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PubMed1994

Reduction in postsynaptic inhibition during maintained electrical stimulation of different nerves in the cat hindlimb.

1. Steady-state postsynaptic potentials (PSPs) were generated by prolonged (approximately 1 s) high-frequency (100-200 Hz) electrical stimulation of nerves in the cat hindlimb. The characteristics of these steady-state PSPs were compared for two polysynaptic afferent pathways (ipsilateral cutaneous sural vs. contralateral peroneal nerves), two animal preparations (decerebrate vs. chloralose), and two motoneuron pools (medial gastrocnemius vs. lateral gastrocnemius-soleus). 2. PSPs from both nerves usually (36 of 51 cases) contained a mixture of depolarizing and hyperpolarizing components. In all 36 cases where the PSP contained a hyperpolarizing component, a consistent qualitative pattern emerged during prolonged stimulation: the hyperpolarization reached a peak approximately 20 ms after stimulation onset and then decayed with a biphasic time course that consisted of an initial rapid phase (20-40 ms) and a later slower phase (200-400 ms) before the steady-state value was reached. This pattern occurred regardless of the differences in polysynaptic afferent pathways, animal preparations, and motoneuron pools. 3. The consistency of this overall pattern was remarkable, given the existence of several quantitative differences among the PSPs. These differences include the following: hyperpolarizing components were least common in the sural and peroneal PSPs in the decerebrate preparation. And only these sural and peroneal PSPs tended to have prolonged afterpotentials after stimulus cessation. The steady-state sural PSPs in the decerebrate preparation tended to generate the largest PSPs and, moreover, these PSPs did not follow the overall trend of having a statistically significant relation between the amplitude of the initial hyperpolarization and the amount of its decay. Finally, transient sural PSPs in lateral gastrocnemius-soleus motoneurons in the decerebrate preparation tended to have the largest hyperpolarizations. 4. To determine whether the decay of the hyperpolarization and the subsequent dominance of depolarization was due to a decreased inhibition or an increased excitation, injected current pulses were utilized to measure the changes in the cell's input resistance during the course of the synaptic input. A strong decrease in input resistance accompanied the initial period of maximal hyperpolarization (50% with respect to the resting input resistance). Input resistance then returned toward resting values as hyperpolarization faded and depolarization became dominant. However, there remained a persistent decrease in input resistance during the final phase of the PSP that amounted to < 10% of the initial decrease. These findings indicated that much of the reduction in hyperpolarization reflected a progressive decrease in synaptic efficacy for the inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1998

Chemoafferent degeneration and carotid body hypoplasia following chronic hyperoxia in newborn rats.

1. To define the role of environmental oxygen in regulating postnatal maturation of the carotid body afferent pathway, light and electron microscopic methods were used to compare chemoafferent neurone survival and carotid body development in newborn rats reared from birth in normoxia (21 % O2) or chronic hyperoxia (60 % O2). 2. Four weeks of chronic hyperoxia resulted in a significant 41 % decrease in the number of unmyelinated axons in the carotid sinus nerve, compared with age-matched normoxic controls. In contrast, the number of myelinated axons was unaffected by hyperoxic exposure. 3. Chemoafferent neurones, located in the glossopharyngeal petrosal ganglion, already exhibited degenerative changes following 1 week of hyperoxia from birth, indicating that even a relatively short hyperoxic exposure was sufficient to derange normal chemoafferent development. In contrast, no such changes were observed in the vagal nodose ganglion, demonstrating that the effect of high oxygen levels was specific to sensory neurones in the carotid body afferent pathway. Moreover, petrosal ganglion neurones were sensitive to hyperoxic exposure only during the early postnatal period. 4. Chemoafferent degeneration in chronically hyperoxic animals was accompanied by marked hypoplasia of the carotid body. In view of previous findings from our laboratory that chemoafferent neurones require trophic support from the carotid body for survival after birth, we propose that chemoafferent degeneration following chronic hyperoxia is due specifically to the loss of target tissue in the carotid body.

Afferent Pathways↗
PubMed2000

Abnormal cerebral processing of oesophageal stimuli in patients with noncardiac chest pain (NCCP).

