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PubMed2001

Estrogen receptor-alpha and beta- immunoreactivity and mRNA in neurons of sensory and autonomic ganglia and spinal cord.

Estrogen receptor-alpha immunoreactivity and mRNAs are present in neurons in locales that innervate genital organs, e.g., parasympathetic pelvic autonomic ganglia, sensory dorsal root and nodose ganglia, and autonomic areas of the lumbosacral spinal cord. With the availability of probes for the beta-isoform of the estrogen receptor, we studied this receptor in autonomic, sensory, and spinal cord neurons and compared it with the distribution of the alpha-receptor. Estrogen receptor-alpha and -beta immunoreactivity were located in the nuclei of neurons, were in subpopulations of parasympathetic neurons in pelvic ganglia, and sensory neurons of dorsal root and nodose ganglia. Both receptor subtypes were present in the lumbosacral spinal cord: in neurons of the outer laminae of the dorsal horn, lateral collateral and medial collateral pathways, sacral parasympathetic nucleus, dorsal intermediate gray, and lamina X. Similar numbers of spinal cord neurons were immunoreactive for estrogen receptor-beta and estrogen receptor-alpha. However, estrogen receptor-beta-immunoreactive neurons appeared less numerous in the outer dorsal horn, but more numerous in the deeper layers of the spinal cord than estrogen receptor-alpha neurons. Retrograde tracing from the uterus revealed "uterine-related" neurons in dorsal root and pelvic ganglia that contained estrogen receptor-alpha and -beta. In situ hybridization revealed both estrogen receptor-alpha and -beta mRNA transcripts in sensory neurons of the dorsal root and nodose ganglia, parasympathetic neurons of pelvic ganglia, and spinal cord neurons in the dorsal horn, sacral parasympathetic nucleus, and dorsal intermediate gray of L6-S1 segments. These studies show that both estrogen receptor-alpha and -beta are synthesized by autonomic and sensory neurons in parts of the nervous system that have connections with the female reproductive system. Such neurons contain neurotransmitters that have important functions in the female reproductive organs; thus, it is likely that estrogen can influence the activity of such neurons and consequently, through them, the activities of the reproductive organs.

Animals↗

PubMed1999

Presence of opioid receptor-like (ORL1) receptor mRNA splice variants in peripheral sensory and sympathetic neuronal ganglia.

The expression of ORL1 receptor mRNA splice variants is determined in peripheral sensory and sympathetic ganglia and compared to mRNA expression for the three classic opioid receptor subtypes (mu, delta, and kappa) using the method of reverse transcription-polymerase chain reaction. ORL1, mu, delta and kappa receptor subtype mRNAs are present in human dorsal root ganglia (DRG) and trigeminal ganglia and rat DRG. ORL1, mu and delta receptor subtype mRNAs are present in rat superior cervical ganglia and only ORL1 and delta receptor mRNAs are present in rat lumbar sympathetic ganglia. Both the ORL1 mRNA splice variants are present in sensory and sympathetic ganglia, however, expression of the shorter ORL1 receptor mRNA dominates over expression of the longer splice variant in rat brain and DRG, whereas, expression of the longer splice variant is dominant in sympathetic ganglia.

Aged↗

PubMed1998

Localization of ATP-gated P2X receptor immunoreactivity in rat sensory and sympathetic ganglia.

The distribution of P2X1, P2X2, P2X3, P2X4, P2X5 and P2X6 receptors, a family of ATP-gated cation channels, in rat trigeminal, dorsal root, nodose, superior cervical, and coeliac ganglia was studied immunohistochemically. It was found that polyclonal antibodies for the six P2X receptor subtypes could label over 90% of neurones in these ganglia to different intensities. There was also considerable variation in intensity of immunoreactivity in individual neurones within each ganglion. In dorsal root and trigeminal ganglia expression of the P2X3 receptor was much higher than for the other five subtypes. P2X3 immunoreactivity was much more intense in the small-diameter neurones than in the large-diameter neurones. In nodose ganglion, both P2X2 and P2X3 antibodies labelled the neurones intensely. In sympathetic superior cervical and coeliac ganglia, immunoreactivity to five P2X receptor subtypes were detected (exception, P2X5), with P2X2, P2X4 and P2X6 showing higher intensity. Low level expression of P2X3 receptor in sympathetic ganglia indicates that this receptor subtype is not limited to the sensory ganglia where it was highly expressed. The results have demonstrated that both sensory and sympathetic ganglia express a variety of P2X receptor subtypes and that different subtypes are expressed to different levels and by different subpopulations of neurones.

