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PubMed1994

Compartmentalization of pattern-initiation and motor functions in the B31 and B32 neurons of the buccal ganglia of Aplysia californica.

1. The B31 and B32 cells in the buccal ganglia of Aplysia californica have unusual electrophysiological features. The somata of these strongly coupled cells do not sustain conventional action potentials. Brief depolarization of the soma produces a complex, sustained regenerative slow depolarization that is followed by a hyperpolarization. This activity in B31/B32 is correlated with a patterned burst of activity expressed in many of the neurons of the buccal ganglia. 2. Intracellular fills of B31/B32 showed that they have many neurites adjacent to the soma, as well as peripheral axons leaving the buccal ganglia via the radular nerve and innervating the Intrinsic-2 (I2) muscle of the buccal mass. Varicosities of B31/B32 axons are seen within the muscle. Backfills from I2 filled two adjacent B31/B32 cells as well as two newly identified neurons: B61 and B62. 3. Intracellular recording from the B31/B32 axons shows that they sustain conventional action potentials. These are recorded in the soma as approximately 10-mV fast depolarizations. Failed spikes in B31/B32, and conventional spikes in B61/B62, are correlated one for one with end-junction potentials (EJPs) in the I2 muscle. The EJPs are present even when the ganglia and muscles are bathed in high-divalent cations seawater. Thus B31/B32 and B61/B62 are motor neurons to the I2 muscle. 4. To determine whether the ability of B31/B32 to initiate patterned bursts is mediated by spikes in the axon or by slow potentials in the soma, the B31/B32 axon was stimulated directly while recording from the B31/B32 soma. Patterned bursts were never seen in the absence of slow potentials in the soma. Thus the ability of B31/B32 to initiate patterned bursts is localized to the soma and adjacent neurites. Slow potentials influence and cause spiking in adjacent neurons even in the absence of axon spikes. 5. These data show that the B31/B32 cells serve two functions that are compartmentalized in different regions of the cell and are mediated via different electrical signaling mechanisms. The B31/B32 somata utilize slow, sustained potentials as part of a network initiating patterned activity in the buccal ganglia. The B31/B32 axons utilize conventional action potentials, and act as motor neurons to the I2 muscle.

Animals↗

PubMed2000

Role of the basal ganglia in the control of purposive saccadic eye movements.

In addition to their well-known role in skeletal movements, the basal ganglia control saccadic eye movements (saccades) by means of their connection to the superior colliculus (SC). The SC receives convergent inputs from cerebral cortical areas and the basal ganglia. To make a saccade to an object purposefully, appropriate signals must be selected out of the cortical inputs, in which the basal ganglia play a crucial role. This is done by the sustained inhibitory input from the substantia nigra pars reticulata (SNr) to the SC. This inhibition can be removed by another inhibition from the caudate nucleus (CD) to the SNr, which results in a disinhibition of the SC. The basal ganglia have another mechanism, involving the external segment of the globus pallidus and the subthalamic nucleus, with which the SNr-SC inhibition can further be enhanced. The sensorimotor signals carried by the basal ganglia neurons are strongly modulated depending on the behavioral context, which reflects working memory, expectation, and attention. Expectation of reward is a critical determinant in that the saccade that has been rewarded is facilitated subsequently. The interaction between cortical and dopaminergic inputs to CD neurons may underlie the behavioral adaptation toward purposeful saccades.

Animals↗

PubMed1994

Basal ganglia lacunes and parkinsonism.

'Arteriosclerotic' parkinsonism is still a subject of debate. The aim of this study was to investigate whether parkinsonism associated with basal ganglia lacunes possesses peculiar clinical features and a clinical course which enables its distinction from idiopathic Parkinson's disease (IPD). 106 consecutive ambulatory patients with the clinical diagnosis of parkinsonism were referred for CT examination. Patients in whom isolated basal ganglia lacunes were found were interviewed and examined, and their clinical characteristics were compared to those of patients suffering from IPD without lacunes (controls). In 20 patients, isolated basal ganglia lacunes were detected; all had risk factors for stroke (significantly more than controls) and 7 of them had had clinically diagnosed strokes. The extrapyramidal disability evolved slowly in all. The clinical picture was indistinguishable from IPD in individual patients. However, tremor was significantly less frequent in this group. Lower body parkinsonism was not observed. Extra-pyramidal signs were frequently asymmetrical (55%), with no consistent relationship to the side of the lacune. Asymmetrical pyramidal signs were present in 30% of those with unilateral lacunes, always on the appropriate side. Only 1 patient was an L-dopa nonresponder. Patients with parkinsonism associated with basal ganglia lacunes showed tremor less frequently than other IPD patients; otherwise, clinical features and course of the disease were indistinguishable from IPD. In these cases, parkinsonism and basal ganglia lacunes might have occurred independently of each other and tremor might have been prevented by ischemic events.

