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PubMed1984

Properties of the GABA receptors located on spinal primary afferent neurones and hypophyseal neuroendocrine cells of the rat.

Electrophysiological techniques have been used to study the pharmacological characteristics of GABA receptors in two in vitro preparations likely to provide the ionic basis for GABAergic inhibition of excitation-secretion coupling. The shortening of Ca2+ spikes duration by GABAB receptors was shown to occur in slow conducting dorsal root ganglion cells, independently of marked depression of inward calcium currents. Ion-selective electrodes (K+ or Ca2+) were used to show the presence of both GABAA and GABAB receptors on the neurosecretory terminals and gland cells from hypophyseal neuro-intermediate lobe (NIL). In this latter preparation, potentiation of hormone release was observed under GABAA receptor activation, whilst inhibition was seen with GABAB agonists.

Afferent Pathways↗
PubMed2006

Dissociation of neural responses and skin conductance reactions during fear conditioning with and without awareness of stimulus contingencies.

This study investigates the effect of awareness of stimulus contingencies on BOLD responses within the amygdala, the orbitofrontal, and the occipital cortex, and on differential skin conductance responses (SCRs) during fear conditioning. Of two geometric figures, the paired conditioned stimulus (CS+) predicted an electrical stimulus (unconditioned stimulus = UCS), whereas the unpaired conditioned stimulus (CS-) was not followed by the UCS. Awareness of stimulus contingencies was manipulated experimentally, creating an aware and an unaware group: a distracter figure and a working memory task were introduced to conceal the stimulus contingencies of the conditioning paradigm, hence preventing contingency detection in the unaware group. The aware group was informed beforehand about the relation between CS+, CS-, and UCS. Differential SCRs were only obtained in the aware but not in the unaware group. Conversely, we observed enhanced responses of the amygdala, the orbitofrontal, and the occipital cortex to the CS+ in the unaware group only. Thus, we found a dissociation of SCR differentiation and the activation of a neural fear network depending on the presence or absence of awareness. These results support a model of fear conditioning that distinguishes between a more cognitive level of learning, reflected in contingency awareness and differential SCRs, and the awareness independent activation of a fear network.

Adult↗
PubMed2002

Gustatory projections from the nucleus of the solitary tract to the parabrachial nuclei in the hamster.

Taste-responsive cells in the nucleus of the solitary tract (NST) either project to the parabrachial nuclei (PbN) of the pons, through which taste information is transmitted to forebrain gustatory nuclei, or give rise to axons terminating locally within the medulla. Numerous anatomical studies clearly demonstrate a substantial projection from the rostral NST, where most taste-responsive cells are found, to the PbN. In contrast, previous electrophysiological studies in the rat have shown that only a small proportion (21-45%) of taste-responsive NST cells are antidromically activated from the PbN, suggesting that less than half the cells recorded from the NST are actually involved in forebrain processing of gustatory information. In the present experiment we investigated the projections from the NST to the PbN electrophysiologically in urethane anesthetized hamsters. Responses of 101 single neurons in the rostral NST were recorded extracellularly following lingual stimulation with 32 mM NaCl, sucrose and quinine hydrochloride (QHCl) and 3.2 mM citric acid. The taste-responsive region of the PbN was identified electrophysiologically and stimulated with a concentric bipolar electrode to antidromically activate each NST cell. Of the 101 taste-responsive NST cells, 81 (80.2%) were antidromically activated from the ipsilateral PbN. The mean firing rates to taste stimulation and the spontaneous activity of these projection neurons were significantly greater than those of non-projecting cells. Every sucrose-best neuron in the sample projected to the PbN. The mean conduction velocity of the 23 QHCl-best neurons was significantly lower than that of the other 58 PbN projection neurons, suggesting that the most QHCl-responsive cells are a subset of smaller neurons. These data show that a large majority of NST cells responsive to taste stimulation of the anterior tongue project to the gustatory subdivisions of the PbN and that these cells have the most robust responses to gustatory stimulation.

Action Potentials↗
PubMed1998

Critical role of axonal A-type K+ channels and axonal geometry in the gating of action potential propagation along CA3 pyramidal cell axons: a simulation study.