Adenosine Triphosphate↗

PubMed1999

Intraventricular infusion of nerve growth factor as the cause of sympathetic fiber sprouting in sensory ganglia.

OBJECT: The results of previous clinical trials have indicated that intraventricular infusion of nerve growth factor (NGF) in patients with Alzheimer's disease is frustrated by the appearance of weight loss and diffuse back pain. The present study tested whether NGF induces sympathetic sprouting in sensory ganglia. Such sprouting has been implicated in previous studies as a possible mechanism of sympathetically maintained pain in neuropathic animals. METHODS: Nineteen Long-Evans rats underwent intraventricular infusion of either artificial cerebrospinal fluid (ACSF; seven animals) or NGF (12 animals). After 14 days of infusion, the sensory ganglia of the trigeminal nerve and the C-2, C-8, T-1, L-4, and L-5 dorsal roots were examined for sympathetic sprouting by using tyrosine hydroxylase immunohistochemical analysis. CONCLUSIONS: In the animals receiving NGF, 52 of 144 ganglia showed sympathetic fiber sprouting. In the control animals receiving ACSF, only two of 72 ganglia showed minor sympathetic fiber sprouting. A preferential sprouting of sympathetic fibers was demonstrated at lower lumbar ganglia compared with the cervical and thoracic ganglia. The data presented here demonstrate that in the rat intraventricular NGF infusion caused sympathetic sprouting in dorsal root ganglia (p < 0.01). These findings may have importance both for the treatment of Alzheimer's disease and the understanding of neuropathic pain.

Alzheimer Disease↗

PubMed1999

Stimulant-induced exocytosis from neuronal somata, dendrites, and newly formed synaptic nerve terminals in chronically decentralized sympathetic ganglia of the rat.

Loss of preganglionic neurones underlies the autonomic failure of human multiple system atrophy. In rat sympathetic ganglia decentralization leads to new synapse formation. We explored whether these synapses are functional, and whether chronically decentralized neurones respond normally to activation, in terms of exocytosis. Potassium depolarization and cholinergic agonists were applied to freshly excised rat superior cervical sympathetic ganglia, preganglionically denervated with prevented reinnervation 5 months earlier. Ganglia were incubated and stimulated in the presence of tannic acid, which stabilizes released vesicle cores for subsequent electron microscopy. In denervated ganglia exocytosis was observed from newly formed synaptic nerve terminals, and from nonsynaptic surfaces of neurone somata and dendrites. The results demonstrated that the new intraganglionic synapses, which are mostly catecholaminergic, can function and that chronically decentralized sympathetic neurones remain capable of stimulant-induced exocytosis from somata and dendrites. The maximal release upon potassium depolarization did not differ significantly between denervated and contralateral ganglia. Relative to this, the exocytotic responses of decentralized somata and dendrites to nicotine resembled those of contralateral ganglia. Responses to muscarine were significantly less in denervated than in contralateral ganglia, indicating inhibition in dendrites. Responses to carbachol suggested interactions between nicotinic and excitatory muscarinic effects. Nerve terminals in denervated ganglia showed high basal release. Their responses to muscarine and carbachol resembled those of the decentralized neurones, from which most may originate. Their response to nicotine evidenced inhibition. Their actions, coupled with nonsynaptic effects of soma-dendritic exocytosis, might modulate responses of the decentralized neurone population to other surviving inputs. This modulation could be influential in disease-induced decentralization in man.

Animals↗

PubMed1998

Latent varicella-zoster virus is located predominantly in neurons in human trigeminal ganglia.

