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PubMed1988

Excitant amino acids and audiogenic seizures in the genetically epilepsy-prone rat. I. Afferent seizure initiation pathway.

The afferent pathway involved in initiation of audiogenic seizures in the genetically epilepsy-prone rat was investigated by bilateral microinfusion of the excitant amino acid antagonist 2-amino-7-phosphonoheptanoate into the major brain stem and subcortical nuclei of the auditory system. This antagonist has been shown to possess anticonvulsant properties in other seizure models, and an excitant amino acid has been implicated as a putative neurotransmitter in several of these nuclei. Seizure severity was significantly reduced following infusion of this agent into the cochlear nucleus, superior olivary complex, inferior colliculus, and medial geniculate body. Many of these animals exhibited a complete blockade of seizures. The smallest effective dose in the cochlear nucleus and the medial geniculate body was 5 nmol per side. The smallest effective dose in the olive was 1 nmol, and in the inferior colliculus 0.1 nmol per side was protective. The onset of anticonvulsant effectiveness was earliest in the inferior colliculus. These findings showed that the inferior colliculus was the most sensitive auditory center to the anticonvulsant action of 2-amino-7-phosphonoheptanoate and that imbalance between inhibitory and excitatory transmission within this brain structure may be crucial in the initiation of audiogenic seizures in the genetically epilepsy-prone rat.

2-Amino-5-phosphonovalerate↗
PubMed1992

Further evaluation of the afferent nervous pathways from the rectum.

To evaluate the visceral afferents from the rectum, we recorded cerebral evoked potentials (EPs) in 26 healthy subjects after electrical stimulation of the rectum, pudendal nerve, and posterior tibialis nerve. We found two distinctly different EPs after rectal stimulation, with differences in latencies and pattern. In 13 subjects (group 1), the EP after rectal stimulation had multiple prominent peaks with early onset latencies ranging from 22 to 29 ms (mean 26 ms). In 13 subjects (group 2), the EP after rectal stimulation had a trifid configuration due to a very prominent negative peak between 97 and 108 ms (mean 101 ms) and longer onset latencies ranging from 50 to 61 ms (mean 55 ms). Latencies after pudendal nerve and posterior tibialis nerve stimulation were similar in the two groups. On further study, we found that both types of afferent pathways are present in the distal colon, since both types of EPs were found in the same subjects either in the rectum or in the rectum and sigmoid. We speculate that the early onset EP is a visceral pathway using the same afferents as the pudendal nerve because the early onset EP after rectal stimulation appears similar in number of peaks and interpeak latencies to EPs recorded after pudendal nerve stimulation, and the late onset EP is a visceral pathway using afferents along the pelvic nerve. Early onset EPs were also recorded after sigmoid stimulation, suggesting that both kinds of EPs are visceral afferents.

Adult↗
PubMed1987

Central organization of afferent renal nerve pathways.

Although afferent renal nerves have been studied for over a quarter of a century, their physiological role remains unclear. There is considerable experimental evidence indicating that afferent renal nerves convey sensory information from renal receptors to integrative circuits in the central nervous system which gives rise to command signals controlling the function of effector organs. In addition, it has been demonstrated that these integrative neural circuits are found at several different levels of the neuraxis; the spinal cord, the medulla and the hypothalamus. In this review, recent neuroanatomical and electrophysiological data on the central pathways of afferent renal nerves is discussed with reference to their possible role in homeostasis.

Afferent Pathways↗
PubMed2003

Phox2b controls the development of peripheral chemoreceptors and afferent visceral pathways.

We report that the afferent relays of visceral (cardiovascular, digestive and respiratory) reflexes, differentiate under the control of the paired-like homeobox gene Phox2b: the neural crest-derived carotid body, a chemosensor organ, degenerates in homozygous mutants, as do the three epibranchial placode-derived visceral sensory ganglia (geniculate, petrosal and nodose), while their central target, the nucleus of the solitary tract, which integrates all visceral information, never forms. These data establish Phox2b as an unusual 'circuit-specific' transcription factor devoted to the formation of autonomic reflex pathways. We also show that Phox2b heterozygous mutants have an altered response to hypoxia and hypercapnia at birth and a decreased tyrosine hydroxylase expression in the petrosal chemosensory neurons, thus providing mechanistic insight into congenital central hypoventilation syndrome, which is associated with heterozygous mutations in PHOX2B.

