Removal Of Superior Cervical Ganglion Research Articles

Sensory nerve-deficient microenvironment impairs tooth homeostasis by inducing apoptosis of dental pulp stem cells.

ObjectivesThe aim of this study is to investigate the role of sensory nerve in tooth homeostasis and its effect on mesenchymal stromal/stem cells (MSCs) in dental pulp.Materials and methodsWe established the rat denervated incisor models to identify the morphological and histological changes of tooth. The groups were as follows: IANx (inferior alveolar nerve section), SCGx (superior cervical ganglion removal), IANx + SCGx and Sham group. The biological behaviour of dental pulp stromal/stem cells (DPSCs) was evaluated. Finally, we applied activin B to DPSCs from sensory nerve‐deficient microenvironment to analyse the changes of proliferation and apoptosis.ResultsIncisor of IANx and IANx + SCGx groups exhibited obvious disorganized tooth structure, while SCGx group only showed slight decrease of dentin thickness, implying sensory nerve, not sympathetic nerve, contributes to the tooth homeostasis. Moreover, we found sensory nerve injury led to disfunction of DPSCs via activin B/SMAD2/3 signalling in vitro. Supplementing activin B promoted proliferation and reduced apoptosis of DPSCs in sensory nerve‐deficient microenvironment.ConclusionsThis research first demonstrates that sensory nerve‐deficient microenvironment impairs tooth haemostasis by inducing apoptosis of DPSCs via activin B/SMAD2/3 signalling. Our study provides the evidence for the crucial role of sensory nerve in tooth homeostasis.

Role of the ganglioglomerular nerve in response to hypoxia in juvenile rats

The superior cervical ganglion (SCG) sends sympathetic input to the carotid body (CB) via the ganglioglomerular nerve (GGN) in order to modulate carotid sinus nerve (CSN) chemosensory afferent discharge via controlling vascular tone. This chemoafferent discharge is then relayed to the nucleus tractus solitarius (NTS) where the information is processed resulting in a compensatory increase in respiration. Hypoxic gas challenge stimulates the GGN. However, little is known as to the effects of ganglioglomerular nerve transection (GGNx) on carotid body chemosensory afferent response to hypoxia (HX).Our objective was to determine the effect of unilateral GGNx on the ventilatory responses elicited by HX (10% O2, 90% N2) gas challenge (5 episodes of 5 min in duration separated by 15 min) in freely‐moving juvenile (P25) Sprague‐Dawley rats.Male rats postnatal (P) 21 were subjected to sham or unilateral (right or left) GGNx and were allowed 4 days to recover. On the day of the experiment, P25 rats were placed in whole‐body plethysmography chambers and subjected to the hypoxic gas exposure. Ventilatory parameters included frequency of breathing, tidal volume, minute ventilation (= frequency x tidal volume), inspiratory and expiatory times, end inspiratory and expiratory pauses, peak inspiratory and expiratory flows, inspiratory and expiratory drive, EF50 (expiratory flow at 50% expired tidal volume) and rejection index (percentage of abnormal breaths).The HX challenge elicited altered ventilatory responses in sham‐operated rats compared to unilateral GGNx. Rejection Index (%) was diminished in unilateral (left and right) GGNx rats compared to sham, in addition to Rpef in only the right GGNx rats. Peak inspiratory flow (mL/s) was increased in only left GGNx rats, while the peak expiratory flow (mL/s) rates were increased in both the right and left GGNx subjects. Minute ventilation (mL/min) exhibited ventilatory roll‐off in sham animals while no such trend was observed in left GGNx rats. Although peak inspiratory flow, inspiratory drive (mL/s), and expiratory drive (mL/s) reached similar plateaus in right GGNx, the onset of the responses was delayed when compared to their sham counterparts. End expiratory pause (msec) showed a more robust response following hypoxic challenge in right GGNx when viewed against the sham. These findings follow a similar trend to those previously demonstrated from unilateral SCG removal, but still possess characteristics that are unique to the GGN alone. This which suggests the role the SCG has in modulating the hypoxic response is through the GGN and the CB, as well as other yet unknown mechanisms.Support or Funding InformationNIH SPARC 1OT2OD023860‐02 SJLewisThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Superior Cervical Ganglionectomy Affects the Cardiorespiratory Network of the In Situ Arterially Perfused Brainstem Preparation