In noncardiac chest pain (NCCP), altered visceral perception may result from abnormal cerebral processing of sensory input rather than abnormalities of afferent pathways. However, the interactions between symptoms, autonomic function and oesophageal stimuli are poorly studied. Oesophageal stimulation elicits reproducible cortical evoked potentials [CEP] and modulates heart rate variability via vagal pathways, as visible on power spectrum analysis of heart rate variability [PS-HRV]. These methods are increasingly used to study the function of visceral afferent neural pathways in human. The aim of this study was to compare EP and PS-HRV during oesophageal stimuli in NCCP and controls. Twelve healthy volunteers (one female, 11 male; aged 24-51 years; mean 32 +/- 8 years), and eight NCCP patients (three female, five male; age range 26-58, mean 40.5 +/- 10 years) were studied. Electrical oesophageal stimulation (EOS; 200 microseconds, 0.2 Hz, 25 stimuli) was applied to the oesophageal wall 5 cm above the lower oesophageal sphincter (LOS), and perception thresholds (measured in mA) determined. EP responses were recorded using 22 standard electroencephalogram scalp electrodes. Autonomic activity was assessed using PS-HRV, before, during, and after oesophageal stimulation. Measured PS-HRV indices included high frequency (HF; 0. 15-0.5 Hz) and low frequency (LF; 0.06-0.15 Hz) power, respectively, assessing vagal and sympathetic activity, and the LF/HF ratio. EOS perception occurred at lower thresholds in NCCP than in controls (3. 6 +/- 1 vs. 7.8 +/- 2 mA, P < 0.05). EP amplitude was greater (13 +/- 2 vs. 6 +/- 1 microV, P < 0.0001), and latency longer in controls vs. NCCP (191 +/- 7 ms vs. 219 +/- 6 ms, P < 0.001). In NCCP, EOS decreased sympathetic outflow (low frequency peak on PS-HRV) and increased cardiovagal activity (high frequency peak, P < 0.02) to a significantly higher degree in comparison with controls. During EOS, heart rate decreased in NCCP from 68 vs. 62 beats min-1 (P < 0.003) but not in controls. In NCCP patients, EOS was perceived at lower intensities and was associated with a greater cardiovagal reflex response. EP responses associated with EOS were smaller in NCCP than in controls, suggesting that an increased perception of oesophageal stimuli results from an enhanced cerebral processing of visceral sensory input in NCCP, rather than from hyperalgesic responses in visceral afferent pathways.

Adult↗
PubMed1991

Free radicals accelerate the decay of long-term potentiation in field CA1 of guinea-pig hippocampus.

Free radicals have been implicated in a number of pathological conditions. To evaluate the neurophysiological consequences of free radical exposure, slices of hippocampus isolated from guinea-pigs were exposed to hydrogen peroxide which reacts with tissue iron to generate hydroxyl free radicals. Long-term potentiation, a sustained increase in synaptic responses, was elicited in field CA1 by high frequency stimulation of an afferent pathway. We found that 0.002% peroxide did not directly affect the responses evoked by stimulation of the afferent pathway but did prevent maintenance of long-term potentiation. Short-term potentiation and paired-pulse facilitation were not affected by peroxide treatment. Peroxide was less effective if removed following high frequency stimulation and was ineffective if applied only after high frequency stimulation. Input/output analysis showed that the increase in synaptic efficacy was reduced with peroxide treatment. Changes in the enhanced ability of the synaptic potential to generate a spike were less apparent. These data show that the interference of free radicals with long-term potentiation may contribute to pathological deficits. It is possible that intracellular calcium regulation is disrupted by peroxide treatment. A number of second messenger systems involved with long-term potentiation are potential targets for free radical attack.

Animals↗
PubMed1992

Symptomatic responses to stimulation of sensory pathways in the jejunum.