Afferent Pathways↗
PubMed2004

Afferent pain pathways: a neuroanatomical review.

Painful experience is a complex entity made up of sensory, affective, motivational and cognitive dimensions. The neural mechanisms involved in pain perception acts in a serial and a parallel way, discriminating and locating the original stimulus and also integrating the affective feeling, involved in a special situation, with previous memories. This review examines the concepts of nociception, acute and chronic pain, and also describes the afferent pathways involved in reception, segmental processing and encephalic projection of pain stimulus. The interaction model of the cerebral cortex areas and their functional characteristics are also discussed.

Afferent Pathways↗
PubMed2001

A re-examination of the possibility of controlling the firing rate gain of neurons by balancing excitatory and inhibitory conductances.

It has been suggested that balancing excitatory and inhibitory conductance levels can control the firing rate gain of single neurons, defined as the slope of the relation between discharge frequency and excitatory conductance. According to this view the increase in firing rate produced by an input pathway can be controlled independently of the ongoing firing rate by adjusting the mixture of excitatory and inhibitory conductances produced by other pathways converging onto the neuron. These conclusions were derived from a simple RC-neuron model with no active conductances, or firing threshold mechanism. The analysis of that model considered only the subthreshold behaviour and did not consider the relation between total trans-membrane conductance and firing rate. Similar conclusions were also derived from a simple parallel conductance based model. In this paper I consider, as an example of a repetitively firing neuron, a generic model of cat lumbar alpha-motoneurons with excitatory and inhibitory inputs and a second independent excitatory pathway. The excitatory and inhibitory inputs can be thought of as central descending controls while the second excitatory pathway may represent, for example, the monosynaptic Ia-afferent pathway. I have re-examined the possibility that the firing rate gain of the "afferent" pathway can be controlled independently of the ongoing firing rate by balancing the excitatory and inhibitory conductances activated by the descending inputs. The steady state firing rate of the model motoneuron increased nearly linearly with the excitatory current, as it does in real motoneurons (primary firing range). The model motoneuron also showed a secondary firing range, whose slope was steeper than in primary range. The firing rate gain was measured by increasing the conductance of the "afferent" pathway. The firing rate gain (in the primary and secondary firing range) of the "afferent" pathway was found to be the same regardless of the particular mixture of excitatory and inhibitory conductances acting to produce the ongoing firing rate. This result was obtained for a single-compartment model, as well as for a two-compartment model consisting of an active somatic compartment and a dendritic compartment containing an L-type calcium conductance. Put simply, the firing rate gain of an input to a neuron cannot be controlled by balancing excitatory and inhibitory conductances produced by other independent input pathways, or by the spatial distribution of excitation and inhibition across the neuron. Three potential ways of controlling the firing rate gain are presented in the "Discussion". Firing rate gain can be controlled by actions at the presynaptic terminal, by inhibitory feedback, which is a function of the neuron's firing rate, or by neuromodulator substances that affect intrinsic inward or outward currents.

Action Potentials↗
PubMed1999

Mechanisms of cardiac pain.

Angina pectoris often results from ischemic episodes that excite chemosensitive and mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals, including adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways. This review focuses on the spinothalamic tract, but other pathways are excited as well. Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to excite upper cervical spinothalamic tract cells. This innervation contributes to the anginal pain experienced in the neck and jaw. The spinothalamic tract projects to the medial and lateral thalamus and, based on positron emission tomography studies, activates several cortical areas, including the anterior cingulate gyrus (BA 24 and 25), the lateral basal frontal cortex, and the mesiofrontal cortex.

Afferent Pathways↗
PubMedDate not supplied

Determining the pathway of the blink reflex through transcutaneous electrical stimulation of the facial nerve over the stylomastoid foramen.

The afferent pathway of the late response (R2 component) of the blink reflex in response to transcutaneous electrical stimulation of the facial nerve over the stylomastoid foramen remains uncertain. The two major hypotheses regarding the afferent pathway of R2 are that it may consist of either the trigemino-facial or the facio-facial reflex. This study was performed to determine the afferent pathway of R2. Ninety-one patients with acute unilateral peripheral facial palsy and 21 controls were studied. The degree of facial nerve damage was classified into three groups: mild, moderate, and severe according to their electroneurographic value. In each group, the appearance rate, latency, and area under the curve of contralateral R2 elicited by electrical stimulation of the injured facial nerve over the stylomastoid foramen were measured and compared with those of controls. The contralateral R2 parameters did not differ between the patient groups and the controls. The results indicate that the afferent pathway of R2 is mediated not only through the facial nerve. We conclude that the auriculotemporal nerve (V3) and the great auricular nerve (C2, C3) may also contribute to the afferent pathway of R2.