A model of CA3 pyramidal cell axons was used to study a new mode of gating of action potential (AP) propagation along the axon that depends on the activation of A-type K+ current (Debanne et al., 1997). The axonal membrane contained voltage-dependent Na+ channels, K+ channels, and A-type K+ channels. The density of axonal A-channels was first determined so that (1) at the resting membrane potential an AP elicited by a somatic depolarization was propagated into all axon collaterals and (2) propagation failures occurred when a brief somatic hyperpolarization preceded the AP induction. Both conditions were fulfilled only when A-channels were distributed in clusters but not when they were homogeneously distributed along the axon. Failure occurs in the proximal part of the axon. Conduction failure could be determined by a single cluster of A-channels, local decrease of axon diameter, or axonal elongation. We estimated the amplitude and temporal parameters of the hyperpolarization required for induction of a conduction block. Transient and small somatic hyperpolarizations, such as simulated GABAA inhibitory postsynaptic potentials, were able to block the AP propagation. It was shown that AP induction had to occur with a short delay (<30 msec) after the hyperpolarization. We discuss the possible conditions in which such local variations of the axon geometry and A-channel density may occur and the incidence of AP propagation failures on hippocampal network properties.

Action Potentials↗
PubMed1979

Excitatory synaptic ensemble properties in the visual cortex of the macaque monkey: a current source density analysis of electrically evoked potentials.

The spatio-temporal distributions of excitatory synaptic ensemble activities in A17 and A18 of the visual cortex of the macaque monkey have been investigated. The synaptic activities were elicited by electrical stimulation of the primary efferents and were localized by applying the current source density analysis to the intracortically recorded field potentials. The principal results are as follows: 1. In A17, two groups of activity, evoked by fast and slow afferents, respectively, were distinguishable. 2. The fast afferents induced monosynaptic activity in layer IV C alpha and layer VI, disynaptic activity in layer IV C alpha and in the supragranular layers and trisynaptic activity in layer IV B. 3. The slow efferents induced monosynaptic activity in lower layers IV C beta and layer VI, disynaptic activity via strong connections in upper layer IV C beta, further disynaptic activity in layers III and IV B and trisynaptic activity in layers V A and II. 4. With the exception that the CSD data reveal more polysynaptic activity within layer IV, there is good agreement between the spatio-temporal distribution of synaptic activities and the cortical circuit diagrams proposed in anatomical studies. 5. In A18, activities from the slow and fast conducting afferent systems are revealed in layer IV, both most likely mediated by the monosynaptically activated target cells of A17. These activities are passed on to the supra-and infragranular layers. 6. In the lateral geniculate nucleus the safety factor of transmission is higher for activity conveyed by slow-than by fast-conducting retinal afferents. 7. The spatial distribution of monocularly evoked surface potentials failed to reveal the ocular dominance columns. 8. Comparison with the cat indicates that, with respect to the intracortical circuitry and LHN-transmission, there are more similarities between the fast-group activity in the monkey and the y-system in the cat and between the slow-group activity in the monkey and the x-system in the cat than vice versa.

Animals↗
PubMed1991

Extracellular characteristics of putative cholinergic neurons in the rat laterodorsal tegmental nucleus.

The extracellular electrophysiological properties of neurons in the laterodorsal tegmental nucleus (LDT), a major source of cholinergic afferents to the thalamus, were studied in chloral hydrate-anesthetized rats. A combination of antidromic activation from the thalamus and histological verification of recording sites was used to correlate the identity of extracellular recordings in the rat LDT with cholinergic neurons in that region. All neurons antidromically activated by stimulation of the anteroventral thalamus were histologically verified to be within clusters of cholinergic (NADPH-d-positive) cells in the LDT or in the adjacent nucleus locus coeruleus (LC). The thalamically projecting LDT neurons had a homogeneous neurophysiological profile consisting of long duration action potentials (mean = 2.5 ms), slow conduction velocities (mean = 0.78 m/s), and lengthy chronaxie values (mean = 0.725 ms). The appearance and axonal characteristics of these neurons resembled those of noradrenergic LC neurons, but the two populations exhibited substantially different spontaneous activity patterns and sensory responsiveness. These characteristics may be useful in the preliminary identification of putative cholinergic neurons in vivo, and thereby provide a foundation for exploring the neuropharmacology, afferent modulation, sensory responsiveness and behavioral correlates of the brainstem cholinergic system.

