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PubMed1998

Dopamine-glutamate interactions in the basal ganglia.

In an attempt to formulate a working hypothesis of basal-ganglia functions, arguments are considered suggesting that the basal ganglia are involved in a process of response selection i.e. in the facilitation of "wanted" and in the suppression of "unwanted" behaviour. The meso-accumbal dopamine-system is considered to mediate natural and drug-induced reward and sensitization. The meso-striatal dopamine-system seems to fulfill similar functions: It may mediate reinforcement which strengthens a given behaviour when elicited subsequently, but which is not experienced as reward or hedonia. Glutamate as the transmitter of the corticofugal projections to the basal ganglia nuclei and of the subthalamic neurons is critically involved in basal ganglia functions and dysfunctions; for example Parkinson's disease can be considered to be a secondary hyperglutamatergic disease. Additionally, glutamate is an essential factor in the plasticity response of the basal-ganglia. However, opposite to previous suggestions, the NMDA-receptor blocker MK-801 does not prevent psychostimulant- nor morphine-induced day to day increase (sensitization) of locomotion. Also the day to day increase of haloperidol-induced catalepsy was not prevented by MK-801.

Basal Ganglia↗
PubMed1986

Autoradiographic study of 3H-lysine uptake by superior cervical and stellate ganglia in prehypertensive spontaneously hypertensive rats.

In order to compare the functional state of sympathetic ganglia in spontaneously hypertensive (SHR) with those in normotensive Wistar Kyoto rats (WKY), protein synthetic activity was examined by light microscopic autoradiography with 3H-lysine. The number of silver grains over the cytoplasm of ganglion cells in the superior cervical and stellate ganglia of newborn and 30-day-old animals were counted on photographic enlargements. In both sympathetic ganglia there were significantly more silver grains over ganglion cells in SHR compared with age-matched WKY at 15, 60, and 120 min after injection of 3H-lysine. The increased incorporation of the label by both sympathetic ganglia was more marked in newborn than in 30-day-old animals. This result shows that protein synthetic activity in these ganglion cells is increased in SHR from the newborn stage. It is suggested that a congenital hyperfunction of sympathetic ganglia occurs in SHR.

Animals↗
PubMed1987

Autoradiographic study of 3H-DOPA uptake by superior cervical and stellate ganglia of spontaneously hypertensive rats during the prehypertensive stage.

The functional state of sympathetic ganglia in spontaneously hypertensive rats (SHR) was compared with that of ganglia in normotensive Wistar Kyoto rats (WKY) by examining catecholamine synthetic activity by light microscopic autoradiography 3H-L-dihydroxyphenyl alanine (3H-DOPA). The number of silver grains over the perikarya of ganglion cells in the superior cervical (SCG) and stellate ganglia (SG) of newborn, 10-day-old and 30-day-old animals was counted on photographic enlargements. There were significantly more silver grains over ganglion cells in SHR compared with those in age-matched WKY at almost all incorporation times at all ages examined in SCG, at all incorporation times in newborn rats, and at incorporation times of 15 and 60 min in SG of 10-day-old rats. The increased incorporation of the label by both sympathetic ganglia was more marked in newborn than in 30-day-old animals. These results indicate that catecholamine synthetic activity in these ganglion cells is increased in SHR from the newborn stage, suggesting that a congenital hyperfunction of sympathetic ganglia occurs in SHR.

Animals↗
PubMed2006

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: implications for the pathophysiology of Parkinson's disease, schizophrenia and attention deficit hyperactivity disorder.