Varicella-zoster virus (VZV) is a human herpesvirus that causes varicella (chicken pox) as a primary infection and, after a variable period of latency in trigeminal and dorsal root ganglia, reactivates to cause herpes zoster (shingles). Both of these conditions may be followed by a variety of neurological complications, especially in immunocompromised individuals such as those with human immunodeficiency virus (HIV) infection. There have been a number of conflicting reports regarding the cellular location of latent VZV within human ganglia. To address this controversy we examined fixed wax-embedded trigeminal ganglia from 30 individuals obtained at autopsy, including 11 with HIV infection, 2 neonates, and 17 immunocompetent individuals, for the presence of latent VZV. Polymerase chain reaction (PCR), in situ hybridization, and PCR in situ amplification techniques with oligonucleotide probes and primer sequences to VZV genes 18, 21, 29, and 63 were used. VZV DNA in ganglia was detected in 15 individuals by using PCR alone, and in 12 individuals (6 normal non-HIV and 6 positive HIV individuals, but not neonatal ganglia) by using PCR in situ amplification. When in situ hybridization alone was used, 5 HIV-positive individuals and only 1 non-HIV individual showed VZV nucleic acid signals in ganglia. In all of the VZV-positive ganglia examined, VZV nucleic acid was detected in neuronal nuclei. Only occasional nonneuronal cells contained VZV DNA. We conclude from these studies that the neuron is the predominant site of latent VZV in human trigeminal ganglia.

Acquired Immunodeficiency Syndrome↗

PubMed1983

Colonization of murine ganglia by a superinfecting strain of herpes simplex virus.

We report on the colonization of murine trigeminal ganglia after sequential infection of mice by herpes simplex viruses (HSVs). In preliminary studies, we have established that whereas the HSV-1(F) strain efficiently colonizes ganglia when inoculated by either the ear or eye routes, the HSV-1 X HSV-2 recombinant C7D colonizes ganglia when inoculated by the eye route only. The experimental design consisted of inoculating the right eye with C7D on day 1 and with HSV-1(F) in both left and right eyes on day 26. Both right and left trigeminal ganglia were removed and analyzed independently for latent virus on day 52. Our studies indicate that HSV-1(F) viruses were recovered from all left trigeminal ganglia but from only a small number of right trigeminal ganglia. Some right trigeminal ganglia yielded no viruses, whereas others yielded both C7D and HSV-1(F) viruses identified on the basis of plaque morphology and restriction enzyme cleavage patterns of viral DNA. The results indicate that more than one virus may colonize the same ganglion and that trigeminal ganglia may be protected from colonization by a superinfecting virus by determinants acting at a local level in the absence of demonstrable virus.

Animals↗

PubMed2001

The transgenic ICP4 promoter is activated in Schwann cells in trigeminal ganglia of mice latently infected with herpes simplex virus type 1.

Herpes simplex virus type 1 (HSV-1) establishes a latent infection in neurons of sensory ganglia, including those of the trigeminal ganglia. Latent viral infection has been hypothesized to be regulated by restriction of viral immediate-early gene expression in neurons. Numerous in situ hybridization studies in mice and in humans have shown that transcription from the HSV-1 genome in latently infected neurons is limited to the latency-associated transcripts. In other studies, immediate-early gene (ICP4) transcripts have been detected by reverse transcription-PCR (RT-PCR) in homogenates of latently infected trigeminal ganglia of mice. We used reporter transgenic mice containing the HSV-1(F) ICP4 promoter fused to the coding sequence of the beta-galactosidase gene to determine whether neurons in latently infected trigeminal ganglia activated the ICP4 promoter. Mice were inoculated via the corneal route with HSV-1(F). At 5, 11, 23, and 37 days postinfection (dpi), trigeminal ganglia were examined for beta-galactosidase-positive cells. The numbers of beta-galactosidase-positive neurons and nonneuronal cells were similar at 5 dpi. The number of positive neurons decreased at 11 dpi and returned to the level of mock-inoculated transgenic controls at 23 and 37 dpi. The number of positive nonneuronal cells increased at 11 and 23 dpi and remained elevated at 37 dpi. Viral proteins were detected in neurons and nonneuronal cells in acutely infected ganglia, but were not detected in latently infected ganglia. Colabeling experiments confirmed that the transgenic ICP4 promoter was activated in Schwann cells during latent infection. These findings suggest that the cells that express the HSV-1 ICP4 gene in latently infected ganglia are not neurons.