Acetylcholine↗
PubMed1991

Magnetic stimulation of motor cortex and motor roots for painless evaluation of central and proximal peripheral motor pathways. Normal values and clinical application in disorders of the lumbar spine.

Magnetic stimulation of the motor cortex, motor roots, and proximal nerve trunks was performed in 46 healthy adults and in 73 consecutive patients with disorders of the lumbar spine. In combination with neurography and F-wave recordings, the fractionated stimulation of the motor pathways allowed calculation of conduction times of the pyramidal tract fibers, of the motor roots (ie, caudal fibers), and of the motor fibers of the lumbosacral plexus. Normal values for motor conduction times to the quadriceps, anterior tibial, and extensor digitorum brevis muscles were established. Patients had clinical and radiologic diagnoses of spinal stenosis (n = 43) and nerve root compression syndromes (n = 30). Motor conduction times to lower limb muscles were significantly delayed (above mean normal value +/- 2 x SD) in 65% of the patients with spinal stenosis and 50% of the patients with nerve root compression syndromes. Conduction slowing could be localized within the motor root and caudal fiber segment of the motor pathways in 80% of the patients in whom F-waves could be recorded. This method can be used to verify, quantify, and locate lesions of the motor pathways in conditions such as compression of the spinal cord, the caudal fibers (spinal stenosis), or the motor root passing through the intervertebral canal.

Adult↗
PubMed1990

Parasympathetic postganglionic pathways to the sinoatrial node.

Vagal ganglia that innervate the canine sinoatrial node (SAN) have been localized to a fat pad overlying and surrounding the right pulmonary vein complex (PVFP). The ventral epicardial surface of the right atrium was mapped in seven dogs anesthetized with alpha-chloralose after beta-blockade (timolol) and cardiac sympathetic and parasympathetic decentralization. A small, concentric bipolar exploring electrode was used to stimulate (during the atrial refractory period and using trains of five to eight stimuli per beat) systematically in the epicardial regions between the PVFP and the SAN. Changes in SAN rate with stimulation were measured, and the anatomic location was identified on a 150-point grid fitted to conform to size and shape of the atrium. Mapping was performed before and after local (PVFP) and systemic ganglionic blockade (hexamethonium). Data reveal that the primary vagal postganglionic pathways to the sinoatrial nodal region are subepicardial and adjacent to the SAN artery along the sulcus terminalis. Hexamethonium in the PVFP abolishes SAN inhibition during preganglionic vagal excitation, without interrupting vagal suppression of atrioventricular conduction. However, SAN slowing (with varying attenuation) continued to occur after hexamethonium (either PVFP or systemically) when the exploring electrode was applied directly over intramural postganglionic fibers between PVFP and sinus node. Attention is directed to existence of a very few synapses closer to SAN, probably in isolated ganglia immersed in fatty connective tissues along the sulcus terminalis.

Animals↗
PubMed2003

Study of neuronal gain in a conductance-based leaky integrate-and-fire neuron model with balanced excitatory and inhibitory synaptic input.

Neurons receive a continual stream of excitatory and inhibitory synaptic inputs. A conductance-based neuron model is used to investigate how the balanced component of this input modulates the amplitude of neuronal responses. The output spiking rate is well described by a formula involving three parameters: the mean mu and variance sigma of the membrane potential and the effective membrane time constant tauQ. This expression shows that, for sufficiently small tauQ, the level of balanced excitatory-inhibitory input has a nonlinear modulatory effect on the neuronal gain.

Computer Simulation↗
PubMedDate not supplied

Electrophysiological observations on the spinal cord of the normal and dystrophic mouse.