The basal ganglia form a forebrain system that collects signals from a large part of the neocortex, redistributes these cortical inputs both with respect to one another and with respect to inputs from the limbic system, and then focuses the inputs of this redistributed, integrated signals into particular regions of the frontal lobes and brainstem involved in aspects of motor planning and motor memory. Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorder (from which Parkinson's disease, PD, is the best-known-example) at one extreme to the hyperkinetic disorder (exemplified by Huntington's disease and hemiballism) at the other. In addition to disorders of movement, major mental disorders including schizophrenic-like states and attention deficit hyperactivity disorder (ADHD) have been linked to abnormalities in the basal ganglia and their allied nuclei. In this paper we discuss recent evidence indicating that a dopamine-induced dysbalance of basal ganglia neurocircuitries may be an important pathophysiological component in PD, schizophrenia and ADHD. According to our model, the deprivation of dopaminergic nigro-striatal input, as in PD, reduces the positive feedback via the direct system, and increases the negative feedback via the indirect system. The critical consequences are an overactivity of the basal ganglia output sites with the resulting inhibition of thalamo-cortical drive. In schizophrenia the serious cognitive deficits might be partly a result of a hyperactivity of the inhibitory dopamine D(2) transmission system. Through this dysinhibition, the thalamus exhibits hyperactivity that overstimulates the cortex resulting in dysfunctions of perception, attention, stimulus distinction, information processing and affective regulation (inducing hallucinations and delusions) and motor disabilities. Recent studies have strongly suggested that a disturbance of the dopaminergic system is also involved in the pathophysiology of ADHD. The most convincing evidence comes from the demonstration of the efficacy of psychostimulants such as the dopamine transporter (DAT) blocker methylphenidate in the symptomatic treatment of ADHD. Genetic studies have shown an association between ADHD and genes involved in dopaminergic neurotransmission (for example the dopamine receptor genes DRD4 and DRD5, and the DAT gene DAT1). DAT knockout mice display a phenotype with increased locomotor activity, which is normalized by psychostimulant treatment. Finally, imaging studies demonstrated an increased density of DAT in the striatum of ADHD patients. Which system is disturbed and whether this system is hyper- or hypoactive is not unambiguously known yet.

Antipsychotic Agents↗
PubMedDate not supplied

Effects of depolarizing agents on transglutaminase activity, Ca2+ influx, and protein synthesis in superior cervical and nodose ganglia excised from rats.

Rapid changes in transglutaminase (TG) activity, 45Ca(2+)-influx and [3H]leucine incorporation in superior cervical ganglia (SCG), and nodose ganglia (NG) excised from adult rats were examined following addition of membrane-depolarizing agents veratridine (Ver) or high extracellular [K+]o during aerobic incubation in vitro at 37 degrees C. Addition of KCl (50 mM) stimulated TG activity to a maximal extent (four to six-fold) in SCG and NG after 30 min. Ver (0.2 mM) also increased TG activity in both ganglia after 30 min. Kinetic studies showed that the stimulation of TG activity in both ganglia caused by each depolarization condition was associated with a decrease in Km and an increase in Vmax value. The depolarizing agents Ver and high [K+]o also caused significant increases in 45Ca2+ influx into both ganglia. The Ver-induced increases in TG activity and 45Ca2+ accumulation were antagonized by tetrodotoxin (TTX, 1 microM), a sodium channel blocker. The K(+)-induced increase in TG activity was not blocked by tetraethylammonium (TEA, 20 mM), a potassium channel antagonist, although TEA did block the K(+)-induced increase in 45Ca2+ accumulation. The membrane-perturbing, sialic acid-containing compounds, GM1-ganglioside (GM1, 5 nM) and alpha-sialyl cholesterol (alpha-SC, 20 microM), were moderate inhibitors of the K(+)-induced effects on TG activity and 45Ca2+ accumulation. The sialyl compounds had little effect on Ver-induced accumulation of 45Ca2+ but enhanced the Ver-evoked stimulation in TG activity. These results suggests that the veratridine- and K(+)-induced increases in TG activity occur via modulation of Ca2+ and Na+ channel gating mechanisms that are pharmacologically distinct for each depolarizing agent. The veratridine- and K(+)-induced decrease in [3H]leucine incorporation could be a result of stimulation of TG activity as a consequence of degenerative alterations.

Animals↗
PubMed2000

Projections from basal ganglia to tegmentum: a subcortical route for explaining the pathophysiology of Parkinson's disease signs?