Recently we found that the superior cervical ganglia projects to the nucleus tractus solitarii. Here, we report the effect of superior cervical ganglionectomy (SCGx) on cardiorespiratory activity in the in situ, arterially perfused brainstem preparation. For these studies, we used male Sprague‐Dawley rat pups (P25). Five days after either bilateral removal of superior cervical ganglia (n=14) or sham surgery (n=14), we recorded efferent activities of the phrenic nerve, cervical vagus nerve, and thoracic sympathetic chain and monitored heart rate and perfusion pressure. Baseline cardio‐respiratory patterns were recorded for 10 min to assess differences in patterning between the SCGx and sham groups. Then, we evoked the peripheral chemoreceptor reflex by injecting (intra‐arterially) sodium cyanide (100 μL of a 0.03% solution) and the baroreceptor reflex by increasing perfusion pressure (increasing the speed of the roller pump to its maximum). Baseline respiratory frequency was similar in the SCGx and sham group. However, the SCGx group had a greater but delayed response to chemoreceptor stimulation. Similarly, the SCGx group had a greater response to baroreceptor stimulation. Baseline heart rates (HR) were similar in both groups. For the SCGx group, HR decreased less than sham group during chemoreceptor stimulation; but, decreased more than the sham group during baroreceptor stimulation. Finally, the SCGx group required a greater perfusion pressure (PP) than the sham group during baseline; and had smaller increase in PP during chemoreceptor stimulation. These data indicate that superior cervical ganglia modulate vasomotor tone at rest and buffer cardio‐respiratory responses to chemoreceptor and baroreceptor reflexes.Support or Funding InformationNIH‐SPARC 1OT2OD023860‐02SJLewisThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Evidence For a Central Pathway in the Cerebrovascular Effects Of Spinal Cord Stimulation

Cervical spinal cord stimulation (SCS) augments cerebral blood flow (CBF) in a number of animal models. The mechanisms underlying the cerebrovascular effects of SCS are not yet well delineated. In this study, we analyzed two alternative pathways in CBF alterations induced by SCS in rats, one involving direct modulation of sympathetic outflow and the other through central vasomotor influence. Resection of the superior cervical ganglion (SCG), SCS alone, or SCS after SCG removal was performed in adult male Sprague-Dawley rats. CBF was measured with (14)C-inosine monophosphate radiotracer studies. In another set of experiments, SCS was performed after spinalization at the cervicomedullary junction or after laminectomy alone. Baseline CBF in the SCG removal group was 71 +/- 8 ml/100 g/min, similar to controls. SCS alone significantly increased blood flow to 100 +/- 10 ml/100 g/min (P < 0.05). Animals that underwent SCS after SCG removal demonstrated a similar robust augmentation in CBF. SCS-induced changes in CBF were completely attenuated by spinalization. The profound effects of spinal cord transection on SCS-induced CBF augmentation, together with the lack of effect of surgical sympathectomy, suggest that the mechanisms underlying the effects of SCS involve central influences rather than cervical sympathetic outflow. These findings suggest a possible role for brainstem vasomotor centers in the cerebrovascular effects of SCS.

Alterations in sympathetic ganglionic transmission in response to angiotensin II in (mRen2)27 transgenic rats.

Hypertension in (mRen2)27 transgenic rats is partly dependent on activation of the sympathetic nervous system, but the role of ganglionic transmission is unknown. We assessed indices of synaptic plasticity (post-tetanic short-term potentiation [PTP] and long-term potentiation [LTP]) and sympathetic ganglionic transmission without tetany in superior cervical ganglia (SCG) of Hannover Sprague-Dawley rats (HnSD) versus (mRen2)27 rats. There were no differences in decay time constants [PTP=9 minutes; LTP=120 to 150 minutes in both (mRen2)27 and HnSD]. However, angiotensin (Ang) II increased PTP and LTP in SCG isolated from (mRen2)27 rats to a greater extent than HnSD. Candesartan (an AT1 antagonist) blocked the potentiation in both groups. Without a preceding tetanic pulse, 16-nM Ang II induced similar significant increases in ganglionic transmission of approximately 14% in both strains. Assessment of Ang II receptors by 125I-[Sar1Thr8]-Ang II binding showed that the AT1-receptor subtype predominates in the ganglia. The density of receptors in the SCG was comparable in (mRen2)27 and HnSD rats, whether measured in tissue from ganglia removed and frozen versus ganglia used in the transmission testing, suggesting that upregulation of receptors in vitro after removal of SCG did not occur. The divergence of effects of Ang II on LTP and PTP [greater in (mRen2)27 than HnSD] and nontetany ganglionic transmission (similar in both strains) may reflect different locations of receptors (pre- versus postsynaptic) or different signaling mechanisms involved in the two responses. We suggest that functional Ang II receptors in SCG mediate physiological actions of Ang II on ganglionic transmission and may play a pivotal role in hypertension.