A method of carrying out electrophysiological experiments on the mouse spinal cord is described. The conduction velocity in the spinal dorsal roots (DR) of the normal mouse was in the range 10-100 m sec-1 and in the ventral roots (VR) 50-70 m sec-1. In the dystrophic mutant (129 ReJ dy/dy) the conduction velocity for both roots was usually in the range 0.1-2.0 m sec-1. Reflexes from DR to VR were recorded in both mutant and wild type animals and it was concluded that the delays in the mutant reflex were probably due to the slower conduction velocity in the roots. Postsynaptic inhibition and presynaptic inhibition were demonstrated and records were made from Renshaw cells and intracellularly from motoneurones. Delayed activity in spinal reflex paths, probably of supraspinal origin, was more pronounced in the dystrophic mutant. It is concluded that if the dystrophic mouse mutant were to be regarded as a model for human disease then similar reflex delays should be demonstrated in human subjects with muscular dystrophy.

Afferent Pathways↗
PubMed1993

Effects of adenosine triphosphate (ATP) on somatosensory evoked potentials in humans anesthetized with isoflurane and nitrous oxide.

In order to examine the usefulness of adenosine triphosphate (ATP) as an adjuvant to anesthesia for surgery requiring intraoperative somatosensory evoked potential (SSEP) monitoring, we have studied the effects of ATP on SSEPs in patients anesthetized with isoflurane and nitrous oxide (N2O). A control recording of SSEP was performed while anesthesia was maintained with 0.5% end-tidal concentration of isoflurane in 60% N2O. The recordings were repeated after an ATP infusion had been added to this basal anesthesia at the rates of 100 micrograms.kg bw-1.min-1 and 200 micrograms.kg bw-1.min-1. SSEP was also studied when end-tidal isoflurane concentration was increased to 1.5% after cessation of ATP infusion. An infusion of ATP combined with 0.5% isoflurane and 60% N2O effectively inhibited an increase in blood pressure during surgery. The amplitude of the cortical component of SSEP was lowered by 1.5% isoflurane, which also increased both cortical and spinal latencies as well as central conduction time (CCT). In contrast ATP infusions at both rates induced no significant changes in latencies, amplitude and CCT. The results indicate that ATP infusion combined with 0.5% isoflurane in 60% N2O can be a useful anesthetic technique for intraoperative SSEP monitoring because adequate anesthetic depth can be maintained by a low concentration of anesthetics without further suppression of SSEPs.

Adenosine Triphosphate↗
PubMed2006

GABA(B) receptors inhibit backpropagating dendritic spikes in hippocampal CA1 pyramidal cells in vivo.

Spike backpropagation has been proposed to enhance dendritic depolarization and synaptic plasticity. However, relatively little is known about the inhibitory control of spike backpropagation in vivo. In this study, the backpropagation of the antidromic spike into the dendrites of CA1 pyramidal cells was studied by extracellular recording in urethane-anesthetized rats. The population antidromic spike (pAS) in CA1 following stimulation of the alveus was recorded simultaneously with a 16-channel silicon probe and analyzed as current source density (CSD). The pAS current sink was shown to sequentially invade the soma and then the apical and basal dendrites. When the pAS was preceded <400 ms by a conditioning orthodromic CA3 stimulus, the apical and basal dendritic spike sinks were reduced and delayed. Dendritic spike suppression was large after a high-intensity CA3 conditioning stimulus that evoked a population spike, small after a low-intensity CA3 conditioning stimulus, and weak after conditioning by another pAS. The late (150-400 ms latency) inhibition of the backpropagating pAS at the apical and basal dendrites was partially relieved by a GABA(B) receptor antagonist, CGP35348 or CGP56999A, given intracerebroventricularly (icv). CGP35348 icv also decreased the latency of the antidromic spike sinks at all depths. A compartment cable model of a CA1 pyramidal cell with excitable dendrites, combined with a model of extracellular potential generation, confirms that GABA(B) receptor activation delays a backpropagating spike and blocks distal dendritic spikes. GABA(B) receptor-mediated conductance increase and hyperpolarization, amplified by removing dendritic I(A) inactivation, contribute to conditioned dendritic spike suppression. In addition, the model shows that slow Na(+) channel inactivation also participates in conditioned spike suppression, which may partly explain the small dendritic spike suppression after conditioning with a weak orthodromic stimulus or another antidromic spike. Thus, both theory and experiment confirm an important role of the GABA(B) receptors in controlling dendritic spike backpropagation.