Functional changes in the organisation of neuronal circuitries are generally used to explain parkinsonian motor symptoms and levodopa-induced dyskinesias. Based on information from histology and neurophysiological microrecordings of specific basal ganglia nuclei, the most widely accepted scheme is based on a central loop which starts in the cerebral cortex, makes multiple relays in the basal ganglia, and returns to the cerebral cortex. Transcranial magnetic stimulation studies, however, reveal no significant differences in the excitability of the motor cortex between normal subjects and patients with Parkinson's disease. Furthermore, electrophysiological and audiospinal facilitation studies indicate that the activity of reticular nuclei is altered in Parkinson's disease. It therefore appears that a circuit with the cortex as the only recipient of basal ganglia output is an oversimplification. This paper explores the relationships between various basal ganglia nuclei and proposes a subcortical pathway via which modifications in the basal ganglia may influence motor function.

Animals↗
PubMed2006

Bilateral basal ganglia activation associated with sensorimotor adaptation.

Sensorimotor adaptation tasks can be classified into two types. When subjects adapt movements to visual feedback perturbations such as in prism lens adaptation, they perform kinematic adaptations. When subjects adapt movements to force field perturbations such as with robotic manipulanda, they perform kinetic adaptations. Neuroimaging studies have shown basal ganglia involvement in kinetic adaptations, but have found little evidence of basal ganglia involvement in kinematic adaptations, despite reports of deficits in patients with diseases of the basal ganglia, such as Parkinson's and Huntington's disease, in these. In an effort to resolve such apparent discrepancy, we used FMRI to focus on the first few minutes of practice during kinematic adaptation. Human subjects adapted to visuomotor rotations in the context of a joystick aiming task while lying supine in a 3.0 T MRI scanner. As demonstrated previously, early adaptive processes were associated with BOLD activation in the cerebellum and the sensory and motor cortical regions. A novel finding of this study was bilateral basal ganglia activation. This suggests that, at least for early learning, the neural correlates of kinematic adaptation parallel those of other types of skill learning. We observed activation in the right globus pallidus and putamen, along with the right prefrontal, premotor and parietal cortex, which may support spatial cognitive processes of adaptation. We also observed activation in the left globus pallidus and caudate nucleus, along with the left premotor and supplementary motor cortex, which may support the sensorimotor processes of adaptation. These results are the first to demonstrate a clear involvement of basal ganglia activation in this type of kinematic motor adaptation.

Adaptation, Physiological↗
PubMed2002

Dopamine transporter density in the basal ganglia assessed with [123I]IPT SPET in children with attention deficit hyperactivity disorder.

Attention deficit hyperactivity disorder (ADHD) is a psychiatric disorder in childhood that is known to be associated with dopamine dysregulation. In this study, we investigated dopamine transporter (DAT) density in children with ADHD using iodine-123 labelled N-(3-iodopropen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl) tropane ([(123)I]IPT) single-photon emission tomography (SPET) and postulated that an alteration in DAT density in the basal ganglia is responsible for dopaminergic dysfunction in children with ADHD. Nine drug-naive children with ADHD and six normal children were included in the study. We performed brain SPET 2 h after the intravenous administration of [(123)I]IPT and carried out both quantitative and qualitative analyses using the obtained SPET data, which were reconstructed for the assessment of the specific/non-specific DAT binding ratio in the basal ganglia. We then investigated the correlation between the severity scores of ADHD symptoms in children with ADHD assessed with ADHD rating scale-IV and the specific/non-specific DAT binding ratio in the basal ganglia. Drug-naive children with ADHD showed a significantly increased specific/non-specific DAT binding ratio in the basal ganglia compared with normal children. However, no significant correlation was found between the severity scores of ADHD symptoms in children with ADHD and the specific/non-specific DAT binding ratio in the basal ganglia. Our findings support the complex dysregulation of the dopaminergic neurotransmitter system in children with ADHD.