Blinking↗
PubMed2003

Electrophysiological assessment of the afferent sensory pathway in cardiac arrest survivors.

BACKGROUND: Hypoxic-ischaemic brain damage in cardiac arrest survivors is global, but postmortem histology could identify parts of the brain that are selectively vulnerable to ischaemia, comprising the thalamus and cortex. We hypothesized that hypoxic-ischaemic brain damage increases along the afferent sensory pathway with a stepwise decrease of detectable somatosensory evoked potential peaks. METHODS: Somatosensory evoked potentials were recorded within 72 h after cardiac arrest in 305 comatose patients after cardiopulmonary resuscitation. We measured the short latency SEP peaks N9, P15, N20, P25 (reflecting the peripheral-thalamo-cortical pathway) and the long latency SEP peaks N35 and N70 (reflecting complex cortico-cortical interactions). Patients with a Cerebral Performance Category score > 2 at 1 year were defined as patients with hypoxic-ischaemic brain damage. RESULTS: Patients with hypoxic-ischaemic brain damage (n = 232) showed a statistically significant decrease of detectable peaks (P < 0.05) along the thalamo-cortical afferent pathway: N13, P15, N20, P25 and N70 peaks were detectable in 99%, 63%, 59%, 55% and 44% patients, respectively. In patients without hypoxic-ischaemic brain damage (n = 73) the N13, P15, N20, P25 peaks were detectable in all, and the N35 and N70 peaks in 98%. Furthermore, in patients with hypoxic-ischaemic brain damage and detectable SEP peaks, P15, N20, P25, N35 and N70, peak latencies were prolonged (P < 0.05) and N20 and N70 amplitudes were decreased (P < 0.05) compared with patients without hypoxic-ischaemic brain damage. CONCLUSION: Extent of hypoxic-ischaemic brain damage in cardiac arrest survivors increases along the afferent sensory pathway, with pronounced vulnerability of thalamic and cortical brain regions.

Adolescent↗
PubMed1999

Contribution of cytochrome P450 epoxygenase and hydroxylase pathways to afferent arteriolar autoregulatory responsiveness.

Previous studies have demonstrated an important role for the cytochrome P450 (CYT-P450) pathway in afferent arteriole autoregulatory responses but the involvement of specific pathways remains unknown. Experiments were performed to determine the role of CYT-P450 epoxygenase and hydroxylase pathways in pressure mediated preglomerular autoregulatory responses. Afferent arteriolar diameter was measured as renal perfusion pressure was increased from 80-160 mmHg. Afferent arteriolar diameter averaged 19+/-2 microm at a renal perfusion pressure of 80 mmHg and decreased by 15+/-2% when pressure was increased to 160 mmHg. Inhibition of the epoxygenase pathway with 6-(2-proparglyloxyphenyl)hexanoic acid (PPOH), enhanced the microvascular response to increasing renal perfusion pressure. In the presence of 50 microM PPOH, afferent arteriolar diameter decreased by 29+/-4% when pressure was increased from 80-160 mmHg. Likewise, the sulphonimide derivative of PPOH, N-methylsulphonyl-6-(2-proparglyloxyphenyl) hexanamide (MS-PPOH, 50 microM), enhanced the afferent arteriolar response to increasing renal perfusion pressure. In contrast, the selective CYT-P450 hydroxylase inhibitor, N-methylsulphonyl-12,12-dibromododec-11-enamide (DDMS) attenuated the vascular response to increasing renal perfusion pressure. In the pressure of 25 microM DDMS, afferent arteriolar diameter decreased by 4+/-2% when pressure was increased from 80-160 mmHg. These results suggest that CYT-P450 metabolites of the epoxygenase pathway alter afferent arteriolar responsiveness and thereby modify the ability of the preglomerular vasculature to autoregulate renal blood flow. Additionally, these results provide further support to the concept that a metabolite of the hydroxylase pathway is an integral component of the afferent arteriolar response to elevations in perfusion pressure.

Amides↗
PubMed1978

Interaction of descending spinal sympathetic pathways and afferent nerves.

