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Characterization of herpes simplex virus type 2 latency-associated transcription in human sacral ganglia and in cell culture.

The ability of herpes simplex virus type 2 (HSV-2) to establish latency in and reactivate from sacral dorsal root sensory ganglia is the basis for recurrent genital herpes. The expression of HSV-2 genes in latently infected human sacral ganglia was investigated by in situ hybridization. Hybridizations with a probe from the long repeat region of HSV-2 revealed strong nuclear signals overlying neurons in sacral ganglia from five of nine individuals. The RNA detected overlaps with the transcript for infected cell protein O but in the opposite, or "anti-sense," orientation. These observations mimic those made previously with HSV-1 in human trigeminal ganglia and confirm the recent findings during latency in HSV-2-infected mice and guinea pigs. Northern hybridization of RNA from infected Vero cells showed that an HSV-2 latency-associated transcript was similar in size to the larger (1.85 kb) latency transcript of HSV-1. Thus, HSV-1 and HSV-2 latency in human sensory ganglia are similar, if not identical, in terms of their cellular localization and pattern of transcription.

Adult↗

Brainstem and basal ganglia lesions in xeroderma pigmentosum group A.

Xeroderma pigmentosum group A (XPA) is a hereditary disorder characterized by cutaneous symptoms and progressive neurodegeneration. Since XPA patients exhibit peripheral neuropathy, neuronal deafness, rigidity, dysphagia, and laryngeal dystonia, it is indispensable for investigation of the neurodegeneration to analyze brainstem and basal ganglia lesions clinically and pathologically; we have previously shown the role of oxidative stress in the development of basal ganglia lesions. Here we immunohistochemically examined the expression of neurotransmitters, calcium-binding proteins, and neuropeptides in the brainstem, basal ganglia, and thalamus in 5 XPA autopsy cases. In the brainstem, immunoreactivity for tyrosine hydroxylase, tryptophan hydroxylase, and calbindin-D28K was severely reduced throughout the brainstem in all the XPA cases. Nevertheless, the expressions of parvalbumin, substance P, and methionine-enkephalin in the brainstem were comparatively preserved; the exception being reduced immunoreactivity for them in the cochlear and dorsal column nuclei in 3 cases. The large cell neurons in the putamen were preferentially reduced, the immunoreactivity for tyrosine hydroxylase reflecting the dopaminergic afferent and efferent pathways was severely affected, and the expression of 3 calcium binding proteins (i.e. parvalbumin, calbindin-D28K, and calretinin) was disturbed in various ways. The expression of substance P and methionine-enkephalin, which are involved in the efferent pathways in the basal ganglia, in the globus pallidus and substantia nigra was spared. It is speculated that the selective damage to the dopamine system in the basal ganglia and the disturbed monoaminergic expression in the brainstem could be related to clinical abnormalities such as the rigidity, laryngeal dystonia, and several neurophysiological changes. Functional analysis of autopsy brains will facilitate clarification of the pathogenesis of the neurodegeneration in XPA.

Adolescent↗

Angiotensinogen-like epitopes are present in the CNS of Aplysia california and co-localize with urotensin I- and urotensin II-like immunoreactivities in the cerebral ganglia.

Immunohistochemistry was used to demonstrate urotensin I (UI), urotensin II (UII), and angiotensinogen (Ao)-like immunoreactivities (ir) in the CNS of Aplysia californica. The fish UI is a 41 amino acid peptide that has 50% identity with mammalian corticotropin-releasing factor (CRF). Identity also exists between UI and angiotensinogen in a tetrapeptide at the N-terminus. Ao-ir neurones were found in the F cluster of the Aplysia cerebral ganglia. Beaded Ao-ir fibres were seen in the neuropile and commissure of the cerebral, pleural and pedal ganglia. Ao neurosecretory material was also seen in the perineural region of the proximal supralabial nerve. Previously we have demonstrated UI and UII immunoreactivities were present in the CNS of Aplysia. A comparison of adjacent sections of the cerebral ganglia immunostained sequentially for UI, UII and Ao revealed that all three immunoreactivities co-existed in the same cells of the F cluster of the cerebral ganglia. Liquid-phase immunoabsorption of the Ao antiserum revealed that porcine or human angiotensinogen but not UI or UII were able to quench Ao immunostaining. Conversely UI and UII staining were quenched by white sucker (Catatomus commersoni) UI and goby (Gillichtys mirabilis) UII, respectively, but they were not modified by angiotensinogen. These results suggest that UI-, UII-, and Ao-like peptides might co-exist as separate entities in the cerebral ganglia of Aplysia californica where they can act in an integrated and/or independent modulatory way.