Attention Deficit Disorder with Hyperactivity↗
PubMed2006

New vistas on the initiation and maintenance of insect motor behaviors revealed by specific lesions of the head ganglia.

In insects, thoracic pattern generators are modulated by the two head ganglia, the supraesophageal ganglion (brain) and the subesophageal ganglion, which act as higher-order neuronal centers. To explore the contribution of each head ganglion to the initiation and maintenance of specific motor behaviors in cockroaches (Periplaneta americana), we performed specific lesions to remove descending inputs from either the brain or the subesophageal ganglion or both, and quantified the behavioral outcome with a battery of motor tasks. We show that 'emergency' behaviors, such as escape, flight, swimming or righting, are initiated at the thoracic level independently of descending inputs from the head ganglia. Yet, the head ganglia play a major role in maintaining these reflexively initiated behaviors. By separately removing each of the two head ganglia, we show that the brain excites flight behavior and inhibits walking-related behaviors, whereas the subesophageal ganglion exerts the opposite effects. Thus, control over specific motor behaviors in cockroaches is anatomically and functionally compartmentalized. We propose a comprehensive model in which the relative permissive versus inhibitory inputs descending from the two head ganglia, combined with thoracic afferent sensory inputs, select a specific thoracic motor pattern while preventing the others.

Animals↗
PubMed2003

Neuropathological evaluation of the diencephalon, basal ganglia and upper brainstem in alobar holoprosencephaly.

Holoprosencephaly (HPE) is caused by the impaired cleavage of the embryonic prosencephalon, and in the severest type, alobar HPE, the normally bilateral diencephalon and basal ganglia are fused and tend to incorporate into the upper brainstem. The detailed neuropathological features of HPE remain to be elucidated, although disturbed regulation in body temperature and electrolyte balance are frequently observed. We immunohistologically examined the expression of hypothalamic hormones, neurotransmitters, calcium-binding proteins and neuropeptides in six female autopsy cases of alobar HPE. Eight age-matched controls formed the comparative basis for the immunoreactivity of these markers during the fetal period. Neurons immunoreactive for either vasopressin or orexin-A were noted in the fused diencephalon in five HPE cases, and colocalization of vasopressin and tyrosine hydroxylase occurred in HPE cases surviving more than 6 months. Tyrosine hydroxylase-immunoreactive fibers and neurons were observed in the fused diencephalon and basal ganglia in all the six cases. Parvalbumin-immunoreactive structures were identified in the fused diencephalon and basal ganglia in five cases, and the apparent red nucleus was identified by anti-parvalbumin immunostaining in two cases aged more than 1 year. Five cases demonstrated substance P-immunoreactive structures in the diencephalon, and a substantia nigra-like structure in the midbrain was visualized by immunostainings for both tyrosine hydroxylase and substance P in four cases. Only two cases aged more than 1 year had immunoreactivity for methionine-enkephalin in the basal ganglia and substantia nigra. These data suggest that the fused diencephalon and basal ganglia exhibited functional developments in alobar HPE, and the disturbed expression of the markers may be involved in hypothalamic and/or motor abnormalities in patients.

Basal Ganglia↗
PubMed2006

Apathy and the basal ganglia.