We hypothesized that intestinal afferent pathways inducing perception may be selectively activated by transmucosal electrical nerve stimulation, without disruption of the intrinsic myoelectrical rhythm. Hence, in 12 healthy subjects we measured perception (by a questionnaire) and jejunal slow wave activity (by electromyography), and we randomly applied for 1 min at 5-min intervals graded electrical (15 Hz, 100 microseconds) and mechanical stimuli (balloon distension) in the jejunum up to the respective discomfort threshold. Electrical and mechanical stimuli induced dose-related perception; the perception and discomfort thresholds were 39 +/- 7 and 63 +/- 6 mA and 31 +/- 3 and 49 +/- 5 ml for electrical and mechanical stimuli, respectively. More than one-half of electrical stimuli elicited clinical-type symptoms (abdominal pressure, fullness, colicky or sharp sensation) similar to those induced by mechanical stimuli; the remaining electrical stimuli (38 +/- 10%) induced paresthesia or flutterlike sensation. Similar types of symptoms were perceived with weak and strong stimuli. Jejunal slow wave activity (11.3 +/- 0.4 cycles/min) was not modified by either stimuli. We conclude that activation of intestinal sensory pathways, either by transmucosal nerve stimulation or via mechanoreceptors, induces a similar dose-related symptomatic response, without interfering with the intrinsic myoelectrical activity.

Adult↗
PubMed1996

Induction of members of the Fos/Jun family of immediate-early genes in identified hypothalamic neurons: in vivo evidence for differential regulation.

In situ hybridization was used to measure the expression of members of the Fos/Jun family of immediate-early genes in hypothalamic neurons in vivo following defined stimuli that utilize different afferent pathways. Only c-jun messenger RNA was expressed in the hypothalamic supraoptic and paraventricular nuclei of control animals. Intravenous infusions of sodium chloride solutions of different tonicity produced a range of plasma osmolalities within physiological limits. While the induction of c-fos and jun B messenger RNAs followed the stimulus intensity, the expression of c-jun was repressed at low levels of stimulation. A higher level of osmotic stimulation was able to co-induce c-jun with the c-fos, jun B and fos B genes, suggesting that other signalling pathways may then be activated. Parturition or systemic administration of cholecystokinin, that activate supraoptic and paraventricular neurons via ascending afferent pathways from the brainstem, both induced c-fos, but not the other genes, in the magnocellular nuclei. Use of double in situ hybridization confirmed that, unlike with osmotic stimulation, induction of c-fos only occurred in oxytocin neurons. These two stimuli did not cause a concomitant repression of c-jun messenger RNA expression in magnocellular oxytocin neurons. These patterns of induction provide evidence for the differential regulation of members of this family of genes in a physiological context.

Animals↗
PubMed1989

Somatosensory areas in the telencephalon of the pigeon. II. Spinal pathways and afferent connections.

There are two somatosensory areas in the telencephalon of the pigeon which receive an input from the spinal somatosensory system: one in the rostral Wulst which consists of the three hyperstriatal layers (h. accessorium (HA), h. intercalatus superior (HIS) and h. dorsale (HD] and one in the caudal telencephalon (neostriatum caudale (NC), neostriatum intermedium (NI) and hyperstriatum ventrale (HV]. Recordings of evoked single unit or multi unit activity and of field potentials before and after lesions of spinal pathways at a high cervical level (C4) were made to determine the contribution of these pathways to the transmission of somatosensory signals to these telencephalic areas. The rostral Wulst area receives somatic signals only through dorsal tracts contralateral to the recording site. Inputs from the wing arise mainly through the dorsal columns (DC) and those from the leg largely through the dorsolateral funiculus (DLF). The spinal projection pathway to the caudal neostriatal area includes the dorsal tracts and parts of the lateral funiculi on both sides. There was no difference in response form between the wing and leg responses. Signals transmitted through the lateral pathways were found to elicit the earliest responses (6-13 ms, electrical stimulation) in the caudal forebrain, while signals travelling through the DC arrive later in the caudal area (about 14 ms for wing stimulation) than in the rostral Wulst area (about 9 ms). The afferent thalamic and intratelencephalic connections of the two somatosensory areas in the telencephalon of the pigeon were investigated with retrograde transport of the neuronal tracers horseradish-peroxidase (HRP) or wheatgerm agglutinated HRP (WGA-HRP), Fast Blue (FB) and Rhodamine-isothiocyanat (RITC). Small tracer-injections were made under electrophysiological control at somatosensory responsive locations. These investigations confirm the projection of the caudal part of the nucleus dorsolateralis posterior (DLPc) to the caudal area and of the nucleus dorsalis intermedius ventralis anterior (DIVA) to the rostral area. In addition, it could be shown that the NI/NC projects to the HV thus confirming the electrophysiological results reported in a companion paper (Funke 1989) that the HV is a secondary area. The integrative function of HV is supported by connections to other sensory and motor telencephalic areas. Combined injections of FB and RITC revealed a topographic projection from the DIVA to the anterior Wulst.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1975

Spinal evoked response in the cat.