Angiotensinogen↗

The polypeptide and the DNA restriction enzyme profiles of spontaneous isolates of herpes simplex virus type 1 from explants of human trigeminal, superior cervical and vagus ganglia.

Analysis of the infected cell polypeptides and the DNA restriction profiles of 31 HSV-1 isolates from the trigeminal, superior cervical and vagus ganglia from 17 individuals (12 U.S.A., 2 Japanese, 3 Norwegian) could be classified as 15 different virus strains. With the exception of the three Norwegian isolates which gave identical profiles, virus isolates from the ganglia of different individuals could all be distinguished from one another. In contrast virus isolates from the trigeminal, superior cervical and vagus ganglia of the same individual, or virus isolates from the left and right ganglia of the same individual or multiple isolates from different explants of a single ganglion were indistinguishable. In conclusion, a single virus strain infects each individual initially and virus descended from this event subsequently infects and becomes latent in different cells of the same ganglion as well as in different ganglia.

DNA Restriction Enzymes↗

Subthalamic ablation reverses changes in basal ganglia oxidative metabolism and motor response to apomorphine induced by nigrostriatal lesion in rats.

In Parkinson's disease, the functional architecture of the basal ganglia nuclei undergoes profound alterations, one of the most important of which is overactivity of the basal ganglia output nuclei. This phenomenon seems to be intimately related to pathological overactivity of the subthalamic nucleus, which directly modulates the basal ganglia output through its glutamatergic projections. In this study, we investigated the effects of unilateral subthalamic nucleus lesions on the activities of succinate dehydrogenase and cytochrome oxidase, two markers of neuronal activity, in rats with prior unilateral lesions of the nigrostriatal tract. We also explored the effect of subthalamic nucleus lesions on the rotational response to systemic apomorphine. Rats with unilateral lesions of the nigrostriatal tract showed ipsilateral increases in enzyme activity in the basal ganglia output nuclei, entopeduncular nucleus and substantia nigra pars reticulata. Selective subthalamic nucleus destruction completely reversed this phenomenon. In addition, subthalamic nucleus lesions abolished the rotational response to apomorphine. These results confirm that overactivity of the subthalamic nucleus plays a pivotal role in the functional alterations of basal ganglia associated with Parkinson's disease. They also shed further light on the neural mechanisms through which manipulations of subthalamic activity can ameliorate Parkinson's disease symptoms.

Animals↗

Neurite outgrowth and protein phosphorylation in chick embryonic sensory ganglia induced by a brief exposure to 12-O-tetradecanoylphorbol 13-acetate.

An exposure to 12-O-tetradecanoylphorbol 13-acetate (TPA) at 20 nM for as short as 30 min was sufficient to elicit neurite outgrowth from explanted chick embryonic sensory ganglia. Attachment of the ganglia to the collagen-coated substratum during exposure to TPA was essential for subsequent neurite outgrowth. Pulse-labeling with [35S]-methionine indicated no significant difference in protein synthesis between control and TPA-treated ganglia. In vitro phosphorylation assay revealed a prominent protein kinase C substrate with an apparent molecular mass of 66,000 dalton (66 kDa) in chick embryo ganglia extracts. Treatment of intact ganglia with TPA for 30 min also specifically stimulated the phosphorylation of the same protein. When staurosporine, a potent inhibitor of protein kinase C, was present during TPA treatment, both neurite outgrowth and the phosphorylation of the 66-kDa protein were blocked. Biochemical analysis of the phosphorylated 66-kDa protein indicated that (1) phosphorylation was only in serine residue, (2) the pI value was 4.5, (3) after V8 protease digestion, two phosphorylated peptide fragments, 6.0 and 7.5 kDa in size, were produced, and (4) it cross-reacted with an antiserum raised against a 66-kDa neurofilament subunit from rat spinal cord. These results suggest that early activation of protein kinase C and the phosphorylation of the 66-kDa protein may be involved in neuritogenesis.

Alkaloids↗

Age-related changes in tyrosine hydroxylase and choline acetyltransferase in sympathetic ganglia of a rat strain with reduced sympathetic neuron numbers.