Removal of the superior cervical ganglia fails to block Fos induction in the accessory olfactory system of male mice after exposure to female odors

When exposed to female odors, testosterone-primed male mice show a robust expression of immediate early genes in the vomeronasal organ (VNO) and associated accessory olfactory structures. We asked whether the superior cervical ganglia (SCG), which provide autonomic inputs to the VNO, are required for odor induction of Fos. Gonadally intact male mice received sham, unilateral, or bilateral SCG lesions and were exposed to odors from estrous females. In comparison to clean bedding, female odors significantly increased neuronal Fos immunoreactivity in sites throughout the VNO projection pathway, but these responses were not reliably modified by SCG removal. Thus, noradrenergic inputs to the VNO, which regulate a pumping mechanism thought to facilitate entrance of chemosignals into the VNO lumen, are not required for odors to induce Fos in the mouse accessory olfactory system.

Suprachiasmatic control of melatonin synthesis in rats: inhibitory and stimulatory mechanisms.

The suprachiasmatic nucleus (SCN) controls the circadian rhythm of melatonin synthesis in the mammalian pineal gland by a multisynaptic pathway including, successively, preautonomic neurons of the paraventricular nucleus (PVN), sympathetic preganglionic neurons in the spinal cord and noradrenergic neurons of the superior cervical ganglion (SCG). In order to clarify the role of each of these structures in the generation of the melatonin synthesis rhythm, we first investigated the day- and night-time capacity of the rat pineal gland to produce melatonin after bilateral SCN lesions, PVN lesions or SCG removal, by measurements of arylalkylamine N-acetyltransferase (AA-NAT) gene expression and pineal melatonin content. In addition, we followed the endogenous 48 h-pattern of melatonin secretion in SCN-lesioned vs. intact rats, by microdialysis in the pineal gland. Corticosterone content was measured in the same dialysates to assess the SCN lesions effectiveness. All treatments completely eliminated the day/night difference in melatonin synthesis. In PVN-lesioned and ganglionectomised rats, AA-NAT levels and pineal melatonin content were low (i.e. 12% of night-time control levels) for both day- and night-time periods. In SCN-lesioned rats, AA-NAT levels were intermediate (i.e. 30% of night-time control levels) and the 48-h secretion of melatonin presented constant levels not exceeding 20% of night-time control levels. The present results show that ablation of the SCN not only removes an inhibitory input but also a stimulatory input to the melatonin rhythm generating system. Combination of inhibitory and stimulatory SCN outputs could be of a great interest for the mechanism of adaptation to day-length (i.e. adaptation to seasons).

In vivo observation of a non-noradrenergic regulation of arylalkylamine N-acetyltransferase gene expression in the rat pineal complex