Summated evoked potentials to sciatic nerve stimulation were recorded from surface electrodes placed over the spine of cats. The response progressively increased in latency rostrally. It was largest and most complex in configuration in leads placed over the caudal spinal cord where sciatic nerve roots enter and begin to ascend the cord. The conduction velocity of the response was about 90 m/sec from rostral sacral to cervical regions. A comparison of surface-recorded evoked responses to stimulation of the sural nerve, the nerve to the medial head of the gastrocnemius muscle and the sciatic nerve suggest that the peripheral nerve fibers that mediate the response to sciatic nerve stimulation are primarily muscle nerve afferents. In surface, lamina, and dural recordings made over similar segmental levels, the response to sciatic nerve stimulation progressively increased in amplitude, duration, and wave form complexity from surface to depth. Failure of transmission across complete cord transections was demonstrated. Results in preparations with partial cord sections suggest that the surface-recorded response is mediated by multiple spinal cord afferent pathways which are situated primarily ipsilateral to the stimulated peripheral nerve. The data indicate that summated evoked responses arising in spinal cord afferent pathways can be recorded from surface-recording electrodes in cats. They suggest that this animal model may prove useful in the study of certain aspects of spinal cord pathology.

Animals↗
PubMed2001

Projection sites of superficial and deep spinal dorsal horn cells in the nucleus tractus solitarii of the rat.

By using anterograde transport of biotin dextran amine injected into the cervical spinal dorsal horn, we have shown that fibres from superficial and deep dorsal horn project to the nucleus tractus solitarii via two distinct pathways. Afferent fibres from the superficial lamina (I-III) were found to course in the dorsal funiculus and terminate bilaterally in the caudal zone of the nucleus tractus solitarii (NTS), mainly within the commissural subnucleus. In contrast, afferents from the deeper dorsal horn laminae (IV-V) were found to course in the dorsolateral fasciculus and terminate ipsilaterally, mostly in the lateral areas of the caudal nucleus tractus solitarii. Similar, but more extensive patterns of labelled fibres were produced by injections into the white matter of the dorsal funiculus and dorsolateral fasciculus, respectively. These observations suggest that the caudal NTS not only serves as a location of visceral afferent convergence and integration, but may also be a receptive area for monosynaptic projections from dorsal horn neurons receiving sensory afferent inputs. Such projections may represent pathways through which NTS neurons are influenced by nociceptive and non-nociceptive information from the dorsal horn and thereby can co-ordinate the appropriate autonomic response, including adjustments in cardiorespiratory reflex output.

Afferent Pathways↗
PubMed1979

Disorders in somesthesis following lesions of parietal lobe.

1. We determined the effects of lesions of the parietal lobe on the capacities of monkeys to detect and discriminate between mechanical sinusoids delivered to the hand. Tests of discrimination measured the capacity to discriminate between frequencies of flutter (24--36 Hz) and the capacity to make gross discriminations of frequency of flutter-vibration over the range of 10--50 Hz. 2. A unilateral removal of the parietal lobe impaired sensory capacities only on the contralateral hand; detection threshold was elevated, the capacity to discriminate between frequenceis of flutter was permanently lost, and the capacity to discriminate between and identify frequencies of 10--50 Hz was grossly impaired. No defects were found on the hand ipsilateral to the lesion. Detection thresholds, but not discrimination thresholds, decreased during postoperative testing, but in most cases did not recover to preoperative values. The impairments in frequency discrimination remained through the last day of postoperative testing. 3. A unilateral, subtotal parietal lesion that completely destroyed the primary and secondary somatic areas and Brodmann's area 5 resulted in the same sensory impairments as those produced by total removal of the parietal lobe. In most cases, detection threshold was elevated; flutter-frequency discrimination was lost, and the capacity to discriminate between frequencies of 10--50 Hz over the extended range of flutter and vibration was impaired. 4. The loss in discriminative capacity following lesions of the somatosensory cortex is interpreted as due to the absence of a cortical mechanism that determined differences in the temporal pattern of cyclically entrained activity in the somatic afferent pathway. This loss was dissociated from the remaining capacity, although impaired, to detect the presence of any neural activity in the afferent pathways or to determine gross differences in the frequency of mechanical sinusoids by a mechanism of coding by the labeled line.