In Wistar rats, a subpopulation of sympathetic ganglionic neurons dies during ageing, but in the GH strain, these same neurons die during the period of perinatal maturation. We have compared tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) in superior cervical ganglia of GH and control rats at different ages. Ganglionic TH rose to near adult levels between postnatal weeks 1 and 2. No significant differences in TH values were seen between GH and control ganglia at any age, indicating that reduced neuron numbers are compensated for by increased cellular activity. Ganglionic ChAT rose initially in parallel with TH and then more slowly over postnatal weeks 3-4, reaching adult levels that were about 20% lower in GH than in normal ganglia. During ageing, TH remained constant but ChAT continued to rise slowly in GH ganglia, whereas ChAT in normal ganglia fell by about 10%. Both the strain difference in ChAT during development and the fall in ChAT during ageing in normal animals parallel the differences in ganglion cell numbers seen under these circumstances.

Aging↗

Effect of chemical destruction of adrenergic neurones on some cholinergic mechanisms in adult rat sympathetic ganglia.

Rats were treated for 2-6 weeks with guanethidine after which their superior cervical ganglia were removed. Ganglionic tyrosine hydroxylase and alpha-bungarotoxin binding sites were reduced by the guanethidine treatment indicating adrenergic cell body destruction. Choline acetyltransferase activity and acetylcholine content of ganglia were not clearly changed by the guanethidine treatment, indicating that the drug does not destroy presynaptic terminals and that these presynaptic indicators do not adapt markedly to postsynaptic loss. The cholinesterase in the ganglia was reduced by guanethidine treatment, but such ganglia retained their ability to accumulate surplus acetylcholine when they were incubated with physostigmine. This is interpreted as indicating surplus acetylcholine accumulation is a presynaptic phenomenon. Choline uptake by resting ganglia was not reduced as a result of guanethidine treatment nor was it affected by preganglionic denervation. This is interpreted as indicating that during rest, choline uptake is into supporting cells or intraganglionic cells rather than cholinergic nerve terminals or adrenergic cell bodies.

Acetylcholine↗

Differences in neurokinin receptor pharmacology between rat and guinea-pig superior cervical ganglia.

1. The depolarizations elicited by seven neurokinin receptor agonists were examined in both rat and guinea-pig superior cervical ganglia by use of grease-gap methodology in the presence of tetrodotoxin (0.1 microM). Responses were normalised with respect to 1 microM eledoisin. 2. The rank order of agonist potency in the rat ganglia was senktide greater than substance P greater than substance P methyl ester = eleidosin = Sar-Met-substance P greater than neurokinin B greater than neurokinin A, whereas in guinea-pig superior cervical ganglion (SCG) the rank order was senktide greater than Sar-Met-substance P greater than neurokinin B = eledoisin = substance P methyl ester. The concentration-effect curves for substance P and neurokinin A in guinea-pig ganglia were biphasic which precluded the determination of meaningful potency values. 3. The maximal depolarization achieved by subtype selective ligands was different between these two species. On rat and guinea-pig SCG, the NK3-selective ligand, senktide, produced a maximal depolarization of 27% and 274% respectively, whereas the NK1-selective ligand, substance P methyl ester, produced depolarizations of 77% and 64% respectively. 4. The depolarizations induced by substance P methyl ester and senktide in either species were unaffected by atropine (1 microM), suggesting a lack of involvement of presynaptic neurokinin receptors in the generation of the response. 5. The potency of substance P methyl ester, senktide, and neurokinin A were unaffected by pretreating ganglia with the peptidase inhibitors bacitracin (40 micrograms ml-1), leupeptin (4 micrograms ml-1), and chymostatin (2 micrograms ml-1). Similarly, these peptidase inhibitors had no effect on the maximal depolarizations achieved by any of these agonists.6. It is evident that rat and guinea-pig superior cervical ganglia possess both NK, and NK3 receptors, but that their net contribution to depolarizations are different between the two species. The depolarizations in guinea-pig SCG are mediated predominantly by an NK3 subtype and in rat SCG by an NK, receptor subtype.

Animals↗

Physiological properties and receptive fields of mechanosensory neurones in the head ganglion of the leech: comparison with homologous cells in segmental ganglia.