Aged↗

PubMed1981

An orthograde labelling study of axons of the dorsal motor nucleus of the vagus to rat cardiac ganglia as demonstrated by autoradiography.

Central organization of the cardiac vagus has not been clarified. Retrograde changes produced in medulla oblongata neurons after section of vagal branches has favored the dorsal motor nucleus of the vagus (DMNX). Current information concerning the origin, course, and termination of vagal preganglionic fibers within cardiac ganglia is conflicting. The explicit purpose of this study was to determine if vagal fibers originated specifically within the DMNX proper. Fibers within the cardiac ganglia were labelled with 3H-leucine following injection into the DMNX. 12 adult albino rats were studied. DMNX were injected with 25 microCi 3H-leucine reconstituted to microliter. Animals were sacrificed by transcardial perfusion following a 4-day survival period. Serial cross-sections of the caudal pons, medulla oblongata, and thoracic viscera were processed for autoradiography. DMNX possessed a heavy incorporation of the radiochemical. Label was observed within the axons of the vagi. Cardiac ganglia contained labelled vagal fibers in close proximity to the postganglionic somata. Cardiac ganglia containing labelled preganglionic vagal axons were located in the cardiac plexuses and in the epicardium. Results show a labelled vagal preganglionic input to cardiac ganglia from the DMNX.

Animals↗

PubMed1997

A preliminary investigation of the effects of aging on the nerve cell number in the myenteric ganglia of the human colon.

We have examined the number of nerve cells present in the myenteric plexus of the human large intestine using a nonhistochemical method (Giemsa) in laminar preparations of the muscularis externa in two groups of subjects aged 20-35 and over 65 years. The collagen and elastic system related fibers in the myenteric ganglia were also qualitatively evaluated. The total number of neurons decreased in the old subjects by over 37%. The perikaryal area of most of the neurons in both the young and old subjects fell from 101 to 200 microns2. A ganglionic capsule was present and was thicker in the ganglia from the old subjects as were the septa within the ganglia. Both collagen and elastic system fibers were more numerous in the ganglia from the old subjects. We conclude that the decrease in neuron density with age is accompanied by an apparent increase in the fibrous components of the myenteric ganglia.

Adult↗

PubMed1992

Neurotransmission through sympathetic ganglia of spontaneously hypertensive rats.

Transmission of neuronal activity was assessed by recording preganglionic and postganglionic compound action potentials in superior cervical ganglia isolated from adult spontaneously hypertensive rats (SHR), Wistar-Kyoto (WKY) rats, and Wistar rats as well as young SHR and WKY rats to determine if previously observed alterations of membrane excitability, synaptic transmission, or both, have an effect on the transmission of preganglionic activity in SHR. Single stimuli induced more postganglionic neurons to fire over a wide range of preganglionic stimulation intensities in superior cervical ganglia from adult SHR as compared with those from adult normotensive controls. Short stimulation trains confirmed that SHR are able to maintain this greater number of active postganglionic neurons during low-frequency stimulation (1-20 Hz). However, by the end of a train of high-frequency stimulation (70-100 Hz) fewer neurons fired in ganglia from SHR compared with those from normotensive controls. These differences in transmission were not observed in the young rats. The results from the present study demonstrate that physiological frequencies of preganglionic activity are more effectively transmitted through sympathetic ganglia from adult SHR compared with those from normotensive controls, and this enhanced transmission through ganglia may contribute to the elevated sympathetic activity and the consequent hypertension seen in this model.

Action Potentials↗

PubMed1994

Localization of muscarinic receptor mRNAs in rat heart and intrinsic cardiac ganglia by in situ hybridization.

