

GABAb receptors are coupled to a barium-insensitive outward rectifying potassium conductance in premotor respiratory neurons.

1. Labeled premotor respiratory neurons from neonatal rats in culture were used to study the effects of (+/-)baclofen, a selective gamma-aminobutyric acid (GABA)b receptor agonist known to inhibit rhythmic breathing movements in mammals. Bath application of (+/-)baclofen-activated outward currents in cell-attached patches, suggesting that a second messenger system linked the (+/-)baclofen-activated conductance (GBac) to the GABAb receptor. 2.GBac channels exhibited outward rectification and were insensitive to blockade by Ba2+ and Cs+. The single-channel conductance was 100 pS in symmetrical K+ solutions and decreased as [K+]o was reduced. The reversal potential for the GBac channel shifted 45 mV/decade when [K+]o was changed indicating that it was predominantly selective for K+ ions. These properties were similar to those of the S-channel in Aplysia sensory neurons. 3. The properties of GBac channels were distinct from those associated with the GABAb mediated slow inhibitory postsynaptic potential (IPSP), indicating that GABAb receptors can be associated with more than one type of K+ channel. We propose that GBac channels modulate the repetitive firing activity of premotor respiratory neurons and may also participate in presynaptic inhibition.

Animals↗

PubMed1989

Differential actions of cocaine and amphetamine on dorsal raphe neurons in vitro.

Intracellular recordings of membrane potential were made from neurons in nucleus dorsal raphe in the rat brain slice. Cocaine (300 nM-30 microM) caused a concentration-dependent hyperpolarization of the membrane potential, with a maximum effect of 13.3 +/- 2.2 mV (N = 6) and an EC50 of 4.2 microM. This action was antagonized by spiperone (1 microM), suggesting that the hyperpolarization was mediated indirectly through endogenous 5-hydroxytryptamine (5-HT). Cocaine (300 nM) increased the time constant for decay (tau 2) of the 5-HT inhibitory postsynaptic potential (IPSP) from 432 +/- 57 msec to 708 +/- 81 msec (N = 14); 10 microM increased tau 2 by about 9-fold. Amphetamine (100 nM-10 microM) caused a depolarization that was antagonized by prazosin (100 nM). In slices taken from reserpine-treated animals (5 mg/kg, 12 hr), the 5-HT-mediated IPSP, the noradrenaline-mediated slow excitatory postsynaptic potential and the amphetamine-induced depolarization were absent. These results indicate that the amphetamine-induced depolarization resulted from the release of endogenous noradrenaline. In the presence of prazosin (100 nM), amphetamine caused a hyperpolarization at a threshold concentration of 10 microM, had an EC50 of 26 microM and a maximum effect of 10 +/- 0.9 mV (N = 8). This hyperpolarization as well as the cocaine-induced hyperpolarization were not reduced by prior treatment with reserpine. Amphetamine (10 microM) caused a 2.2-fold increase in the time constant of decay of the IPSP with no change in the amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗

PubMed1982

Electrical development in spinal cord cell culture.

Parallel electrophysiological and neurochemical studies of development are reported for mouse spinal cord cell cultures. The time course of electrical activity and the stage-dependent effects of tetrodotoxin on levels of the neuronal enzyme choline acetyltransferase were compared to establish the presence of spontaneous electrical activity at a time when tetrodotoxin adversely affects development. The extracellular patch electrode makes it possible to examine the ongoing electrical activity of the small cells present in young cultures. A rapid increase in spontaneous electrical activity during the first 2 weeks in culture was found to correlate closely with the onset of tetrodotoxin-induced depression of choline acetyltransferase activity, supporting the idea that ongoing electrical activity plays a role in neuronal development. The development of inhibitory synaptic activity occurs gradually throughout the period of culture, whereas excitatory synaptic activity and action potentials develop in unison, reaching maximal levels during the 2nd week in culture. For all cultures tested, ranging in age from 9 to 45 days old, acute bath application of gamma-aminobutyric acid (GABA) abolished spontaneous electrical activity. Glycine is relatively ineffective in abolishing spontaneous activity in young cultures which have few inhibitory postsynaptic potentials (IPSPs), but glycine becomes as effective as GABA at a later stage of development. This suggests rather different timetables of development for GABA and glycine receptors, with glycine receptors developing in parallel with IPSPs.