A study of the head ganglion of the leech was made to compare the properties of specific sensory cells in this ganglion with those of homologous neurones in the segmental ganglia. 1. In the head ganglion, cells were identified that had electrical properties, sensory modalities and adaptation properties similar to those of touch (T), pressure (P) and nociceptive (N) cells in the segmental ganglia. The cell bodies of these neurones were situated in characteristics positions that could be correlated with those in the segmental ganglia. Several lines of evidence suggested that they were primary sensory neurones. Fewer T, P and N neurones were identified in the head ganglion than would be expected from its six constituent segmental ganglia. 2. The receptive fields of identified T, P and N cells were situated on the external surface of the head and the interior of the mouth with considerable overlap. They were generally smaller in size than those situated on the main part of the body. The receptive fields were also displaced anteriorly so that some of them were situated in segments anterior to those of the innervating cells. 3. The morphology of the sensory cells in the head ganglion was studied by intracellular injection of horseradish perioxidase. The general branching characteristics of the cells and the structural appearance of their processes resembled those of homologous cells in the segmental ganglia. However, the routes taken to the periphery by some of the cells were not constant from head ganglion to head ganglion. This variability was confirmed by electrophysiological evidence, and differed from the constancy seen in segmental sensory cells.

Action Potentials↗

Reflex pathways in the abdominal prevertebral ganglia: evidence for a colo-colonic inhibitory reflex.

1. In vitro experiments were performed on preparations consisting of prevertebral ganglia attached to the entire colon of guinea-pigs. The colon was divided into an orad and a caudad segment and intraluminal pressure was recorded from the terminal end of each segment. Intracellular recordings were simultaneously obtained from neurones in the coeliac plexus. 2. The source of mechanosensory input from the colon paralleled the responses to mesenteric nerve stimulation. That is, section of the mesenteric nerve that contributed the strongest synaptic input to a neurone eliminated most of the mechanosensory input to that neurone. 3. The origin of the mechanosensory input to some neurones could be localized as coming from either the orad or caudad segment of the colon. In the coeliac ganglia 68% of the neurones tested responded primarily to orad distension and 37% to caudad distension. In the superior mesenteric ganglion 57% responded to orad distension and 43% to caudad distension. 4. Repetitive stimulation of the mesenteric nerve trunks arising from the prevertebral ganglia inhibited contractions differentially in the orad and caudad segments. The inferior coeliac nerves inhibited primarily the orad segments of colon and the lumbar colonic nerves inhibited primarily the caudad segments of colon. Stimulation of the superior coeliac nerves did not alter the motility of either segment. 5. When one of the colonic segments was distended, contractions in the other colonic segment were inhibited in 71% of the distensions. This inhibition operated in both directions: either orad inhibiting caudad or vice versa. 6. Cutting the intermesenteric nerve which communicates between the orad and caudad prevertebral ganglia eliminated the inhibitory reflex. 7. These experiments provide evidence for a colo-colonic inhibitory reflex mediated through pathways in the prevertebral ganglia.

Afferent Pathways↗

Childhood onset generalised dystonia can be modelled by increased gain in the indirect basal ganglia pathway.

Clinical experience suggests an important role of the indirect basal ganglia pathway in the genesis of childhood onset generalised dystonia, but it has been difficult to reconcile the increased muscle activity in dystonia with the current model of basal ganglia function in which the indirect pathway is considered primarily inhibitory. The aim of this study was to present a modification of the direct-indirect pathway model, in which the indirect pathway is inverting rather than purely inhibitory, so that while high signals are inhibited, low signals are amplified. As the basal ganglia may be a feedback loop that modifies cortical activity, instability from excessive gain in this feedback loop could explain features of dystonia. A detailed mathematical model is provided, together with simulations of cortical cell population spiking behaviour when connected through a basal ganglia loop. The simulations show that increased gain in the indirect pathway relative to the direct pathway can lead to unstable uncontrolled synchronous oscillations in cortex and basal ganglia. This behaviour could result in dystonia. The model provides a consistent explanation for the association of dystonia with parkinsonism and disorders characterised by dopamine depletion, the ability to treat some dystonias with dopamine, the ability of neuroleptic drug treatment to cause an acute dystonic reaction treatable with anticholinergic drugs, and the ability of pallidotomy or deep brain stimulation of the internal pallidum to alleviate symptoms of generalised dystonia.

Basal Ganglia↗

Parkinson's disease and other basal ganglia or movement disorders in a large nationwide cohort of Swedish welders.