Although the heart is considered a relatively pure source of m2 muscarinic receptors, the possible expression of other muscarinic receptor genes at discrete sites within the myocardium or by intrinsic cardiac ganglia had not been evaluated. Accordingly, the present study used in situ hybridization histochemistry with 35S-labeled oligonucleotide probes to address this issue. Initial experiments demonstrated that the localization of m2 mRNA was similar to that reported for muscarinic receptors labeled with the nonselective muscarinic antagonist quinuclidinyl benzilate; however, there were two important exceptions. The conducting system contained less message than expected, whereas the intrinsic cardiac ganglia contained more. The mismatch between muscarinic receptor and m2 mRNA densities in the conducting system could not be explained by the local expression of other muscarinic receptor genes, since m1, m3, and m4 mRNAs were not detected at this or any other site within the myocardium. However, the presence of a high density of prejunctional muscarinic receptors in the conducting system would be consistent with such a mismatch. Surprisingly, the intrinsic cardiac ganglia contained more than four times as much m2 mRNA as found in the atria. This level of message may be necessary for the production of prejunctional receptors on cholinergic nerve fibers within the heart and receptors localized to the ganglion cell bodies. The ganglia also contained smaller amounts of m1 and m4 mRNAs. These observations suggest that prejunctional muscarinic receptors could have a prominent role in regulating cholinergic neurotransmission in the conducting system and that multiple muscarinic receptors are present in the intrinsic cardiac ganglia.

Animals↗

PubMed2001

Upregulation of immunoreactive angiotensin II release and angiotensinogen mRNA expression by high-frequency preganglionic stimulation at the canine cardiac sympathetic ganglia.

The possible involvement of the local angiotensin system in ganglionic functions was investigated in the canine cardiac sympathetic ganglia. Positive chronotropic responses to preganglionic stellate stimulation at high frequencies, after intravenous administration of pentolinium plus atropine, were inhibited by the nonpeptide angiotensin AT(1) receptor antagonist forasartan or the angiotensin I-converting enzyme inhibitor captopril, whereas the rate increases elicited by the postganglionic stellate stimulation and norepinephrine given intravenously failed to be inhibited by these antagonists. The levels of endogenous immunoreactive angiotensin II, as determined by radioimmunoassay in the incubation medium of the stellate and inferior cervical ganglia, were increased after the high-frequency preganglionic stimulation of the isolated ganglia. The increment of the peptide was also antagonized by the pretreatment with captopril but not by a chymase inhibitor, chymostatin. The expression of angiotensinogen mRNA was observed in the stellate ganglion, adrenal, liver, and lung but not in the ovary and spleen. The expression of the mRNA in the stellate and inferior cervical ganglia increased after high-frequency preganglionic stimulation of the in vivo dogs for a period of 1 hour. These results indicate that an intrinsic angiotensin I-converting enzyme-dependent angiotensin system exists in the cardiac sympathetic ganglia, which is activated by high-frequency preganglionic stimulation.

Angiotensin II↗

PubMed2003

Dissociating hippocampal versus basal ganglia contributions to learning and transfer.

Based on prior animal and computational models, we propose a double dissociation between the associative learning deficits observed in patients with medial temporal (hippocampal) damage versus patients with Parkinson's disease (basal ganglia dysfunction). Specifically, we expect that basal ganglia dysfunction may result in slowed learning, while individuals with hippocampal damage may learn at normal speed. However, when challenged with a transfer task where previously learned information is presented in novel recombinations, we expect that hippocampal damage will impair generalization but basal ganglia dysfunction will not. We tested this prediction in a group of healthy elderly with mild-to-moderate hippocampal atrophy, a group of patients with mild Parkinson's disease, and healthy controls, using an "acquired equivalence" associative learning task. As predicted, Parkinson's patients were slower on the initial learning but then transferred well, while the hippocampal atrophy group showed the opposite pattern: good initial learning with impaired transfer. To our knowledge, this is the first time that a single task has been used to demonstrate a double dissociation between the associative learning impairments caused by hippocampal versus basal ganglia damage/dysfunction. This finding has implications for understanding the distinct contributions of the medial temporal lobe and basal ganglia to learning and memory.