The rodent pineal gland is the end point of several peripheral and central fibers innervating the superficial and deep parts of the gland. Up to now, only the sympathetic transmitter norepinephrine is thought to regulate melatonin synthesis, although numerous biochemical experiments have reported in vitro effects of various transmitters on melatonin synthesis. To find out whether there is non-noradrenergic regulation of in vivo pineal metabolism, the mRNA encoding the enzyme arylalkylamine N-acetyltransferase was studied using the highly sensitive technique of in situ hybridization. The existence of a marked nocturnal increase of arylalkylamine N-acetyltransferase mRNA in the superficial pineal gland was confirmed. Interestingly and for the first time, a similar daily variation was observed in the deep pineal. After removal of superior cervical ganglia, the daily rhythm in arylalkylamine N-acetyltransferase mRNA was abolished in both the superficial and deep pineal indicating that the rhythm is driven by sympathetic input in the entire pineal complex. Interestingly, the remaining arylalkylamine N-acetyltransferase mRNA level in the pineal of day- and night-time ganglionectomized rats was significantly higher than in the pineal of day-time intact animals. These data reveal a sympathetic-dependent day-time inhibition of arylalkylamine N-acetyltransferase gene expression. In addition, the day-time pineal arylalkylamine N-acetyltransferase mRNA expression in ganglionectomized rats persisted after adrenal gland removal but was reduced by 50% after propranolol injection. These results indicate that arylalkylamine N-acetyltransferase mRNA in ganglionectomized rats is not induced by circulating catecholamines and may be caused by both a centrally originated norepinephrine, as already suggested, and other non-adrenergic transmitter(s). In conclusion, this work shows that norepinephrine drives the nocturnal increase of arylalkylamine N-acetyltransferase gene expression both in the superficial and deep pineal and strongly suggests that other neurotransmitters are involved in day-time inhibition and night-time stimulation of pineal metabolism.

LOCALIZATION OF DOPAMINE RECEPTOR SUBTYPES IN SYSTEMIC ARTERIES

Dopamine D1-D5 receptor protein immunoreactivity was investigated in different sized pial, renal and mesenteric artery branches using immunohistochemical techniques and anti-dopamine D1-D5 receptor protein antibodies. Faint dopamine D1 receptor protein immunoreactivity was observed in smooth muscle of tunica media of pial, renal and mesenteric artery branches. Dopamine D2 receptor protein immunoreactivity was located in the adventitia and adventitia-media border of pial and renal artery branches and to a lesser extent of mesenteric artery branches. No dopamine D3 receptor protein immunoreactivity was observed in pial and mesenteric arteries. In renal arteries a moderate dopamine D3 receptor immunoreactivity was detectable in the adventitia and adventitia-media border. A strong dopamine D4 receptor protein immunoreactivity displaying the same localization of dopamine D2 receptor protein was observed in pial and mesenteric arteries, but not in renal artery branches. Moderate dopamine D5 receptor protein immunoreactivity was observed in smooth muscle of the tunica media of pial, renal and mesenteric artery branches.Bilateral removal of superior cervical ganglia, from which sympathetic supply to cerebral circulation originate abolished dopamine D2 and D4 receptor protein immunoreactivity in pial arteries but was without effect on dopamine D1 and D5 receptor protein immunoreactivity. These findings indicate that systemic arteries express dopamine D1-like (D1 and D5) and D2-like (D2, D3 and D4) receptor subtypes displaying respectively a muscular (postjunctional) and prejunctional localization. The specific distribution of dopamine D2-like receptor subtypes in systemic arteries suggests that they may have a different role in regulating blood flow through the vascular beds investigated.

Cervical gangliectomy does not affect in vitro trytophan hydroxylase activity in rat brain base arteryes

The presence of a serotonergic innervation in rat cerebral arteries of peripheral origin was explored. Superior cervical ganglia removal did not change tryptophan hydroxylase activity measured in cell-free extracts of brain base vessels. A low enzyme activity was detected in the ganglia. These results suggest that rat cerebral arteries do not receive a serotonergic innervation from the superior cervical ganglia.

In vivo tryptophan hydroxylase activity in rat major cerebral arteries is decreased by dorsal raphe nucleus lesions.

The in vivo presence of tryptophan hydroxylase activity in rat major cerebral arteries as well as the possible origin of the structure containing it were explored. Enzyme activity was appraised by accumulation of 5-hydroxytryptophan after inhibition of aromatic L-amino acid decarboxylase. Decarboxylase inhibition evoked a significant increase in 5-hydroxytryptophan levels in rat cerebral arteries, striatum, hippocampus, hypothalamus, and plasma but had no effect on aorta. p-Chlorophenylalanine reduced 5-hydroxytryptophan accumulation in the cerebral vessels and brain nuclei, whereas alpha-methyltyrosine did not modify it except in hypothalamus, where it was enhanced. alpha-Methyltyrosine significantly reduced noradrenaline levels in cerebral arteries and L-dopa accumulation after inhibition of the decarboxylase in striatum. Dorsal raphe nucleus lesioning significantly diminished 5-hydroxytryptophan formation in cerebral arteries, striatum, and hypothalamus, without affecting it in hippocampus. Lesion of median raphe nucleus reduced 5-hydroxytryptophan accumulation in hippocampus and in hypothalamus but not in cerebral blood vessels or striatum. Superior cervical ganglia removal decreased noradrenaline levels in cerebral blood vessels without affecting 5-hydroxytryptophan accumulation. These results indicate the presence of a functionally active tryptophan hydroxylase in rat cerebral arteries associated with fibers originating from dorsal raphe nucleus. This supports that rat major cerebral arteries receive serotonergic innervation from central origin.