INTRODUCTION: Although it has been hypothesised that metal welding and flame cutting are associated with an increased risk for Parkinson's disease due to manganese released in the welding fume, few rigorous cohort studies have evaluated this risk. METHODS: The authors examined the relation between employment as a welder and all basal ganglia and movement disorders (ICD-10, G20-26) in Sweden using nationwide and population based registers. All men recorded as welders or flame cutters (n = 49,488) in the 1960 or 1970 Swedish National Census were identified and their rates of specific basal ganglia and movement disorders between 1964 and 2003 were compared with those in an age and geographical area matched general population comparison cohort of gainfully employed men (n = 489,572). RESULTS: The overall rate for basal ganglia and movement disorders combined was similar for the welders and flame cutters compared with the general population (adjusted rate ratio (aRR) = 0.91 (95% CI 0.81 to 1.01). Similarly, the rate ratio for PD was 0.89 (95% CI 0.79 to 0.99). Adjusted rate ratios for other individual basal ganglia and movement disorders were also not significantly increased or decreased. Further analyses of Parkinson's disease by attained age, time period of follow up, geographical area of residency, and educational level revealed no significant differences between the welders and the general population. Rates for Parkinson's disease among welders in shipyards, where exposures to welding fumes are higher, were also similar to the general population (aRR = 0.95; 95% CI 0.70 to 1.28). CONCLUSION: This nationwide record linkage study offers no support for a relation between welding and Parkinson's disease or any other specific basal ganglia and movement disorders.

Adult↗

Somatostatin release from isolated ganglia of the myenteric plexus.

Somatostatin neurons of the myenteric plexus project caudad exclusively within the plexus synapsing with neurons in the same or other ganglia. Isolated ganglia offer a unique opportunity to examine peptide transmitter release from these interneurons. Ganglia were isolated from the myenteric plexus by sequential enzymatic digestion, centrifugation, and filtration. Single ganglia were harvested by suction and dispersed in polyacrylamide gel. The ganglia were placed in chambers (200 ganglia/chamber) and perfused with Krebs medium at the rate of 1 ml/min. Addition of the nicotinic agonist, dimethylphenylpiperazinium (DMPP), caused a concomitant increase in somatostatin (152%; P less than 0.001) and vasoactive intestinal peptide (VIP) (79%; P less than 0.05) release above basal level that was abolished by hexamethonium. Addition of the VIP antagonist, VIP-(10-28), (5 microM), to the perfusate augmented significantly DMPP-induced somatostatin release (440%; P less than 0.05), implying that the concomitant release of VIP attenuates somatostatin release. Addition of VIP (1 microM) to the perfusate abolished somatostatin release, confirming the ability of VIP to inhibit somatostatin release. The study shows that VIP interneurons exert a regulatory feedback control over somatostatin interneurons in the myenteric plexus.

Animals↗

Differential expression of substance P, somatostatin, and VIP in neurons from cultured myenteric ganglia.

The expression of three enteric neuropeptides was examined in freshly dispersed ganglia and in ganglia cultured for up to 28 days. During culture, glial cells grew into a flat sheet surrounding a cluster of neurons identified with neuron-specific enolase (13 +/- 2/ganglion), which remained constant throughout the period of culture. The neurons underwent a distinctive temporal change, resulting in overexpression of substance P (SP), normal expression of somatostatin, and virtual suppression of vasoactive intestinal peptide (VIP). Three weeks after the start of culture, the ganglia contained and released (in response to 55 nM KCl, 0.1 mM 1,1-dimethyl-4-phenylpiperazinium, or 1 microM gastrin-releasing peptide) twice as much SP as freshly dispersed ganglia, corresponding to a sevenfold increase per cultured neuron; content and release of somatostatin did not change. SP content and release declined to 1.5% of those found in control cultures when nonneuronal cells were suppressed with cytosine arabinoside but were partially restored (13-17% of control) by nerve growth factor. In marked contrast, VIP was minimally (< 1%) present in and released from ganglia after the third day in culture. Suppression of VIP could reflect a selective loss of VIP neurons and/or VIP expression.

Animals↗

Activation of ETB receptors increases superoxide levels in sympathetic ganglia in vivo.