With the use of computer-aided techniques, the interaction of descending spinal sympathetic pathways and afferent nerve fibers (cervical dorsal roots and tibial nerve) in regulation of thoracic (T2) preganglionic nerve activity was investigated in anesthetized, vagotomized, and paralyzed cats. High-frequency activation of a sympathoinhibitory pathway (ventrolateral funiculus) depressed the evoked discharges in the T2 preganglionic nerve elicited by stimulation of a sympathoexcitatory pathway (dorsolateral funiculus) and the spinal component of the somatosympathetic reflex. Submaximal evoked responses were also inhibited through baroreceptor reflex activation (blood pressure elevations up to 225 mmHg). Facilitation of the spinal component of the somatosympathetic reflex occurred during stimulation of the excitatory pathway. Carotid occlusion (baroreceptor inactivation) facilitated the submaximal evoked discharges from stimulation of the descending excitatory pathway. These data support the contention that sympathetic nerve activity can be modified by the integration of excitatory and inhibitory impulses at the spinal level.

Afferent Pathways↗
PubMed1992

Increased c-fos expression in spinal neurons after irritation of the lower urinary tract in the rat.

This study utilized neuronal c-fos expression to examine the spinal pathways involved in processing nociceptive and non-nociceptive afferent input from the lower urinary tract (LUT) of the urethane-anesthetized rat. C-fos protein was detected immunocytochemically in only a small number of cells (< 2 cells/L6 section) in control animals. However, chemical irritation with 1% acetic acid or mechanical stimulation of the LUT markedly increased the number of c-fos-positive neurons (56-180 cells/L6 section) in four regions of the caudal lumbosacral (L6-S1) spinal cord: medial dorsal horn (MDH), lateral dorsal horn, dorsal commissure (DCM), and sacral parasympathetic nucleus (SPN). Only small numbers of c-fos-positive cells were detected in rostral lumbar segments, a region that is thought to receive nociceptive input from the LUT via afferent pathways in sympathetic nerves. The distribution of c-fos-positive cells in the L6 spinal cord varied according to the stimulus (i.e., urethral catheter, bladder distension, or chemical irritation). Distension of the urinary bladder increased the number of c-fos-positive cells mainly in DCM and SPN regions of the cord. In contrast, irritation of the LUT increased c-fos expression largely in DCM and MDH areas. Spinal cord transection (T8 level) did not alter the c-fos expression induced by a catheter or chemical irritation, indicating that gene expression was mediated by spinal pathways. Denervation experiments showed that c-fos expression was induced by activation of afferent pathways in the pelvic and pudendal nerves. These results suggest that neurons in several regions of the spinal cord are involved in processing afferent input from different parts of the LUT. Neurons in the DCM appear to have an important role since they respond to both nociceptive and non-nociceptive inputs and to visceral (pelvic nerve) and somatic (pudendal nerve) afferent pathways. Thus, these neurons may be involved in the mechanisms of visceral-somatic referred pain.

Afferent Pathways↗
PubMed1991

A large proportion of afferent neurons innervating the uterine cervix of the cat contain VIP and other neuropeptides.

Axonal tracing techniques were used in combination with immunohistochemistry to examine the distribution of neuropeptides in afferent pathways from the uterine cervix of the cat. Primary afferent neurons innervating the uterine cervix were identified by axonal transport of the dye, fast blue, injected into the cervix. Fifteen to twenty-five days after the injection, dorsal root ganglia (L1-S3) were removed and incubated for 48-72 h in culture medium containing colchicine to increase the levels of peptides. Calcitonin gene-related peptide (CGRP), cholecystokinin (CCK), leucine-enkephalin (LENK), somatostatin, substance P and vasoactive intenstinal polypeptide (VIP) were identified by use of indirect immunohistochemical techniques. Eighty-four percent of uterine cervix afferent neurons were identified in the sacral dorsal root ganglia (S1-S3), and 16% in the middle lumbar dorsal root ganglia (L3-L4). In sacral dorsal root ganglia, VIP was present in the highest percentage of dye-labeled cells (71%), CGRP in 42%, and substance P in 18% of the cells. CCK and LENK were present in 13% of the cells. In lumbar dorsal root ganglia, CGRP (51%) was most prominent peptide followed by VIP (34%), substance P (28%), LENK (17%) and CCK (13%). Somatostatin was present in the ganglia but did not occur in dye-labeled neurons. In conclusion, the uterine cervix of the cat receives a prominent VIP- and CGRP-containing afferent innervation. The percentage of neurons containing VIP is three to five times higher than the percentage of these neurons in afferent pathways to other pelvic organs. These observations coupled with the results of physiological studies suggest that VIP is an important transmitter in afferent pathways from the cervix.