We should like to emphasize the following points: 1. Apathy is defined here as a quantified and observable behavioral syndrome consisting in a quantitative reduction of voluntary (or goal-directed) behaviors; 2. Therefore, apathy occurs when the systems that generate and control voluntary actions are altered; 3. These systems are mostly represented by the different subregions embedded in the Prefrontal cortex (PFC) and in the basal ganglia regions that are closely connected with the PFC; 4. In consequence, clinically, apathy is a prefrontal syndrome either due to direct lesions of the PFC or to lesions of basal ganglia areas that are closely related to the PFC; 5. Apathy is not a single entity but rather heterogeneous. Several different mechanisms may lead to apathy; Because there are several anatomical-functional prefrontal-basal ganglia circuits, the underlying mechanisms responsible for apathy may differ according to which prefrontal-basal ganglia circuit is affected; 6. In this context, apathy is the macroscopic results of the disruption of one or several elementary steps necessary for goal-directed behavior that are subserved by different prefrontal-basal ganglia circuits; 7. Intense apathy is related to caudate nucleus and GPi, disrupting associative and limbic pathways from/to the PFC; 8. in progressive supranuclear palsy (PSP) and focal lesions (caudate nuclei, GPi), apathy may be due to a loss of PFC activation; 9. In Parkinson's disease (PD), apathy may be due to a loss of signal focalization; 10. More globally, we propose that apathy may be explained by the impact of lesions or dysfunctions of the BG, because these lesions or dysfunctions lead to a loss of amplification of the relevant signal and/or to a loss of temporal and spatial focalization, both of which result in a diminished extraction of the relevant signal within the frontal cortex, thereby inhibiting the capacity of the frontal cortex to select, initiate, maintain and shift programs of action.

Basal Ganglia↗
PubMed1997

A dynamic model of motor basal ganglia functions.

Fast aiming movements were measured in a choice reaction paradigm in a healthy control group and in Parkinsonian patients. The patients were tested without ('off') and with 3,4-dihydroxyphenylalanine ('on') (L-dopa) medication. The movement trajectories were used to estimate the parameters of a dynamic linear model. The model is based on the functional structure of the basal ganglia-thalamocortical circuit with direct and indirect pathways linking the putamen to the basal ganglia output nuclei (Albin et al. 1989). The output of the circuit is connected to a model for the motor neuron-musculo-skeletal system. The gain kd for the direct pathway and the gain ki for the indirect pathway were estimated. They were found to be significantly decreased for Parkinsonian patients in 'off' compared with the control group. L-dopa therapy in Parkinsonian patients increased the gains of the direct and the indirect pathway almost to normal values which implies that the long-term dopamine level in the striatum was excitatory for the direct and for the indirect pathway. This result is restricted to movements of correct size. For movements of diminished size, which are typical for Parkinsonian patients, the model predicts that the dopamine level in the striatum is excitatory for the direct pathway but inhibitory for the indirect pathway. The simulated values for neuronal activities are in agreement with expected values according to the experimental data. The proposed model of the 'motor' basal ganglia thalamocortical circuit implies that information about biomechanical properties of the musculo-skeletal system is stored in the 'motor' basal ganglia-thalamocortical circuit, and that the basal ganglia are involved in computation of the desired movement amplitude.

Antiparkinson Agents↗
PubMed1999

Morphological and electrophysiological features of F76 and D1 neurones of the sub-oesophageal ganglia of Helix aspersa in vitro and in culture.

Identified neurones F76 and D1 of the suboesophageal ganglia of Helix aspersa were studied in the isolated ganglia in vitro and in culture. The neurones were examined electrophysiologically with current clamp and morphologically either with intracellular injections of Lucifer Yellow or biocytin. These nerve cells had very similar resting membrane potentials and responses to injected current. The projections of D1 and F76 have been characterised, with both neurones having two main axons. The F76 neurones project to the left pallial, right pallial, anal, and visceral nerves as well as to the left and right pleural ganglia. The D1 neurones have similar projections except that they do not project to the anal and visceral nerves. The bilateral symmetry to the pallial nerves and pleural ganglia is discussed. These cells were also studied electrophysiologically after mechanical isolation and culture. F76 and D1 neurones were separated by dissection (no enzymes) and cultured in three ways. In normal snail Ringer they remained viable for up to two weeks with no development. In Ringer preincubated with a ganglia or containing endothelial growth factor, neurite outgrowths were seen. Membrane potentials were significantly lower in cultured neurones than in vitro and the after hyperpolarization never went below resting in cultured cells but it did in vitro.

Action Potentials↗
PubMed2005

Presence and co-localization of vasoactive intestinal polypeptide with neuronal nitric oxide synthase in cells and nerve fibers within guinea pig intrinsic cardiac ganglia and cardiac tissue.