Aged↗

PubMed1988

Idiopathic basal ganglia calcification and organic mood disorder.

Idiopathic basal ganglia calcification is a syndrome consisting of bilateral basal ganglia calcifications, neuropsychiatric abnormalities, disturbances of movement, and normal calcium and phosphorus metabolism. The best described neuropsychiatric alterations are dementia and an organic psychosis. Organic mood disorder has been reported less often, and mania secondary to idiopathic basal ganglia calcification has not been noted previously. The authors describe five patients with idiopathic basal ganglia calcification and organic mood changes, including one patient with secondary mania. Symptoms of idiopathic basal ganglia calcification resemble those of other disorders affecting subcortical structures and support an association between mood, affect, cognition, and the extrapyramidal nuclear system. Treatment may ameliorate the mood disorder.

Adult↗

PubMed1994

Basal ganglia: functional anatomy and physiology. Part 1.

Advances in knowledge about basal ganglia structure and connectivity from 1925 to date are reviewed. Current concepts about neuronal populations, transmitters, and input and output of each of the basal ganglia nuclei are presented. The portrayal by Wilson, in 1925, of the striatum as a simple homogeneous structure has been replaced by the recognition, based on staining characteristics, connectivity, and function, that the neostriatum is compartmentalized into striosomes, matrisomes, and matrix compartments. Electrophysiologic studies have further shown the existence, in the neostriatum, of neuronal clusters that represent basic functional units much like the functional columns described much earlier for the cerebral cortex. Whereas the neostriatum is considered the major receiving area of the basal ganglia, the globus pallidus and substantia nigra pars reticulata constitute the major output nuclei. Combined neuroanatomic and neurophysiologic studies have revealed precise somatotopic organization throughout the basal ganglia system such that the leg, arm, and face areas of the cerebral cortex related to respective topographic areas within the striatum, pallidum, substantia nigra, and subthalamus. The previous concept of an inhibitory role for dopamine on striatal neurons has been modified. It is now acknowledged that dopamine exerts an inhibitory effect on striatal neurons that project to the external pallidum and a facilitatory effect on striatal neurons that project to the internal pallidum and substantia nigra pars reticulata. The previous concept of serial connectivity of the neostriatum (funnel concept) has been replaced by the concept of parallel connectivity. Within the internal connectivity of the basal ganglia, there is a fast system in which the neurotransmitter is gamma-aminobutyric acid (GABA) and a slow system modulated by neuropeptides. The slow system is believed to give identity to an otherwise homogenous GABAergic system.

Basal Ganglia↗

PubMed2001

The place of the thalamus in frontal cortical-basal ganglia circuits.

The thalamus has long been thought to convey subcortical information to the cortex. Indeed, models of basal ganglia function attribute the primary role for the thalamus to a simple relay of information processed in the basal ganglia to the cortex. The thalamic nuclear groups that are associated primarily with this function are the ventral anterior and ventral lateral nuclei and the mediodorsal thalamic nucleus. However, recent studies have shown that the corticothalamic projection is important for the dynamics of the thalamocortical processing. Furthermore, the relay nuclei that carry basal ganglia output to the cortex have recently been shown to project back to the basal ganglia directly. These two recent developments indicate a more dynamic role for the thalamus in basal ganglia information processing than a passive relay.

Animals↗

PubMed2004

Molecular regulation of gene expression of catecholamine biosynthetic enzymes by stress: sympathetic ganglia versus adrenal medulla.

Stress induces tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) gene expression in sympathetic ganglia and adrenal medulla (AM). However, distinct molecular mechanisms appear to regulate these genes in these locations. The elevation of TH mRNA in response to single immobilization stress (IMO) in AM is robust, but transient, while the induction of TH and DBH mRNAs in sympathetic ganglia is slower and more long lasting. Injections of adrenocorticotropic hormone (ACTH) elicited induction of TH and DBH gene expression in rat sympathetic ganglia, but not in AM. The superior cervical (SCG) and stellate (StG) ganglia, but not AM, were found to express mRNA for the MC-2 receptor, the major ACTH responsive receptor in adrenal cortex. IMO led to increase in MC-2 receptor mRNA levels in SCG. Thus, ACTH, via the MC-2 receptor, may be directly involved in the stress-elicited regulation of norepinephrine biosynthesis in sympathetic ganglia. The signaling pathways triggered by IMO differed in these locations. In AM, IMO triggered activation of the MAP kinase, JNK, and induction of AP1 factors, Egr1 and phosphorylation of CREB. In contrast in the SCG, with IMO we did not observe changes in JNK and little binding to the AP1 motif of the TH promoter. However, there was an increase in CREB binding to the CRE site of the TH promoter. The results reveal differential mechanisms of regulation of catecholamine biosynthetic enzymes by stress in two components of the sympathoadrenal system and should provide basis for possible selective pharmacologic interventions.