Dai and colleagues (Dai X, Galligan JJ, Watts SW, Fink GD, and Kreulen DL. Hypertension 43: 1048-1054, 2004) found that endothelin (ET) stimulated O2- production in sympathetic ganglion neurons in vitro by activating ET(B) receptors. The objective of the present study was to determine whether activation of ET(B) receptors in vivo elevates O2- levels in sympathetic ganglia. Because ET(B) receptor activation increases blood pressure, we also sought to determine whether alteration in O2- levels was a direct effect of ET(B) receptor activation on sympathetic ganglia or an indirect consequence of hypertension. Male Sprague-Dawley rats received intravenous infusions of either the specific ET(B) receptor agonist sarafotoxin 6c (S6c; 5 pmol.kg(-1).min(-1)) or isotonic saline at 0.01 ml/min (control) for 120 min. To measure O2- levels, we removed the inferior mesenteric ganglion immediately after infusion and stained it with dihydroethidine (DHE). Mean arterial pressure increased 26.6 +/- 1.7 mmHg in the S6c-treated rats and 3.65 +/- 6 mmHg in control rats. Measurements of average pixel intensity revealed that the DHE fluorescence in ganglionic neurons and surrounding glial cells were 96.7% and 160% greater in S6c-treated than in control rats, respectively. To evaluate the effect of elevated blood pressure on O2- production, a separate group of rats received phenylephrine (PE; 10 mug.kg(-1).min(-1) iv) for 2 h. MAP increased 31 +/- 1.2 mmHg in PE-infused rats. The DHE fluorescence intensity in ganglia of PE-infused rats was significantly greater than that of control rats, 137.7% in neurons and 104.6% in glia but significantly lower than in ganglia from S6c rats. We conclude that ET(B) receptor activation in vivo significantly enhances O2- levels in sympathetic ganglia, due to both pressor effects and direct stimulation of ET(B) receptors in ganglion cells.

Animals↗

Metabolic mapping of a cardiac reflex mediated by sympathetic ganglia in dogs.

The hypothesis tested was that some cardiac reflexes can be mediated by the neural mechanisms in thoracic sympathetic ganglia in addition to those existing in the spinal cord or brain stem. In mongrel dogs anesthetized with pentobarbital sodium the left stellate (SG) and middle cervical (MCG) ganglion were decentralized, and the left thoracic vagosympathetic trunk was cut cranial to the MCG and caudal to the MCG but above the heart. The left thoracic vagosympathetic trunk below the MCG was then stimulated afferently. A single bolus of 2-[14C]deoxyglucose was injected intravenously and the stimuli repeated periodically toward the decentralized ganglia for 45 min. The heart and ganglia were then removed, frozen, and sectioned for autoradiography. Significant increases in glucose utilization were found in both the SG and MCG compared with ganglia from nonstimulated control animals. Significant increases in the glucose utilization of the endocardial third of the left ventricle were also observed in the reflexly stimulated hearts. Neural mechanisms in the acutely decentralized SG and MCG could modify cardiac glucose utilization within specific areas of the heart. In addition, such ganglionic mechanisms may be concentrated within the caudal half of the SG. These data suggest that many neurons in the thoracic autonomic ganglia may be involved in local cardiac reflexes.

Afferent Pathways↗

Rostral ganglia are required for induction but not expression of crayfish escape reflex habituation: role of higher centers in reprogramming low-level circuits.

It is widely assumed that learning results from alterations in the strength of synapses within the neural pathways that mediate a learned behavioral response and that these alterations are directly caused by training-induced activity of neurons connected by the changing synapses. Initial evidence for this view came from studies of habituation of defensive reflexes in several invertebrate species. However, more recent studies of habituation of the escape reflex in one of these species, the crayfish, have shown that habituation is substantially caused by tonic inhibitory input from cephalic ganglia; this descending inhibition suppresses the activity of neurons within the escape circuit, which reside in caudal ganglia. Such control by descending inhibition indicates that animals with encephalized nervous systems do not entirely abdicate to low-level circuitry the important decision of whether to habituate to stimuli that might warn of danger. Higher centers in fact play a major role in controlling the habituation of this potentially life-saving protective response. Another way for higher centers to control lower ones would be to induce alteration of the lower center's intrinsic properties. Here, we show that, whereas descending input from higher ganglia is needed to induce habituation, once established, habituation persists even after rostral ganglia are disconnected. This provides evidence that lower-level neural circuits can be reprogrammed through transient interaction with higher ganglia to decrease their intrinsic tendency to produce escape.

Animals↗