Changes in mediobasal hypothalamic dopamine and indoleamine metabolism after superior cervical ganglionectomy of rats.

Eight days after bilateral superior cervical ganglionectomy (Gx) of rats, norepinephrine content of medial basal hypothalamus (MBH) decreased significantly by 44-50%. To obtain information on other possible neurochemical sequela of Gx in MBH, we examined the metabolism of dopamine and serotonin in MBH of Gx rats by employing a high pressure liquid chromatography procedure. Eight days after Gx, MBH dopamine levels augmented significantly. Assessment of dopamine metabolism by measuring dihydroxyphenylacetic acid (DOPAC)/dopamine and homovanillic acid (HVA)/dopamine indexes indicated a significant decrease of MBH DOPAC/dopamine ratio after Gx. MBH serotonin levels increased, and 5-hydroxyindoleacetic acid (5-HIAA)/serotonin index decreased significantly in Gx rats. To examine the interaction Gx-induced changes on MBH dopamine and serotonin with the modified hormonal milieu produced by an ectopic pituitary transplant, adult male rats bearing an ectopic pituitary within the pectoral muscles from day 5 of life were submitted to Gx on day 60 of life and were studied 8 days later. MBH dopamine content increased significantly after pituitary grafting, an effect counteracted by a subsequent Gx, while Gx alone augmented MBH dopamine levels. DOPAC and HVA contents augmented in pituitary-grafted animals, an effect counteracted by Gx. Gx increased MBH serotonin content in control but not in pituitary-grafted rats. After pituitary grafting a decrease in MBH 5-HIAA levels was found, an effect reversed by Gx. Pituitary transplants brought about a significant increase of MBH DOPAC/dopamine index, and a significant decrease in 5-HIAA/serotonin index, both effects being counteracted by Gx. Gx of control rats resulted in a significant decrease of MBH 5-HIAA/serotonin index. Analyzed as a main effect in a factorial analysis of variance, Gx decreased MBH DOPAC/dopamine and HVA/dopamine indexes significantly. Plasma prolactin increased in pituitary-grafted rats, an effect further increased by a subsequent Gx. In pituitary-grafted, Gx rats plasma GH levels augmented significantly. The data suggest that superior cervical ganglion removal affects differentially dopamine and indoleamine metabolism in MBH of control and pituitary-grafted rats.

Alterations in α-adrenoceptors in aging intraocular hippocampal grafts

Age-related changes of hippocampal α 1- and α 2-adrenoceptors were investigated using intraocular hippocampal transplants combined with 3H-prazocin and 3H-para-aminoclonidine ( 3H-PAC) autoradiography. Young hippocampal grafts in young hosts and old grafts in old hosts innervated by noradrenergic sympathetic fibers were studied. In addition, young and old hippocampal grafts were examined following noradrenergic denervation by superior cervical ganglion removal. The 3H-PAC binding was significantly reduced in aged grafts as compared to young grafts whereas the 3H-prazocin binding did not change with age. After sympathetic denervation, both 3H-PAC and 3H-prazocin binding increased significantly in young grafts. In aged adrenergically denervated grafts, α 2-receptor binding was again significantly reduced whereas α 1-receptor binding was not significantly different from that in young denervated grafts. Taken together, these results indicate a selective age-related reduction in hippocampal postsynaptic α 2-receptors which is intrinsically determined.

Effects of neonatal removal of superior cervical ganglion on serotonin and thyrotropin-releasing hormone immunoreactivity in the intermediolateral cell column of the rat spinal cord.