Animals↗

PubMed2004

Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences.

The in vivo ganglionic environment directs the latent herpes simplex virus transcriptional program. Since stress-driven perturbations in sensory neurons are thought to play a critical role in the transition from latency to reactivation, a primary concern in the selection of a valid model of the molecular interactions leading to reactivation is the faithful recapitulation of these environments. In this study reactivation of latently infected ganglia excised and cultured in vitro (explanted) is compared to reactivation occurring in latently infected ganglia in vivo following hyperthermic stress. Three notable points emerged. (i). Neurons in explanted ganglia exhibited marked morphological changes within 2 to 3 h postexplant. DNA fragmentation in neuronal nuclei was detected at 3 h, and atypical expression of cell cycle- and stress-regulated proteins such as geminin, cdk2, cdk4, and cytochrome c became apparent at 2 to 48 h. These changes were associated with axotomy and explant and not with the initiation or progression of reactivation and were not observed in ganglia following in vivo hyperthermic stress. (ii). Despite these differences, during the first 22 h primary reactivation events were restricted to a very small number of neurons in vivo and in explanted ganglia. This suggests that at any given time only a few latently infected neurons are competent to reactivate or that the probability of reactivation occurring in any particular neuron is very low. Importantly, the marked changes detected in explanted ganglia were not correlated with increased reactivation, demonstrating that these changes were not associated with the reactivation process per se. (iii). Secondary spread of virus was evident in explanted ganglia within 36 h, an event not observed in vivo. We conclude that explant reactivation may provide an ancillary system for selected studies of the early events in reactivation. However, clear signs of neuronal degeneration within 2 to 3 h postexplant indicate that these ganglia are undergoing major physiological changes not associated with the reactivation process. This ongoing neurodegeneration could alter even the early virus-host interactions in reactivation, and thus caution in the extrapolation of results obtained in explants to the in vivo interactions initiating reactivation is warranted.

Animals↗

PubMed1997

Intraarticular ganglia of the knee: prevalence, presentation, etiology, and management.

OBJECTIVE: The aim of this study was to present a comprehensive review of intraarticular ganglia of the knee. MATERIALS AND METHODS: Cases of intraarticular ganglia of the knee were collected from a group of 1767 consecutive patients referred for MR imaging examinations of the knee. Medical records and radiologic, arthroscopic, and pathologic reports were reviewed. RESULTS: Twenty-three patients (17 men and six women) had intraarticular ganglia of the knee. Three ganglia were found in Hoffa's fat pad, 10 were associated with the anterior cruciate ligament, eight were associated with the posterior cruciate ligament, and two had no definite association with either the anterior or the posterior cruciate ligament. Of the 23 ganglia, 14 (61%) were located in the intercondylar notch. Pain was the most common complaint: medial joint line tenderness, lateral joint line tenderness, or retropatellar pain. Two of the three patients with ganglia in Hoffa's fat pad had a palpable mass on physical examination. Of the 23 patients with intraarticular ganglia of the knee, 18 (78%) had no associated internal derangement. Five patients underwent arthroscopic surgery, confirming the diagnosis of ganglionic cyst. Of these five patients, none had a recurrence. CONCLUSION: With the advent of MR imaging of the knee, intraarticular ganglia of the knee have been found to occur more commonly than once thought, with a prevalence of 1.3% in this series. Radiologists interpreting knee MR images must be aware of this entity and its management.

Adult↗

PubMed1987

Paracervical ganglia of the female rat: histochemistry and immunohistochemistry of neurons, SIF cells, and nerve terminals.