Afferent Pathways↗
PubMed1991

[Disorders of the afferent visual pathway in HIV infection. 1. Optic nerve and 2. Visual pathways/visual cortex].

Up to now little involvement of the afferent visual pathway (optic nerve and optic radiation and visual cortex) in HIV infection has been apparent. These results are based on our prospective investigations of 538 HIV-infected individuals, among them 261 patients with full-blown AIDS carried out by the same examiner over a 6-year period (1984-1990). Diseases of the optic nerve were observed in 22/261 (8.4%) of Aids patients but in only 1/227 (0.4%) of patients with earlier stages of HIV infection. Optic neuritis was the most common disease (in 14/261 = 5.4% of Aids patients), for the most part occurring in the course of CMV (cytomegalovirus) retinitis. For this form the prognosis was primarily good under virustatic therapy with ganciclovir in contrast to primary CMC papillitis. Furthermore, a few cases of optic perineuritis, optic neuropathy in basal meningitis, ischemic optic neuropathy and papilloedema with increased intracranial pressure were observed, most of them caused by opportunistic infections of the central nervous system. In single cases the HIV might hypothetically have played a role in the etiology. Visual impairment of the patients varied from subtle disturbances to blindness. Often optic atrophy resulted. Homonymous hemianopsia was the principal sign in diseases of the visual pathway between the lateral geniculate body and the visual cortex (in 10/261 = 3.8% of Aids patients). This symptom resulted from cerebral toxoplasmosis in 7 cases, progressive multifocal leukoencepalopathy (PML) in 2 cases and primary intracerebral malignant lymphoma in 1 case. The visual fields and neuroradiological findings are demonstrated. In 3 cases the homonymous hemianopsia was the first clinical appearance of Aids. Involvement of the afferent visual pathway in HIV infection may be a cause of blindness or visual disturbances despite normal findings on examination of the eyes themselves.

Fluorescein Angiography↗
PubMed1994

Prolactin in winter depression.

Women with winter depression have low serum prolactin concentration that is independent of both season and efficient bright light treatment administered in winter. A defect of neural pathways afferent to the paraventricular nucleus may explain these findings. Estrogen is thought to play a key role in modulation of the rhythmic responses in winter depression.

Afferent Pathways↗
PubMed1991

Vagal involvement in the action of exogenous adenosine triphosphate on reflex renal sympathetic nerve activity.

The reason why adenine compounds when used as hypotensive agents are devoid of significant reflex sympathetic activity, such as rebound hypertension and tachycardia, is not clearly understood. This study, performed on alpha-chloralose-anesthetized dogs, examined, first, the effects of adenosine triphosphate (ATP) and adenosine as compared with those of sodium nitroprusside on efferent renal sympathetic nerve activity (RSNA), as an indicator of general reflex sympathetic activity, and second, whether vagal involvement could be demonstrated in the action of ATP and adenosine on RSNA. Renal sympathetic nerve activity increased progressively with increasing doses of sodium nitroprusside (5, 10, and 20 micrograms/kg) and adenosine (0.5, 2.0, and 4.0 mg/kg), whereas ATP suppressed RSNA at 2.0 and 4.0 mg/kg. High doses of ATP and adenosine (4.0 mg/kg) were injected into intact (n = 7) and vagotomized dogs (n = 7). Both ATP and adenosine induced rapid onset of hypotension without rebound hypertension and tachycardia. After vagotomy, the attenuation of RSNA by ATP was completely abolished and rebound hypertension and tachycardia were observed. Vagotomy did not alter the effect of adenosine on RSNA. It is concluded that ATP-induced hypotension is associated with attenuation of sympathetic efferent nerve activity mediated through vagal afferent pathways. Vagal afferent impulses are thought to be one of the mechanisms that inhibit reflex sympathetic activities, such as rebound hypertension after ATP-induced hypotension. The mechanisms by which adenosine inhibits reflex sympathetic activity are not, however, secondary to vagal afferent involvement and must be multifactorial.

Adenosine↗