In this study, we investigated the effects of the neonatal removal of the right superior cervical ganglion on the serotonin-like and thyrotropin-releasing-hormone-like immunoreactivities (5-HT-LI and TRH-LI) in the intermediolateral cell column (IML) of the spinal cord by quantitative image analysis. Two weeks after the lesion, we observed a 60% reduction in 5-HT-LI, while TRH-LI was not significantly reduced, in the right IML (lesioned side) at T1-2 levels. One month after the lesion, 5-HT-LI and TRH-LI were significantly reduced by 60% in the right IML at T1-2 levels. After 3 months, this decrease persisted at this level. In addition, we observed a 30% loss of the 5-HT-LI in the right IML at T3-4 levels, whereas TRH-LI did not decrease significantly at T3-4 levels. These findings are discussed and compared with those of other experimental studies on serotonergic reorganization in the rat spinal cord.

Short-day stimulation of testicular activity and immunoreactivity of the hypothalamic GnRH system in mink following deafferentation of the pineal body by bilateral superior cervical ganglionectomy and melatonin replacement

The effects of superior cervical ganglionectomy on testicular function (testis volume and plasma testosterone levels) and the immunocytochemical activity of the GnRH hypothalamic system were studied in the mink, a short-day breeder. Animals reared in a natural photo-period were (i) ganglionectomized at four different times during the period extending from the end of summer to the end of autumn (September 15, October 20, October 28, and December 1), and (ii) reared for 50 days in a short gonadostimulatory photoperiod (4L:20D). Lastly, an attempt was made to overcome the effects of superior cervical ganglion removal by administering melatonin to mink reared in a natural photoperiod. In mink reared in a natural photoperiod, deafferentation of the pineal on September 15 ( L= 12.5h) or October 20 ( L= 10.5h) resulted in consistently low values of testicular volume and plasma testosterone until the end of the experiment (February). When the operation was performed on October 28 ( L= 10h) testicular activity was initiated but only lasted a short time and did not allow maximal gonadal development. When superior cervical ganglionectomy was carried out on December 1 ( L= 8.5h), during the phase of renewed testicular activity, the increases in testicular volume and testosterone levels were not affected by the operation and the subsequent variation of these parameters was identical to that observed in intact animals. Similarly, in mink reared for 50 days in a photoperiod of 4L:20D before superior cervical ganglionectomy, deafferentation of the pineal did not prevent gonadostimulation induced by short days. These results show that once the hypothalamic system secreting GnRH is triggered by short days, its activity is no longer controlled by the photoperiod. The immunohistochemical study of GnRH-secreting hypothalamic neurons, carried out in December without prior colchicine treatment in animals ganglionectomized in September or October, showed the presence of only a small number of GnRH-positive perikarya. Similarly, positive axonal endings in the external layer of the median eminence were scarce and weakly immunoreactive. On the other hand, in intact animals, in those ganglionectomized on December 1, and those exposed to the short photoperiod of 4L:20D, perikarya and immunoreactive endings were numerous and intensely labeled. In mink ganglionectomized in October ( L= 10.5h) and thereby maintained in a phase of sexual quiescence, insertion of melatonin implants in January triggered testicular activity 50 days later.

Nerve growth factor and septal grafts: a study of behavioral recovery following partial damage to the septum in rats

Previous studies have produced conflicting results about the effects of intracerebral injection of NGF after septal damage in rats: in one experiment, behavioral deficits in maze tasks were exacerbated by NGF administration whereas they were alleviated in another one. The present investigation aimed to clarify the effects of NGF and to identify factors liable to induce different behavioral outcomes. Behavioral effects were assessed following a postsurgical delay of five months using various parameters: food consumption in a novel environment, spontaneous activity, locomotion in an open-field, immobility in a tail suspension test, spontaneous alternation in a T-maze and performance in a radial eight-arm maze. Possible influence of intrahippocampal sympathetic fiber ingrowth occurring after septal lesions was ruled out, as the comparison of rats subjected to superior cervical ganglia removal with their lesion-control counterparts showed few behavioral differences, even after NGF administration. All lesioned rats showed reduced adaptability in most of these tests. Grafts partially reversed the lesion-induced deficit in spontaneous alternation. A single intracerebral NGF injection was found to ameliorate radial maze performance, whether rats were grafted or not. However, it appeared that the number of strategies available to NGF-rats in the radial maze task was as limited as for lesion-control rats. These findings suggest that NGF-rats do not recover spatial abilities lost after septal lesions, but are able to make more efficient use of remaining capacities to master the maze task.