Animals↗
PubMedDate not supplied

[Physiology of the autonomic nervous system].

INTRODUCTION: The autonomic nervous system (ANS) is made up of a complex set of neurons and pathways that control the functioning of the different body systems within the organism. Its overall function is that of maintaining a state of homeostasis in the organism and of performing the adaptation responses when faced with changes in the external and internal environment. METHODS: The ANS is composed of visceral afferent pathways, integration centres at the brain stem, hypothalamus and cerebral cortex levels, as well as sympathetic and parasympathetic efferent pathways. The efferent pathways innerve the cardiac muscle, the smooth muscle and the exocrine and endocrine glands, while the afferent pathways are arranged in two patterns: oligosynaptic circuits, which mediate reflex adaptation responses of the visceral systems, and complex circuits, with projections to nuclei in the brain stem and the brain, where the information is collected and responses are produced that affect numerous systems. The afferent signals activate or inhibit the efferent components of the ANS by means of reflex pathways, independently of the will. These reflex circuits are also modulated by means of signals from central structures, and constitute a central autonomic neuronal network that integrates somatic, autonomic and affective responses. CONCLUSION: Dysfunctions of the ANS are possibly due to increases or decreases in autonomic control activity, which can appear because of lesions to the brain, spinal cord or peripheral nerves.

Autonomic Denervation↗
PubMed1997

Increased renal interstitial hydrostatic pressure causes c-fos expression in the rat's spinal cord dorsal horn.

To describe a sympathetic afferent circuit, interstitial hydrostatic pressure in the left kidney was increased in anesthetized rats for 1.5 h to activate renal mechanoreceptor afferents. Following renal afferent stimulation, the number of immunocytochemically stained cells for the immediate early gene c-fos was increased within the dorsal horn of the spinal cord. Relative to the surgical control procedure, increasing renal interstitial hydrostatic pressure produced more immunocytochemically stained cells per tissue section in laminae I and II of the dorsal horn both ipsilateral and contralateral to the stimulated kidney in the three most caudal thoracic spinal segments. Further, the number of c-fos immunocytochemically stained cells per section in the dorsal horn ipsilateral to the stimulated kidney was 28% greater than the number of stained cells contralateral to it. The staining patterns in the dorsal horns of stimulated and control animals were similar with most labeled cells in laminae I and II. These results indicate that (1) c-fos immunocytochemical staining may be useful for tracing specific sympathetic afferent pathways, (2) sensory pathways affected by increased renal interstitial hydrostatic pressure include spinal neurons located at lower thoracic levels, and (3) some of this sympathetic afferent pathway is located contralateral to the stimulated kidney. Neurons in the contralateral dorsal horn activated by renal stimulation may mediate renorenal reflexes.

Animals↗
PubMed1999

Duodenal acid-induced gastric relaxation is mediated by multiple pathways.

In this study, we used an in vivo anesthetized rat model to investigate the mechanisms responsible for duodenal acid-induced inhibition of gastric motility. Intraduodenal infusion of HCl produced a rate-dependent decrease in intragastric pressure. Infusion of HCl at 2 ml/h produced a physiological plasma secretin level and elicited a decrease in intragastric pressure of 3.0 +/- 0. 2 cmH20. Infusion of rabbit secretin antiserum reduced the acid-induced inhibition of gastric motility by 85 +/- 5%, suggesting mediation mainly by endogenous secretin. Administration of the cholecystokinin (CCK)-A antagonist MK-329 caused only a modest 10 +/- 3% reduction in gastric relaxation, whereas the serotonin antagonist ICS-205930 had no effect. In contrast, immunoneutralization with the secretin antibody caused only a 15% reduction in the relaxation evoked by a higher rate of HCl infusion (3 ml/h), whereas MK-329 and ICS-205930 caused a 20 +/- 4% reduction and no reduction, respectively. Bilateral truncal vagotomy or perivagal application of capsaicin completely abolished gastric relaxation in response to low rates (1-2 ml/h) of 0.1 N HCl infusion but only partially affected gastric relaxation in response to a higher infusion rate (3 ml/h). These observations indicate that multiple pathways mediate the duodenal acid-induced inhibition of gastric motility. At low rates of HCl infusion, gastric relaxation is mediated primarily by endogenous secretin, which acts through vagal afferent pathways. At higher rates of HCl infusion, gastric relaxation is mediated by endogenous secretin, CCK, and possibly by the direct action of HCl on vagal afferent pathways or yet unidentified neuropathways.