The paracervical ganglia of the female rat were studied to elucidate the variety of neural elements in the ganglia. Light and electron microscopy, histochemistry, and immunohistochemistry were employed to reveal subtypes of neurons; small, intensely fluorescent (SIF) cells; and nerve terminals and to examine the relationships between these elements. On the basis of their histochemical markers, four subtypes of principal neurons were identified: acetylcholinesterase (ACHE)-positive, noradrenergic, neuropeptide tyrosine-immunoreactive (NPY-I), and vasoactive intestinal polypeptide-immunoreactive (VIP-I). The NPY-I neurons appeared to be the most numerous and the noradrenergic the least common type of neuron. Four subtypes of chemically coded SIF cells were revealed: catecholamine-containing, NPY-I, and those immunoreactive for calcitonin-gene-related peptide (CGRP-I) and cholecystokinin-octapeptide (CCK-8-I). The SIF cells were present as single cells among and adjacent to principal neurons and as large clusters near the edges of the ganglia or in nearby nerve trunks. Synaptic contacts on SIF cells, or between SIF-cell processes and neurons, were not observed. Seven subtypes of nerve terminals were stained: ACHE-positive, CGRP-I, CCK-8-I, VIP-I, substance P-I, enkephalin-I, and atrial natriuretic factor-I. Nerve terminals enwrapped the neurons as perineuronal plexuses in synaptic-like relationships. These results demonstrate that the paracervical ganglia of the female rat are a complex system of neural elements. For example, several classes of chemically coded neurons, SIF cells, and terminals exist in the ganglia. Each of these components contains a number of substances, some of which are putative neurotransmitters, which could influence activity in the ganglia or in the effector organs innervated by the ganglia.

Acetylcholinesterase↗

PubMed1986

Effects of estrogen on the basal ganglia.

Recent research suggests that estrogen regulates the activity of dopamine-containing fibers originating in the midbrain and terminating in the basal ganglia, and/or dopamine-sensitive cells in the basal ganglia. The mechanism by which estrogen acts is not clear, since cells in neither of these regions concentrate estrogens. Nevertheless, estrogens clearly affect behaviors mediated by the basal ganglia, as illustrated in human patients suffering from extrapyramidal disorders. Both biochemical and behavioral research in animals has confirmed that estrogen modulates basal ganglia function, but there has not been agreement concerning either the locus, the direction, or the mechanism of its action. These topics are the focus of this review. The effects of estrogen on behaviors mediated by DA in the basal ganglia depend on the dose of estrogen administered, the time interval between estrogen treatment and testing, the behavior measured, and the part of the basal ganglia from which the behavior is elicited. A high dose of estrogen results in an initial suppression and later enhancement of DA-related behaviors elicited from the striatum. However, no later enhancement of these behaviors occurs if a low dose of estrogen is given. Even after low doses of estrogen, the latency to behavioral suppression varies depending upon the behavior measured. These varying latencies suggest that more than one mechanism is involved in the effects of estrogen on basal ganglia output. In addition, estrogen may also act on some regions in the mesolimbic DA system. While estrogen may act indirectly via the catechol estrogens and prolactin, it has been demonstrated that estrogen can act directly on the striatum. These findings are related to the effects of estrogen on human extrapyramidal disorders.

Acetylcholine↗

PubMed1983

The development of substance P, somatostatin and vasoactive intestinal polypeptide in sympathetic and spinal sensory ganglia of the chick embryo.

Antisera to substance P, somatostatin and vasoactive intestinal polypeptide were produced in rabbits and used to establish radioimmunoassays. The specificities and sensitivities of the assays were characterised before using them to measure the levels of these peptides in the paravertebral sympathetic ganglia and spinal sensory ganglia of embryonic chicks. The immunoreactive materials in the developing ganglia were shown to be identical with the peptides by the criterion of co-elution on reverse-phase high performance liquid chromatography. The levels of the peptides varied independently during the developmental period studied between day 8 and hatching at day 20 of incubation. Vasoactive intestinal polypeptide was first detectable on day 12 in the sympathetic ganglia and the levels increased through to hatching, at which time it first became detectable in the sensory ganglia. In contrast, substance P and somatostatin were detectable in both sensory and sympathetic ganglia throughout the period studied: the content of substance P increased up to day 18 after which time it declined, and somatostatin was present initially (day 8) at high levels before rapidly declining to a minimum at day 10 and then slowly increasing again, in parallel with the general growth of the ganglia, reflected by their protein contents. The differential changes in levels of substance P, somatostatin and vasoactive intestinal polypeptide during development indicates that different regulatory mechanisms are responsible for the ontogenesis of individual peptide phenotypes in the peripheral nervous system.