Animals↗
PubMed1976

Heterogeneity of motor units activating single Golgi tendon organs in cat leg muscles.

The aim of this study was to investigate whether an individual Golgi tendon organ can signal the contraction of motor units with different physiological properties. The axonal conduction velocity and tetanic tension of motor units were examined in four muscles of the cat leg (peroneus brevis, peroneus longus, tibialis anterior and soleus). The motor units which were found to activate a given tendon organ had contractile properties dispersed over the same range as those of the whole muscle population. The proportion of tendon organ-activating motor units found in the studied samples suggests that altogether, the Golgi tendon organs of a muscle monitor the contraction of every motor unit in this muscle.

Animals↗
PubMed2004

Activation of slowly conducting medullary raphe-spinal neurons, including serotonergic neurons, increases cutaneous sympathetic vasomotor discharge in rabbit.

Neurons in the rostral medullary raphe/parapyramidal region regulate cutaneous sympathetic nerve discharge. Using focal electrical stimulation at different dorsoventral raphe/parapyramidal sites in anesthetized rabbits, we have now demonstrated that increases in ear pinna cutaneous sympathetic nerve discharge can be elicited only from sites within 1 mm of the ventral surface of the medulla. By comparing the latency to sympathetic discharge following stimulation at the ventral raphe site with the corresponding latency following stimulation of the spinal cord [third thoracic (T3) dorsolateral funiculus] we determined that the axonal conduction velocity of raphe-spinal neurons exciting ear pinna sympathetic vasomotor nerves is 0.8 +/- 0.1 m/s (n = 6, range 0.6-1.1 m/s). Applications of the 5-hydroxytryptamine (HT)(2A) antagonist trans-4-((3Z)3-[(2-dimethylaminoethyl)oxyimino]-3-(2-fluorophenyl)propen-1-yl)-phenol, hemifumarate (SR-46349B, 80 microg/kg in 0.8 ml) to the cerebrospinal fluid above thoracic spinal cord (T1-T7), but not the lumbar spinal cord (L2-L4), reduced raphe-evoked increases in ear pinna sympathetic vasomotor discharge from 43 +/- 9 to 16 +/- 6% (P < 0.01, n = 8). Subsequent application of the excitatory amino acid (EAA) antagonist kynurenic acid (25 micromol in 0.5 ml) substantially reduced the remaining evoked discharge (22 +/- 8 to 6 +/- 6%, P < 0.05, n = 5). Our conduction velocity data demonstrate that only slowly conducting raphe-spinal axons, in the unmyelinated range, contribute to sympathetic cutaneous vasomotor discharge evoked by electrical stimulation of the medullary raphe/parapyramidal region. Our pharmacological data provide evidence that raphe-spinal neurons using 5-HT as a neurotransmitter contribute to excitation of sympathetic preganglionic neurons regulating cutaneous vasomotor discharge. Raphe-spinal neurons using an EAA, perhaps glutamate, make a substantial contribution to the ear sympathetic nerve discharge evoked by raphe stimulation.

Anesthesia↗
PubMed2002

Diverse synaptic mechanisms generate direction selectivity in the rabbit retina.

The synaptic conductance of the On-Off direction-selective ganglion cells was measured during visual stimulation to determine whether the direction selectivity is a property of the circuitry presynaptic to the ganglion cells or is generated by postsynaptic interaction of excitatory and inhibitory inputs. Three synaptic asymmetries were identified that contribute to the generation of direction-selective responses: (1) a presynaptic mechanism producing stronger excitation in the preferred direction, (2) a presynaptic mechanism producing stronger inhibition in the opposite direction, and (3) postsynaptic interaction of excitation with spatially offset inhibition. Although the on- and off-responses showed the same directional tuning, the off-response was generated by all three mechanisms, whereas the on-response was generated primarily by the two presynaptic mechanisms. The results indicate that, within a single neuron, different strategies are used within distinct dendritic arbors to accomplish the same neural computation.