The presence of vasoactive intestinal polypeptide (VIP) has been analyzed in fibers and neurons within the guinea pig intrinsic cardiac ganglia and in fibers innervating cardiac tissues. In whole-mount preparations, VIP-immunoreactive (IR) fibers were present in about 70% of the cardiac ganglia. VIP was co-localized with neuronal nitric oxide synthase (nNOS) in fibers innervating the intrinsic ganglia but was not present in fibers immunoreactive for pituitary adenylate cyclase-activating polypeptide, choline acetyltransferase (ChAT), tyrosine hydroxylase, or substance P. A small number of the intrinsic ChAT-IR cardiac ganglia neurons (approximately 3%) exhibited VIP immunoreactivity. These few VIP-IR cardiac neurons also exhibited nNOS immunoreactivity. After explant culture for 72 h, the intraganglionic VIP-IR fibers degenerated, indicating that they were axons of neurons located outside the heart. In cardiac tissue sections, VIP-IR fibers were present primarily in the atria and in perivascular connective tissue, with the overall abundance being low. VIP-IR fibers were notably sparse in the sinus node and conducting system and generally absent in the ventricular myocardium. Virtually all VIP-IR fibers in tissue sections exhibited immunoreactivity to nNOS. A few VIP-IR fibers, primarily those located within the atrial myocardium, were immunoreactive for both nNOS and ChAT indicating they were derived from intrinsic cardiac neurons. We suggest that, in the guinea pig, the majority of intraganglionic and cardiac tissue VIP-IR fibers originate outside of the heart. These extrinsic VIP-IR fibers are also immunoreactive for nNOS and therefore most likely are a component of the afferent fibers derived from the vagal sensory ganglia.

Afferent Pathways↗
PubMed2005

Primary afferent neurons intrinsic to the guinea-pig intestine, like primary afferent neurons of spinal and cranial sensory ganglia, bind the lectin, IB4.

The plant lectin, IB4, binds to the surfaces of primary afferent neurons of the dorsal root and trigeminal ganglia and is documented to be selective for nociceptive neurons. Physiological data suggest that the intrinsic primary afferent neurons within the intestine are also nociceptors. In this study, we have compared IB4 binding to each of these neuron types in the guinea-pig. The only neurons in the intestine to be readily revealed by IB4 binding have Dogiel-type-II morphology; these neurons have been previously identified as intrinsic primary afferent neurons. Most of the neurons that are IB4-positive in the myenteric plexus are calbindin-immunoreactive, whereas those in the submucosal ganglia are immunoreactive for NeuN. The neurons that bind IB4 strongly have a similar appearance in enteric, dorsal root and trigeminal ganglia. Binding is to the cell surface, to the first part of axons and to cytoplasmic organelles. A low level of binding was found in the extracellular matrix. A few other neurons in all ganglia exhibit faint staining with IB4. Strongly reactive neurons are absent from the gastric corpus. Thus, IB4 binding reveals primary afferent neurons with similar morphologies, patterns of binding and physiological roles in enteric, dorsal root and trigeminal ganglia.

Animals↗
PubMed1996

Expression of choline acetyltransferase immunoreactivity in guinea pig cardiac ganglia.

Recent reports indicate that a considerable amount of heterogeneity exists amongst cardiac postganglionic neurons in their chemical coding patterns and electrical properties, and that some of these cells may serve in roles as sensory and interganglionic neurons as well as motor neurons. This study was undertaken to ascertain whether or not all of these neurons are cholinergic by immunostaining whole-mount preparations of the guinea pig heart for choline acetyltransferase (ChAT). Counts of neurons that were immunostained for microtubule-associated protein-2 revealed that about 1000 neurons exist in about 100 ganglia on the posterior atrial surface. ChAT immunoreactivity was expressed by all of the postganglionic neurons in the cardiac ganglia, including the 5% of neurons that also expressed immunoreactivity for nitric oxide synthase. Varicose nerve fibers that were immunoreactive for ChAT were abundant in ganglia, with every cardiac neuron lying in close apposition to one or more labelled varicosities. ChAT-immunoreactive nerve fibers were also observed in large vagosympathetic fiber bundles, in interganglionic fiber bundles, and passing individually within the myocardium. Immunoreactivity for ChAT was also observed in a large proportion of the small tyrosine hydroxylase-immunoreactive neurons that exist in guinea pig cardiac ganglia. These results indicate that all postganglionic neurons in guinea pig cardiac ganglia are likely to utilize acetylcholine as a neurotransmitter, regardless of their functional role in circuitry of cardiac innervation, and each of these neurons is likely to receive cholinergic input.