Animals↗

PubMed1987

Antagonists discriminate muscarinic excitation and inhibition in sympathetic ganglion.

The effect of muscarinic antagonists was studied on the muscarinic slow IPSP (inhibitory postsynaptic potential) and slow EPSP (excitatory postsynaptic potential) in bullfrog sympathetic ganglia using the sucrose-gap recording method. Pirenzepine, alcuronium and atropine reduced slow IPSP amplitude more than slow EPSP amplitude. The most selective antagonists studied were pancuronium and gallamine which blocked or substantially reduced the slow IPSP without significantly affecting slow EPSP amplitude. The results suggest that the muscarinic inhibitory response may involve a different muscarinic receptor subtype, and/or receptor-ion-channel complex, than the muscarinic excitatory response.

Alcuronium↗

PubMed1992

Intracellular electrophysiological and morphological study of the medullary inspiratory neurons of the decerebrate rat.

Intracellular recordings and labelings with horseradish peroxidase (HRP) of inspiratory neurons were performed in decerebrate, paralyzed and ventilated rats. A total of 58 neurons were located within the ventrolateral medulla. They were identified as bulbospinal neurons (n = 15), cranial motoneurons (n = 9) and not antidromically activated (NAA) neurons (n = 34) by antidromic stimulation or HRP labeling, or both. These inspiratory neurons had rhythmical changes in membrane potentials similar to those reported in cats, i.e. an abrupt depolarization at the onset of phrenic discharge followed by trajectories of depolarization which evolved into augmenting I, bell-shaped I or decrementing I patterns until a rapid repolarization at the start of expiration. All types were hyperpolarized during expiration by chloride-dependent inhibitory postsynaptic potentials (IPSPs) which were demonstrated in 13 neurons from which the reversal was obtained. Such IPSPs were apparent in two waves throughout expiration, an early one in post-inspiration (stage I of expiration) and a late one in late expiration (stage II of expiration). These properties are also similar to those of feline inspiratory medullary neurons. Four labeled bulbospinal neurons had axonal collaterals which were ipsi- and contralateral to the site of their somata. Two of 6 labeled NAA neurons exhibited profuse axonal arborizations within various medullary nuclei. No medullary axonal collateral was seen from 6 labeled motoneurons. These results indicate that even though in the rat a single concentration of inspiratory neurons within the ventrolateral medulla has been demonstrated, there is no fundamental difference in the organization of the inspiratory neuronal network compared to that of the cat.

Animals↗

PubMed1985

Synaptic transmission in the rabbit inferior mesenteric ganglion.

Electrical properties, cholinergic neurotransmission and non-cholinergic neurotransmission in the rabbit inferior mesenteric ganglion (IMG) in vitro were examined with intracellular recording techniques. A single ganglionic neuron received an average of 42 nicotinic cholinergic synaptic inputs. An atropine-sensitive slow excitatory postsynaptic potential not followed by a non-cholinergic late slow excitatory postsynaptic potential (LS-EPSP) was observed in 7% of the cells. In 63% of the cells a LS-EPSP insensitive to antagonism of nicotinic and muscarinic receptors was observed following repetitive nerve stimulation. The involvement of substance P (SP) in the genesis of the LS-EPSP was tested by applications of SP, applications of SP antagonists and applications of capsaicin. Neither SP, SP antagonists nor capsaicin affected the LS-EPSP. These findings distinguish the LS-EPSP in the rabbit IMG from its counterpart in the guinea pig IMG where SP has been proposed as the mediator of the LS-EPSP. A late slow inhibitory postsynaptic potential was observed in 13% of the cells. This hyperpolarization followed repetitive nerve stimulation and was insensitive to blockade of cholinergic receptors. There is a marked convergence of subthreshold fast excitatory postsynaptic potentials (F-EPSPs) of both central and peripheral origin onto these cells. The LS-EPSP could provide a mechanism for increasing the likelihood of temporal and/or spatial summation of these fast synaptic inputs, thereby increasing the probability of action potential generation in the ganglion cells.