Animals↗

PubMed1986

Origin and distribution of cerebral vascular innervation from superior cervical, trigeminal and spinal ganglia investigated with retrograde and anterograde WGA-HRP tracing in the rat.

Peripheral sources of cerebral vascular innervation have been investigated with retrograde and anterograde neuronal tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) in the rat. For retrograde identification of sources of innervation, WGA-HRP was applied to the exposed basilar artery through a fine slit in the overlying meninges, and sections of brain and peripheral ganglia were reacted with tetramethylbenzidine for detection of the tracer. A high density of tetramethylbenzidine reaction product was observed around the basilar artery and in the surrounding pial tissue, but the application sites were not completely selective since some tracer always had spread into the ventral brain stem. Retrogradely labelled cell bodies were identified in the superior cervical, stellate, first and second spinal, and trigeminal ganglia, i.e. these ganglia may represent origins of basilar artery innervation. In a second series of experiments, microinjections of WGA-HRP were placed into the indicated ganglia to obtain anterograde labelling of nerve fibres on whole-mounts of the cerebral vessels. Injections into trigeminal ganglia labelled nerve fibres on the ipsilateral half of the circle of Willis, as well as the contralateral anterior cerebral artery and the rostral part of the basilar artery. The first and second spinal ganglia projected to the vertebrobasilar arteries, while the ipsilateral part of the internal carotid (outside the circle of Willis) received fibres from the second spinal ganglion. Nerve fibres originating in trigeminal and spinal ganglia were organised in bundles, and between these a sparse plexus of thin single fibres appeared. Injection of WGA-HRP into superior cervical ganglion labelled a plexus of nerve fibres on the ipsilateral circle of Willis and the (rostral) basilar artery. These experiments demonstrated the origin and distribution of sympathetic and sensory innervation to major cerebral arteries in the rat.

Animals↗

PubMed1994

Sensory ganglia as a target of autonomic and sensory nerve fibres in the guinea-pig.

The distribution of neuropeptide- (neuropeptide Y, substance P, vasoactive intestinal peptide) and catecholamine-synthesizing enzyme-immunoreactive axons in guinea-pig trigeminal, nodose, and cervical dorsal root ganglia was studied by double-labelling immunofluorescence in controls and after extirpation of either the cervical sympathetic trunk or the stellate ganglion; tyrosine hydroxylase- and dopamine-beta-hydroxylase-immunoreactive terminals in dorsal root ganglia were ultrastructurally investigated. Six neurochemically identifiable axons innervated the trigeminal ganglion, five kinds were found in the nodose and dorsal root ganglia. Two of them (catecholaminergic with and without neuropeptide Y) were of sympathetic origin and, besides their termination at arteries, provided a direct innervation of capsule cells of the trigeminal and cervical dorsal root ganglia facing the subarachnoid space. Varicosities which were interpreted as being of sensory origin were equally numerous in all ganglia, whereas those being likely of parasympathetic origin decreased in numbers from the trigeminal to the dorsal root and nodose ganglia. It is concluded that the sensory ganglia are the target of postganglionic sympathetic, parasympathetic and primary afferent neurons, each of which are specifically organized with respect to the neurochemical phenotype and inter- and intraganglionic distribution. Among other targets, these "nervi gangliorum" appear to be intimately linked to the ganglionic capsular cells and meningeal sheaths facing the liquor spaces.

Animals↗

PubMed2003

The basal ganglia: a neural network with more than motor function.