Sympathectomy provides evidence of dopamine storage in rat laryngeal nerve paraganglia.

Catecholamine content in the recurrent and superior laryngeal nerves (RLN and SLN) of the rat was analysed by high-performance liquid chromatography after surgical and chemical sympathectomy. Sympathectomy induced by repeated injections of guanethidine did not lead to any change in the dopamine (DA) level, whereas the noradrenaline (NA) content decreased by 68% and 64% respectively in the RLN and SLN. Surgical excision of the superior cervical ganglion (SCG) did not alter the level of DA in the SLN, but caused a 60% decrease of DA in the RLN. Removal of SCG did not affect the NA levels either in the RLN or in the SLN, unless it was combined with extirpation of the middle cervical ganglion, which induced a decrease in NA in both nerves. The results indicate that much of the DA in the laryngeal nerves is stored outside the sympathetic nerve fibres, probably in the small organs earlier characterized as endoneurial paraganglia.

Nerve growth factor protein level increases in the adult rat hippocampus after a specific cholinergic lesion.

Nerve growth factor (NGF) is the best-characterized neurotrophic substance and has recently been shown to influence cholinergic neurons in the basal forebrain. Hippocampus and neocortex, the primary targets for these central neurons, have further been found to contain high levels of NGF. Using enzyme immunoassay and acetylcholine esterase (AChE) histochemistry we have now studied the levels of NGF and AChE after a specific cholinergic lesion, transection of the fimbria fornix comprising the major cholinergic input to hippocampus. Fimbriectomy in adult rats led to a marked decrease in AChE-positive nerve terminals in both hippocampus and neocortex 10 days later, and to an increase (40%) of NGF protein concentration in hippocampus. thirty days after surgery, NGF had returned to control levels and remained there after 90 days. Removal of superior cervical ganglion did not alter the results. The density of cholinergic terminals in both hippocampus and neocortex increased with time (90 days) after fimbrial transection. The results support the idea that cholinergic neurons in the basal forebrain take up and retrogradely transport NGF from their target areas and suggest that transection of the pathway interrupts the transport thereby increasing NGF distal to the lesion. The return of NGF to control levels probably reflects reestablished cholinergic contracts in the hippocampus.

Recovery of spatial alternation deficits following selective hippocampal destruction with kainic acid.

Elimination of hippocampal CA3 and CA4 pyramidal cells with kainic acid (KA) induces a performance deficit on a forced-choice alternation task, which recovers over time. In order to determine whether superior cervical ganglion (SCG) fibers sprouting into the hippocampus contribute to behavioral recovery, 31 Sprague-Dawley rats were first trained on a forced-choice task. After reaching criterion performance levels, animals received either KA or saline injections into the hippocampus and were again tested on the forced-choice task. Half of the rats had their SCG removed 35 days after injections, and all were again tested on the forced-choice task. Analysis of variance showed animals receiving KA took significantly longer to reach criterion following injections. Removal of the SCG after recovery reintroduced the performance deficit of KA-treated rats on the alternation task; no other group showed any effect for SCG removal. Results are interpreted as indicating that the SCG may have a modulatory effect in behavioral recovery, although other mechanisms may also be operating.

Neuropeptide Y innervation of the rodent pineal gland and cerebral blood vessels

Neuropeptide Y (NPY)-immunoreactivity has been shown to be present in sympathetic nerve fibres in the rat pineal gland and a dense network of NPY-containing nerve fibres demonstrated to innervate the rat circle of Willis. The NPY content of the major rabbit intracranial arteries was determined by radioimmunoassay and maximal levels found in the anterior cerebral arteries. After bilateral superior cervical ganglion (SCG) removal, no NPY was detectable in the rat pineal gland; however, significant NPY-immunoreactive nerve fibres remained throughout the rat vertebrobasilar arteries, and 47% of the assayable NPY was still present. Neither intraventricular 6-hydroxydopamine (6-OHDA) nor the combination of 6-OHDA treatment and SCG removal resulted in any further loss of NPY. In conclusion, the NPY innervation of the pineal gland originates exclusively from the peripheral sympathetic nervous system. In contrast the caudal portion of the rat circle of Willis contains NPY fibres which are resistant to sympathectomy.