Action Potentials↗

PubMed1976

Putative synaptic mechanisms of inhibition in Limulus lateral eye.

Serotonin (5-HT) perfusion of a thin section of Limulus lateral eye hyperpolarizes retinular and eccentric cell membrane potential, and blocks spike action potentials fired by the eccenteric cell. The indoleamine does not directly affect retinular cell receptor potential or eccenteric cell generator potential in response to light stimuli. LSD perfusion blocks both this inhibitory action of 5-HT and light-evoked, synaptically mediated, lateral inhibition. Iontophoretic application of 5-HT to the synaptic neuropil produces shorter latency and duration and larger amplitude of inhibition than does the perfusion technique. This inhibition is dose dependent; the accompanying inhibitory postsynaptic potential (IPSP) appears to have an equilibrium potential more hyperpolarized than normal resting potential levels of ca. -50 mV. IPSP amplitude is sensitive to extracellular potassium ion concentration: it increases with decreased [K+]0 and decreases with increased [K+]0. LSD blocks the inhibition produced by iontophoretic application of 5-HT. Interaction between light-evoked, natural synaptic transmitter-mediated IPSP's and 5-HT IPSP's suggests a common postsynaptic receptor or transmitter-receptor-permeability change mechanism.

Action Potentials↗

PubMed1997

Relationship between sensory stimuli-elicited IPSPs in motoneurons and PGO waves during cholinergically induced muscle atonia.

Inhibitory postsynaptic potentials (IPSPs) can be produced in masseter motoneurons by sensory stimuli after the injection of carbachol into the nucleus pontis oralis (NPO) of alpha-chloralose-anesthetized cats. We have postulated previously that these IPSPs, which are induced in masseter motoneurons by sensory stimuli, arise as the result of phasic activation of the motor inhibitory system that mediates atonia occurring spontaneously during active sleep. In the present study, we determined that sensory stimuli, which excite different sensory pathways, somatosensory and auditory, also elicit ponto-geniculo-occipital (PGO) waves during the carbachol-induced state. Because the elicitation of PGO waves has been hypothesized to be a central sign of activation of alerting mechanisms, we suggest that these stimuli also excite those CNS structures that are involved in the alerting network. The temporal association of the sensory stimuli-elicited IPSPs and PGO waves also was examined by correlating the intracellular response of masseter motoneurons and the extracellular response of lateral geniculate nuclei neurons to somatosensory and auditory stimuli. Sensory stimuli produced an IPSP that had a similar latency from the foot of the elicited PGO wave as that of spontaneously occurring motoneuron IPSPs and PGO waves that occur during both carbachol-induced muscle atonia and naturally occurring active sleep. In addition, the intensity of the stimulus necessary for elicitation of PGO waves was found to be lower than that required for the elicitation of IPSPs in motoneurons. Additionally, evoked responses in masseter motoneurons during the carbachol-induced state were graded in response to increases in stimulus intensity. The preceding data suggest that some type of processing of sensory input occurs such that only those stimuli that are capable of activating alerting mechanisms involved in the generation of PGO waves result in an increase in activity in the motor inhibitory system. We conclude that there may be a functional link between alerting mechanisms involved in the generation of PGO waves and the motor inhibitory system that generates IPSPs in motoneurons. This functional link may serve to preserve atonia, and thus the state of active sleep, from potentially disruptive PGO-related influences that, during other behavioral states, result in motor activation.

Animals↗

PubMed1987

Conductance changes underlying a late synaptic hyperpolarization in hippocampal CA3 neurons.