Adrenal Medulla↗

PubMed1996

Immobilization stress elevates gene expression for catecholamine biosynthetic enzymes and some neuropeptides in rat sympathetic ganglia: effects of adrenocorticotropin and glucocorticoids.

Sympathetic ganglia are the major contributors to the stress-elicited rise in circulating norepinephrine, enkephalins, and neuropeptide Y. Here we examined the effect of immobilization stress and treatment with ACTH and glucocorticoids on messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), preproneuropeptide Y (pre-NPY), and proenkephalin in rat superior cervical ganglia (SCG) and in stellate ganglia. Our results show a severalfold increase in the relative abundance of TH and NPY mRNAs in response to a single immobilization. Repeated stress elevated expression of all the genes studied and increased TH immunoreactivity in both ganglia. The effect of stress was more pronounced in SCG. Prolonged cortisol administration failed to alter the mRNA levels of TH, DBH, and NPY in control animals but attenuated the response to stress. In contrast, TH and DBH mRNA levels in the SCG, but not in adrenal medulla, were elevated by ACTH administration, similar to the levels attained after immobilization. The results revealed that the regulation of gene expression in response to immobilization stress in sympathetic neurons differs from the regulation in adrenal medulla. The study implicates hormonal involvement in the stress-induced changes in TH, DBH, NPY, and proenkephalin gene expression in sympathetic ganglia.

Adrenocorticotropic Hormone↗

PubMed1979

Calcification of the basal ganglia: computerized tomography and clinical correlation.

During a 1-year period, 4219 consecutive computerized tomograms (CT) were reviewed for basal ganglia calcification; 14 patients with such calcification were identified. Calcifications on CT scan were bilateral in 12 of these cases and unilateral in 2. All bilateral calcifications were symmetric. The globus pallidus was the site of calcification in 13 of the 14 patients. Bilateral dentate nucleus calcification was seen in one patient. Skull radiograms were normal in all but one. Patients had diverse symptoms that were often explained by other findings, suggesting that calcifications may be coincidental and that basal ganglia calcification may not be a nosologic entity. Disturbances of calcium metabolism were not found in these patients, minimizing the pathophysiologic significance of altered calcium metabolism and the need for extensive endocrinologic evaluation. The finding of basal ganglia calcification alone does not justify invasive diagnostic procedures. Extrapyramidal signs may be associated with basal ganglia calcification; parkinsonism associated with basal ganglia calcification differs from idiopathic parkinsonism in being resistant to levodopa therapy.

Adult↗

PubMed2002

Mid-gestation right basal ganglia lesion: clinical observations in two children.

OBJECTIVE: To describe the neurobehavioral syndrome in two children with destruction of the right basal ganglia ostensibly from amniocentesis needle penetration at 17 weeks of gestation. BACKGROUND: Early-life unilateral lesions of the basal ganglia are rare and the resulting syndrome not described. METHODS: Both children had repeated clinical assessments, MRI and (18)F-fluorodeoxyglucose PET scans, and psychometric and achievement testing over 10 years. RESULTS: Right basal ganglia destruction was similar and virtually coextensive in both children; optic nerve and oculomotor dysfunction were disparate. One had a right temporal pole porencephalic cyst with anomalous overlying cortex. The clinical syndrome included left hemiparesis with distal spasticity and without hypotrophy; extraocular movement disorders; severe episodic disinhibition, impulsiveness, hitting reflexively, and extreme emotional lability. Outbursts of screaming and cursing resembled "sham rage." Both had mild intellectual retardation with competent language but poor nonverbal and visual-spatial abilities, visual memory, and daily living and socialization skills. CONCLUSIONS: The shared behavioral and cognitive syndrome is most reasonably attributed to the right basal ganglia lesions, which were complete and coextensive in both, whereas other lesions were partial, milder, and disparate. Early destruction of the right basal ganglia may preclude normal development of right hemisphere functions without evidence of plasticity and appears associated with intense disinhibition and impulsiveness of aggressive attack activities and with general lability and dyscontrol of emotion.