Animals↗
PubMed1997

Laminin immunoreactivity in enteric ganglia of the chick embryo.

The localization and time of appearance of laminin in the duodenum of the chick embryo were studied with an anti-laminin polyclonal antibody and immunofluorescence. Laminin immunoreactivity was observed in the basement membranes of the mesothelium, mucosal epithelium, muscle cells and in the adventitia and basal surface of the endothelium in blood vessels. In addition, laminin immunostaining was detected over the contour of myenteric ganglia from embryonic day 7 and inside these ganglia from embryonic day 13. In colocalization experiments, laminin immunoreactivity occurred outside tubulin immunoreactive neuronal cell bodies, thus indicating that it resides in glial cells or in extracellular spaces. In addition connecting strands of the myenteric plexus and intramuscular nerves expressed laminin immunoreactivity. Similar observations were made in the proventriculus, gizzard, ileum and rectum of chick embryos, and in the duodenum and rectum of quail embryos. In the ganglion of Remak, laminin immunofluorescence was detected in the collagenous sheath that surrounds the ganglion and inside the ganglion, where it outlines neuronal cell bodies. Laminin immunoreactivity within the myenteric ganglia during the 3rd week in ovo, appears to be characteristic of the avian species examined, since it was not observed in the rat and mouse intestine at equivalent developmental stages. Immunocytochemical experiments at the electron-microscope level confirmed that structures with laminin or laminin-like immunoreactivity occur both around and inside myenteric ganglia. It is suggested that laminin, or an immunologically similar molecule, may play a role in the development and maturation of avian enteric ganglia.

Animals↗
PubMed1999

Cholinergic neurons of the pelvic autonomic ganglia and uterus of the female rat: distribution of axons and presence of muscarinic receptors.

Acetylcholine (ACh) stimulates contraction of the uterus and dilates the uterine arterial supply. Uterine cholinergic nerves arise from the paracervical ganglia and were, in the past, characterized based on acetylcholinesterase (AChE) histochemistry. However, the histochemical reaction for acetylcholinesterase provides only indirect evidence of acetylcholine location and is a nonspecific marker for cholinergic nerves. The present study: (1) reevaluated cholinergic neurons of the paracervical ganglia, (2) examined the cholinergic innervation of the uterus by using retrograde axonal tracing and antibodies against molecules specific to cholinergic neurons, choline acetyltransferase and the vesicular acetylcholine transporter, and (3) examined muscarinic receptors in the paracervical ganglia using autoradiography and a radiolabeled agonist. Most ganglionic neurons were choline acetyltransferase- and vesicular acetylcholine transporter-immunoreactive and were apposed by choline acetyltransferase/vesicular acetylcholine transporter-immunoreactive terminals. Retrograde tracing showed that some cholinergic neurons projected axons to the uterus. These nerves formed moderately dense plexuses in the myometrium, cervical smooth muscle and microarterial system of the uterine horns and cervix. Finally, the paracervical ganglia contain muscarinic receptors. These results clearly reveal the cholinergic innervation of the uterus and cervix, a source of these nerves, and demonstrate the muscarinic receptor content of the paracervical ganglia. Cholinergic nerves could play significant roles in the control of uterine myometrium and vasculature.

Acetylcholinesterase↗