1. Single-electrode current- and voltage-clamp techniques were employed to study properties of the conductance underlying an orthodromically evoked late synaptic hyperpolarization or late inhibitory postsynaptic potential (IPSP) in CA3 pyramidal neurons in the rat hippocampal slice preparation. 2. Late IPSPs could occur without preceding excitatory postsynaptic potentials at the resting membrane potential and were graded according to the strength of the orthodromic stimulus. The membrane hyperpolarization associated with the late IPSP peaked within 140-200 ms after orthodromic stimulation of mossy fiber afferents. The late IPSP returned to base line with a half-decay time of approximately 200 ms. 3. As determined from constant-amplitude hyperpolarizing-current pulses, the membrane conductance increase during the late IPSP, and the time course of its decay, were similar whether measurements were made near the resting membrane potential or when the cell was hyperpolarized by approximately 35 mV. 4. When 1 mM cesium was added to the extracellular medium to reduce inward rectification, late IPSPs could be examined over a range of membrane potentials from -60 to -140 mV. For any given neuron, the late IPSP amplitude-membrane potential relationship was linear over the same range of membrane potentials for which the slope input resistance was constant. The late IPSP reversed symmetrically near -95 mV. 5. Intracellular injection of ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid or extracellular application of forskolin, procedures known to reduce or block certain calcium-dependent potassium conductances in CA3 neurons, had no significant effect on the late IPSP. 6. Single-electrode voltage-clamp techniques were used to analyze the time course and voltage sensitivity of the current underlying the late IPSP. This current [the late inhibitory postsynaptic current (IPSC)] began as early as 25 ms after orthodromic stimulation and reached a peak 120-150 ms following stimulation. 7. The late IPSC decayed with a single exponential time course (tau = 185 ms). 8. A clear reversal of the late IPSC at approximately -99 mV was observed in a physiological concentration of extracellular potassium (3.5 mM).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2000

Dual modulation of excitatory synaptic transmission by agonists at group I metabotropic glutamate receptors in the rat spinal dorsal horn.

The effects of group I metabotropic glutamate (mGlu) receptors on excitatory transmission in the rat dorsal horn, but mostly substantia gelatinosa, neurons were investigated using conventional intracellular recording in slices. The broad spectrum mGlu receptor agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S, 3R-ACPD), the group I mGlu receptor selective agonist (S)-3, 5-dihydroxyphenylglycine (DHPG), and the selective mGlu subtype 5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), all induce long-lasting depression of A primary afferent fibers-mediated monosynaptic excitatory postsynaptic potential (EPSP), and long-lasting potentiation of polysynaptic EPSP, and EPSP in cells receiving C-afferent fiber input. The DHPG potentiation of polysynaptic EPSP was partially or fully reversed by (S)-4-carboxyphenylglycine (S-4CPG), the mGlu subtype 1 preferring antagonist. 2-Methyl-6-(phenylethynyl)-pyridine, the potent and selective mGlu subtype 5 antagonist, partially reversed the CHPG potentiation of polysynaptic EPSP. The effects of DHPG on monosynaptic and polysynaptic EPSPs were reduced, or abolished, by the N-methyl-D-aspartate (NMDA) receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5). A clear and pronounced facilitation of the expression of DHPG- and CHPG-induced enhancement of polysynaptic EPSP, and EPSP evoked at C-fiber strength, was seen in the absence of gamma-aminobutyric acid subtype A receptor- and glycine-mediated synaptic inhibition. Besides dual modulation of excitatory synaptic transmission, DHPG induces depression of inhibitory postsynaptic potentials evoked by primary afferent stimulation in dorsal horn neurons. In addition, group I mGlu receptor agonists produced a direct persistent excitatory postsynaptic effect consisting of a slow membrane depolarization, an increase in input resistance, and an intense neuronal discharge. Cyclothiazide and (S)-4-CPG, the mGlu receptor subtype 1 preferring antagonists, significantly attenuated the DHPG-induced depolarization. These results demonstrate that the pharmacological activation of group I metabotropic glutamate receptors induces long-term depression (LTD) and long-term potentiation (LTP) of synaptic transmission in the spinal dorsal horn. These types of long-term synaptic plasticity may play a functional role in the generation of post-injury hypersensitivity (LTP) or antinociception (LTD).

Animals↗

PubMed1992

Medullary expiratory neurons in the decerebrate rat: an intracellular study.