Adolescent↗

PubMed1996

The frontal cortex-basal ganglia system in primates.

The primate basal ganglia receives information from most of the cerebrum, including the frontal cortex, but projects (via the dorsal thalamus) primarily to the frontal lobe, perhaps in its entirety. As such, the frontal cortex and basal ganglia constitute an integrated, distributed neuronal architecture. We review evidence that the frontal lobe and basal ganglia specialize in different, but related, aspects of response learning. Frontal cortex acts when new rules need to be learned and older ones rejected, whereas the basal ganglia potentiate previously learned rules based on environmental context and reinforcement history. Such potentiation increases the probability that the central nervous system will select a particular rule to guide behavior. We outline a possible mechanism for the basal ganglia's proposed role in rule potentiation, one that involves both the direct and indirect striatal output pathways and their dopaminergic input. It has previously been proposed that direct-pathway neurons recognize a pattern of corticostriatal inputs, which promotes activity in recurrent, positive-feedback modules (or loops) of which they are an integral part. We propose that this recurrent activity potentiates a rule associated with those modules. If so, then the dopaminergic system is well situated and organized to modulate rule potentiation in both the short and long term. Dopaminergic neurons of the midbrain increase activity during learning and other periods of relatively unpredictable reinforcement. Dopamine enhances gene expression and other forms of activity in striatal neurons of the direct pathway, while suppressing neurons of the indirect pathway. In the short term, then, dopamine may augment the activity of modules triggered by a recognized context, whereas in the long term it may promote context-dependent activation of the same modules. Together, these modulatory influences could support both rule potentiation and learning the context for potentiating that rule.

Animals↗

PubMed2002

Cubital tunnel syndrome associated with medial elbow Ganglia and osteoarthritis of the elbow.

BACKGROUND: Medial elbow ganglia have been reported in association with cubital tunnel syndrome. This lesion is thought to occur rarely and has not been emphasized in the literature. The purposes of the present study are to report our experience with this lesion in order to elucidate its prevalence as well as its clinical and radiographic features, to describe our operative findings, and to present the results of surgical treatment. METHODS: Four hundred and eighty-seven elbows in 472 patients were treated for cubital tunnel syndrome between 1980 and 1999. We performed a retrospective study of the thirty-eight patients who had a medial ganglion. All of the ganglia were excised, and the ulnar nerve was translocated subcutaneously. Thirty-two patients were followed for a mean of thirty-seven months. RESULTS: Medial elbow ganglion was the third most common causative factor associated with cubital tunnel syndrome, with an overall prevalence of 8%. Resting pain in the medial aspect of the elbow was reported by twenty-five of the thirty-eight patients, and a sudden onset of numbness in the ring and little fingers or of medial elbow pain without prior symptoms was reported by twenty-nine patients. The symptoms lasted two months or less in thirty-one patients. All ganglia originated from the medial aspect of the ulnohumeral joint, and radiographs of that joint showed degenerative changes in thirty-seven patients. At the time of follow-up, all measurements of sensory and motor function of the ulnar nerve had improved and no recurrence of nerve palsy was found. CONCLUSIONS: Although uncommon, medial elbow ganglia have a strong association with osteoarthritis of the elbow and can cause a relatively acute onset of cubital tunnel syndrome. A patient with cubital tunnel syndrome associated with elbow osteoarthritis who complains of medial elbow pain or severe numbness within two months after the onset of the syndrome should be strongly suspected of having a ganglion. Most ganglia are occult, and ultrasonography and magnetic resonance imaging can assist in the preoperative diagnosis. Careful excision of the ganglion performed concurrently with subcutaneous anterior transposition of the ulnar nerve can produce satisfactory results.

Adult↗