Acids↗
PubMed1986

Fast and slow synaptic potentials produced in a mammalian sympathetic ganglion by colon distension.

Radial distension of the large intestine produced a slow depolarization in a population of neurons in the inferior mesenteric ganglion of the guinea pig. The slow potentials often occurred simultaneously with cholinergic fast potentials [( excitatory postsynaptic potentials (EPSPs]) yet persisted in the presence of nicotinic and muscarinic cholinergic antagonists when all fast EPSPs were absent. The amplitude of the distension-induced noncholinergic slow depolarization increased with increasing distension pressure. For distensions of 1-min duration at pressures of 10-20 cm of water, the mean depolarization amplitude was 3.4 mV. The slow depolarization was associated with an increase in membrane resistance, and prolonged periods of colon distension resulted in a tachyphylaxis of the depolarization. Desensitization of ganglion cells to the peptide substance P attenuated the distension-induced slow potential by an average of 49% +/- 17%. Thus, two colonic mechanosensory afferent pathways converge on principal ganglion cells in the inferior mesenteric ganglion: one was previously described to be mediated by acetylcholine, and the other is described here, whose transmitter remains to be determined but which preliminary evidence suggests is mediated in part by substance P. The noncholinergic afferent pathway may enhance the intestinal inhibitory reflex mediated by cholinergic mechanosensory afferent input to the abdominal prevertebral sympathetic ganglia.

Animals↗
PubMed1997

[A case of rapidly progressive HTLV-I-associated myelopathy (HAM)].

We report a 65-year-old woman with HAM who showed rapid progression of the clinical symptoms. The initial symptom was lumbago and she became unable to walk within 4 months after the onset of the lumbago. When seen on admission, she had flaccid paraplegia and areflexia was seen in the lower extremities with positive Babinski and Chaddock reflexes. She had numbness below the level of the navel, vibratory sensation was decreased in both lower limbs, and there was a hyperesthesic zone at the tenth thoracic vertebral level. She had a difficulty in urination and defecation. Laboratory examination revealed elevated anti-HTLV-I antibody titers both in serum (4,096x by PA method) and in cerebrospinal fluid (CSF) (4,096x). The levels of IgG and neopterin in CSF were also increased to 16.6 mg/dl (normal: < 5 mg/dl) and 360.3 pmol/ml (normal: < 30 pmol/ml), respectively. HTLV-I messenger RNA positive cells were detected in 0.1% to 0.01% of cells in CSF by in situ hybridization using an oligonucleotide probe labelled with alkaline phosphatase. Spinal cord MRI detected neither spinal cord compression nor vascular diseases. She was treated with 1,000 mg methylprednisolone for 3 days intravenously, followed by 60 mg oral prednisolone therapy. In several days after receiving the treatments, her muscle tonus became spastic and deep tendon reflexes in the legs became brisk. The hyperesthesia at the tenth thoracic vertebral level and numbness below the level of the navel were also gradually improved. Subsequently, her clinical features were consistant with those of the typical HAM. Therefore, the patient was diagnosed as rapidly progressive HAM. The initial phase of rapidly progressive HAM patients had been described only from clinical history. These patients had common characteristic clinical features, such as older age at onset, relatively severe motor dysfunction, high titers of anti-HTLV-I antibody in CSF, and increased levels of neopterin and IgG in CSF, when compared with those of other HAM patients. The clinical course and laboratory findings in the present patient were compatible with those in the previous cases reported as rapidly progressive HAM. This patient showed flaccid paraplegia and areflexia which have rarely been seen in HAM patients. However, these symptoms were changed to spastic and hyperactive after prednisolone therapy. We speculate that inflammation in the spinal cord in this patient was severe enough to spread to the dorsal root, and disturbed the afferent pathway from the peripheral to the central nervous system. This inflammatory reaction might be suppressed by prednisolone to facilitate the recovery of the afferent pathway, which led to the typical clinical symptoms of HAM.