Action Potentials↗
PubMed1984

Electrophysiological identification of neurons in the parabrachial nucleus projecting directly to the hypothalamus in the rat.

Experiments were done in urethane anesthetized rats to identify single units in the region of the parabrachial nucleus (PBN) projecting directly to 'cardiovascular' responsive sites in either the paraventricular nucleus of the hypothalamus (PVH) or the supraoptic commissure and nucleus (SOC-SON) region. Fifty-five single units were antidromically activated in the ipsilateral PBN by electrical stimulation of either the PVH (n = 27) or SOC-SON region (n = 28) with latencies corresponding to conduction velocities of 0.3-5.1 m/s. The axons of PBN units projecting to the PVH conducted at significantly slower velocities (0.5 +/- 0.04 m/s) than those projecting to the SOC-SON region (1.6 +/- 0.25 m/s). These data suggest that ascending fibers from the PBN to the PVH are unmyelinated, whereas those to the SOC-SON region are primarily a little myelinated. In addition, since the PBN is known to receive cardiovascular and visceral afferent inputs, it is suggested that these neurons likely function in relaying this afferent information to hypothalamic areas involved in autonomic regulation.

Animals↗
PubMed1978

[Further study of the descending sympathoactivating pathways of the dorsolateral funiculus of the spinal cord].

The localization and conduction velocities of descending pathways which activate the different groups of sympathetic preganglionic nerons were studied in the cat cervical spinal cord. Certain evidences have been obtained that the fibres located near the dorsal surface of the dorsolateral funiculi with conduction velocities about 24--29 m/sec. can activate the ventral horn preganglionic neurons monosynaptically. In contrast to previous ideas, the sympathetic preganglionic neurons of the lateral horns seem to be activated not by different but by a single group of descending fibers with the conduction velocity 4--8.9 m/sec and localization in more ventral portions of the dorsolateral funiculus. The transmission from these fibers to the sympathetic preganglionic neurons of the lateral horns occurs in two ways: oligosynaptically (probably, disynaptically) and polysynaptically through a more complicated interneuronal chain. The sympathetic preganglionic neurons with unmyelinated axons, localized in the intermediate zone, for the first time were shown to be activated polysynaptically, probably via the same ways as the lateral horn neurons.

Animals↗
PubMed1981

The effects of tryptamine on transmitter release at a lobster neuromuscular junction.

Electrophysiological techniques were employed to characterize the effects of tryptamine at excitatory and inhibitory neuromuscular junctions of the stretcher muscle in the carpopodite of lobster walking limbs. Tryptamine was found to have a concentration dependent, biphasic effect on excitatory junction potential (EJP) amplitude. At concentrations of 0.01-0.5 mM tryptamine increased the amplitude of evoked EJPs, but at higher concentrations (greater than 0.5 mM) the amplitude was decreased by this amine. The high concentrations also decreased the amplitude of inhibitory junction potentials (IJPs) and reduced the frequency of miniature excitatory junction potentials (MEJPs). When a preparation in which the EJPs had been depressed by tryptamine was washed with the control, artificial sea water solution, the EJPs were increased to an amplitude greater than that of the pre-tryptamine control. Current-voltage relationship studies showed that tryptamine did not affect the effective resistance of the muscle fiber membrane. Tryptamine had no effect on the amplitude of excitatory responses evoked by the iontophoretic application of glutamate. Concentrations of tryptamine ranging to 10.0 mM affected neither the conduction velocity in meropodite or that of giant central nervous system (CNS) axons. We conclude that tryptamine affects synaptic transmission pre-synaptically by influencing the transmitter release process. Mass spectrometric analysis showed tryptamine to be an endogenous substance in the lobster; but the concentrations were low in the tissues analyzed. The highest concentration (approximately 0.3 nmol/g wet tissue) was in the subesophageal ganglion. Tryptamine was not detected in the meropodite nerves or carpopodite muscles.

Animals↗