Intracellular recordings and labelings with horseradish peroxidase (HRP) of expiratory (E) neurons were performed in decerebrate, paralyzed, and ventilated rats. A total of 37 neurons were recorded, from which 4 cells and 1 axon were labeled. They were located in two regions of the ventrolateral medulla. One was in the rostral portion of the nucleus ambiguus just caudal to the facial nucleus, and the other in the nucleus retroambiguus at the level of the caudal medulla. These expiratory neurons had rhythmical changes in membrane potential similar to those reported in cat, i.e., a depolarization in the intervals between phrenic bursts which evolved in an augmenting (E-aug, n = 15), or bell-shaped or 'plateau' (E-all, n = 22) pattern until a rapid hyperpolarization at the start of inspiration. Both types were hyperpolarized during inspiration by chloride-dependent, inhibitory postsynaptic potentials (IPSPs) which were demonstrated in 17 neurons (10 E-aug and 7 E-all) from which reversal was obtained. Such IPSPs also existed during post-inspiration (stage I of expiration) in 4 of the 10 augmenting E neurons. They were identified by antidromic stimulation or HRP labeling, or both, as bulbospinal neurons (n = 2), cranial motoneurons (n = 4), or not antidromically activated (NAA) neurons (n = 31). All the identified bulbospinal neurons and the motoneurons exhibited an E-all pattern. The expiratory neurons of the caudal medulla had various projections as demonstrated with HRP labeling: one bulbospinal neuron with ipsilateral axon giving off intramedullary collaterals, and NAA neurons with rostral medullary projections or with axons crossing the midline.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Octopamine is the synaptic transmitter between identified neurons in the buccal feeding network of the pond snail lymnaea stagnalis.

We report the pharmacological properties of synaptic connections from the three octopamine-containing OC interneurons to identified buccal feeding neurons in the pond snail, Lymnaea stagnalis. Intracellular stimulation of an OC interneuron evokes inhibitory postsynaptic potentials in the B3 motoneurons and N2 (d) interneurons, while the synapse between OC and N3 (phasic) interneurons has two components: an initial electrical excitation followed by chemical inhibition. All synaptic responses persist in a saline with elevated calcium and magnesium suggesting that the connections are monosynaptic. Local perfusion of 10(-4) M octopamine produces the same inhibitory membrane responses from these buccal neurons as OC stimulation. These responses also persist in high Mg(2+)/Ca(2+) saline indicating direct membrane effects. The similarities in reversal potentials for the synaptic hyperpolarization evoked on B3 neurons after OC stimulation (-89.0 mV, S.E.M.=14.1, n=10) and the octopamine response of the B3 neurons (-84.7 mV, S.E.M.=6.6, n=6) indicate that increased K(+)-conductance underlies both responses. Bath application of the octopaminergic drugs phentolamine (10(-6) M), epinastine (10(-6) M) or DCDM (10(-4) M) blocks the inhibitory synapse onto B3 or N2 neurons and the chemical component of the N3 response. They also block the octopamine-evoked inhibition of B3, N2 and N3 neurons. NC-7 (2x10(-5) M) has a hyperpolarizing agonist effect (like octopamine) on these neurons and also blocks their chemical synaptic input from the OC interneurons. These results provide pharmacological evidence that the neurotransmitter between the octopamine-immunopositive OC interneurons and its followers is octopamine. This is the first example of identified octopaminergic synaptic connections within the snail CNS.

Action Potentials↗

PubMed1994

Experimental neurobiology of epilepsies.

Epileptic discharges are a pathological extreme of neuronal synchrony. Experimental models of both focal and primary generalized epilepsies reveal the importance of the interaction of intrinsic (membrane current) properties of neurons and the synaptic networks which connect them. Focal epilepsies depend on excitatory networks within individual cortical structures, but full seizures may require widely dispersed neuronal networks. Absence seizures are generated by the thalamocortical system, and depend on inhibitory postsynaptic potentials, Ca2(+)-activated K+ currents and low threshold "T" currents. Other forms of synchronization can occur under particular circumstances, including field effects and gap junctions, but at the moment appear to be less generally involved in epileptogenesis. The cellular and network mechanisms of chronic experimental epilepsies are more complex and involve synaptic reorganization, and functional disconnection of inhibitory neurons.

Animals↗