Aged↗
PubMed2001

Mechanisms of frequency-specific responses of omega neuron 1 in crickets (Teleogryllus oceanicus): a polysynaptic pathway for song?

In crickets (Teleogryllus oceanicus), the auditory interneuron omega neuron 1 (ON1) responds to sounds over a wide range of frequencies but is most sensitive to the frequency of conspecific songs (4.5 kHz). Response latency is longest for this same frequency. We investigate the mechanisms that might account for the longer latency of ON1 to cricket-like sounds. Intracellular recordings revealed no evidence for appropriately timed postsynaptic inhibition of ON1 that might increase its latency, nor was latency affected by picrotoxin. The onset of excitatory postsynaptic potentials (EPSPs) was delayed for 4.5 kHz stimuli compared with ultrasound stimuli, pointing to a presynaptic locus for the latency difference. When ON1 is stimulated with high frequencies, discrete, apparently unitary EPSPs can be recorded in its dendrite, and these are latency-locked to spikes recorded simultaneously in the auditory nerve. This suggests that input to ON1 from high-frequency-tuned auditory receptor neurons is monosynaptic. In agreement with this, brief ultrasound stimuli evoke a single, short-latency EPSP in ON1. In contrast, the EPSP evoked by a brief 4.5 kHz stimulus consists of an early component, similar in latency to that evoked by ultrasound and possibly evoked by ultrasound-tuned receptors, and a later, dominant component. We interpret the early peak as arising from a monosynaptic afferent pathway and the late peak from a polysynaptic afferent pathway. Multiple-peak EPSPs, with timing similar to those evoked by sound stimuli, were also evoked by electrical stimulation of the auditory nerve.

Acoustic Stimulation↗
PubMed1984

Spacetime body maps and somatosensory evoked potentials.

Scalp-recorded somatosensory evoked potentials (SEPs) in humans and dogs suggest that it takes longer for peripheral information to reach the brain from the anogenital perineum than from the distal hind limbs, in spite of a shorter afferent pathway. The delay seems to be centrally determined, rostral to the lumbar segments, rather than by slower conduction velocities in the peripheral pudendal-sacral afferents. Thus the mammalian brain may temporally conserve the spatial sequence of segmental inputs in spite of variable afferent pathway lengths and/or conduction velocities. Human SEPs indicate the arrival timetable in cortex to be ordered: Lips, fingers, toes, genitals, anus; with a delay between lips and anogenital perineum of 30-40 msec. This delay is comparable to the interpair-interval threshold for human detection of two successive tactile events on the fingers, while ambiguous temporal defusion of two successive identical stimuli can be perceived down to objective separations of about 15 msec. It is suggested that, whereas the metric tensor model proposes central correction of asynchronous sensorimotor signals within an approximately 30 msec predictive function by cerebellar circuitry (in order to avoid spatial distortion in a spacetime tensor of sensorimotor processing), the brain may use longer time differences between proximal and distal receptive fields to develop a Cartesian, four-dimensional body map within its adaptive, behavioral world.

Anal Canal↗
PubMed2000

A gain-control mechanism for processing of chorus sounds in the afferent auditory pathway of the bushcricket Tettigonia viridissima (Orthoptera; Tettigoniidae).

The representation of alternative conspecific acoustic signals in the responses of a pair of local interneurons of the bushcricket Tettigonia viridissima was studied with variation in intensity and the direction of sound signals. The results suggest that the auditory world of the bushcricket is rather sharply divided into two azimuthal hemispheres, with signals arriving from any direction within one hemisphere being predominantly represented in the discharge of neurons of this side of the auditory pathway. In addition, each pathway also selects for the most intense of several alternative sounds. A low-intensity signal at 45 dB sound pressure level is quite effective when presented alone, but completely suppressed when given simultaneously with another signal at 60 dB sound pressure level. In a series of intracellular experiments the synaptic nature of the intensity-dependent suppression of competitive signals was investigated in a number of interneurons. The underlying synaptic mechanism is based on a membrane hyperpolarization with a time-constant in the order of 5-10 s. The significance of this mechanism for hearing in choruses, and for the evolution of acoustic signals and signalling behaviour is discussed.

Acoustic Stimulation↗