The basal ganglia is a group of subcortical nuclei involved in motor control, cognition, and emotion. Basal ganglia disorders are manifested by abnormal movement and a number of neuropsychiatric disorders. Basal ganglia nuclei are organized into sensorimotor, associative, and limbic territories based on their connectivity and function. The caudate nucleus, putamen, and subthalamic nucleus comprise the input nuclei of the basal ganglia. The internal segment of globus pallidus and substantia nigra reticulata are the output nuclei. The input and output nuclei are interconnected by direct and indirect pathways. The cerebral cortex, basal ganglia, and thalamus communicate with each other via closed (segregated) parallel as well as open (split) loops. Recent anatomic, functional, and clinical data have necessitated modifications in the classical models of local connectivity between input and output nuclei of the basal ganglia as well as in the corticobasal ganglia-thalamus-cortical loops.

Animals↗

PubMed1984

The origin and possible significance of substance P immunoreactive networks in the prevertebral ganglia and related structures in the guinea-pig.

The distribution and origin of substance P immunoreactive nerve elements have been studied in the guinea-pig prevertebral ganglia by the indirect immunohistochemical technique, using a monoclonal antibody to substance P. Non-varicose substance P immunoreactive nerve fibres enter or leave the ganglia in all nerves associated with them, traversing the ganglia in larger or smaller bundles. Networks, mainly single-stranded, of varicose substance P immunoreactive nerve fibres also permeate the ganglia, forming a loose meshwork among the neurons. Similar networks are present in the lumbar paravertebral ganglia. In all these ganglia, neuronal somata do not in general show substance P immunoreactivity. The various nerves connected with the inferior mesenteric ganglion have been cut, in single categories and in various combinations, and the ganglion examined, after intervals of up to six days. Cutting the colonic or hypogastric nerves, which connect the ganglion with the hindgut and pelvic organs, leads to accumulation of substance P immunoreactive material in their ganglionic stumps, extending retrogradely to intraganglionic non-varicose fibres traceable through into the intermesenteric and lumbar splanchnic nerves. There is some local depletion of intraganglionic varicose networks. Cutting the intermesenteric nerve, which connects the coeliac-superior mesenteric ganglion complex with the ganglion, leads to accumulation of substance P immunoreactive material in its cranial stump and depletion of its distal stump; a minimal depletion is detectable in the inferior mesenteric ganglion itself. Cutting the lumbar splanchnic nerves, which connect the ganglion with the upper lumbar spinal cord and dorsal root ganglia, leads to accumulation of substance P immunoreactive material in their proximal stumps and total depletion of their distal, ganglionic stumps; in the ganglion there is subtotal loss of non-varicose substance P immunoreactive fibres and of varicose nerve networks, and the few surviving non-varicose fibres are traceable across the ganglion from the intermesenteric nerve to the colonic and hypogastric nerves. Cutting the intermesenteric and lumbar splanchnic nerves virtually abolishes substance P immunoreactive elements from the ganglion within three days postoperatively. It is concluded that these arise centrally to the ganglion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Basal ganglia: functional anatomy and physiology. Part 2.

Advances in knowledge about basal ganglia function and circuitry are reviewed. Despite the voluminous available literature on this subject, the role of basal ganglia in health and disease remains controversial. Experimental data on the effects of stimulation and ablation of the basal ganglia are summarized. The roles of the basal ganglia in the preparation for and execution of cortically initiated movement are described. Newer roles ascribed to the basal ganglia in sensory-motor gating, cognition, emotion, and motivation are discussed. The old and current concepts of information flow between the cerebral cortex, striatum, pallidum, thalamus, and back to the cerebral cortex are reviewed. The "funnel" system of information flow has been discarded in favor of several parallel and largely segregated loops pertaining to motor, oculomotor, cognitive, and limbic functions. The anatomic substrate of each of these loops is described. The specific roles of the striatum, pallidum, substantia nigra, and thalamus in information flow as related to movement are described. The roles of the basal ganglia in reinforcing wanted behavior and suppressing unwanted behavior via direct and indirect striatal loops are discussed. The implications of these loops in the genesis of Parkinson's disease and Huntington's chorea are described. Alteration in basal ganglia neurotransmitters and neuromodulators in Huntington's chorea, Tourette's syndrome, and Parkinson's disease are described.

Basal Ganglia↗