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PubMed1996

Enkephalin terminals form inhibitory-type synapses on neurons in the rat nucleus locus coeruleus that project to the medial prefrontal cortex.

Norepinephrine-containing fibres in the medial prefrontal cortex derive from the locus coeruleus, a brainstem nucleus which also receives a dense innervation of enkephalin-immunoreactive axon terminals. We combined immunogold-silver labelling of retrogradely transported FluoroGold from the medial prefrontal cortex with immunoperoxidase detection of leucine5-enkephalin in the same section of tissue through the locus coeruleus of adult rats. This dual-labelling experiment was conducted to determine whether axon terminals containing lecuine5-enkephalin target neurons in the locus coeruleus that project to the frontal cortex and, if so, what are their morphological characteristics. By light microscopy, enkephalin-labelled processes overlapped FluoroGold retrogradely labelled neurons in the locus coeruleus. By electron microscopy, retrogradely labelled perikarya and dendrites were commonly enveloped by astrocytic processes and received few afferents in the plane of section examined. However, at sites unoccupied by glial processes, abundant afferent input could be identified. In addition, some FluoroGold-labelled perikarya and dendrites lacked this glial ensheathment but were more frequently apposed by axon terminals. Of 163 FluoroGold-labelled perikarya and dendrites examined where enkephalin immunoreactivity was present in the neuropil, 42% were contacted by enkephalin-immunoreactive axon terminals. The peroxidase-labelled enkephalin terminals as well as the unlabelled terminals often contained both small, clear and large dense core vesicles. Both labelled and unlabelled terminals also formed primary symmetric synapses characteristic of inhibitory transmitters with retrogradely labelled perikarya and proximal dendrites. At times, more than one enkephalin-labelled terminal was found to converge on a common retrogradely labelled perikarya or dendrite. These results demonstrate cellular sites where enkephalin-containing afferents may directly modulate and most likely inhibit the activity of cortically projecting neurons in the locus coeruleus.

Animals↗
PubMed1980

Growth interaction between locus coeruleus and trigeminal ganglion after intraocular double grafting.

Fetal trigeminal ganglia were combined in the anterior chamber of eyes of rat recipients with sequentially grafted fetal locus coeruleus transplants. After maturation of both grafts in oculo the growth pattern of locus coeruleus derived noradrenaline fibres in the iris was examined with Falck-Hillarp fluorescence histochemistry. Contrary to what was expected from earlier studies, which revealed a radiating halo of fibres around the CNS tissue on the iris, the locus coeruleus-derived fibres radiated to a large extent from the adjacent trigeminal ganglion attachment. Thus, the presence of a grafted trigeminal ganglion changed the distribution of the central monoamine nerves growing out in the iris. The possible cause of this changed distribution is discussed. Maturated intraocular trigeminal ganglion transplants were retransplanted, together with the whole iris to which it was attached, into a new eye which already harboured a maturated locus coeruleus graft attached to its host iris. The expected reinitiated locus coeruleus fibre ingrowths into the iris transplants were then compared in those iris transplants that had trigeminal ganglia and controls that had not. The surface area of the iris grafts covered by newly formed locus coeruleus noradrenaline fibres was significantly smaller (27% reduction) if trigeminal ganglia were situated on them during the reinnervation process. This finding strongly supports our earlier studies, which suggested that the presence of sensory nerves in the iris inhibits growth of locus coeruleus in that receptor tissue, and furthermore, that the sensory nerves responsible for this inhibitory interaction have their origin within the trigeminal ganglion itself.

Adrenergic Fibers↗
PubMed1995

Hypoxic changes in rat locus coeruleus neurons in vitro.

1. Intracellular recordings were made in a pontine slice preparation of the rat brain containing the nucleus locus coeruleus (LC). Locus coeruleus neurons responded to brief hypoxic stimuli (replacement of 95% O2-5% CO2 with 95% N2-5% CO2) with hyperpolarization and a cessation of spontaneous action potentials. When the cells were continuously hyperpolarized by about 15 mV in order to abolish spontaneous firing, hypoxia induced an early depolarization (HD), followed by a hypoxic hyperpolarization (HH) and after reoxygenation, a posthypoxic hyperpolarization (PHH). These responses were accompanied by a decrease in input resistance, which was larger during HH than during HD but, thereafter, became smaller during PHH. 2. The hypoxia-induced currents associated with the changes in membrane potential, at a holding potential of -70 mV, were an early inward current (HIC), a subsequent outward current (HOC) and after reoxygenation, another outward current (PHOC). The HIC did not change with an increasing holding potential. In contrast, the HOC reversed its amplitude at about -95 mV. Finally, the PHOC decreased, but did not reverse its polarity at more negative holding potentials. When the external K+ was elevated from 2.5 to 10.5 mM, the current-voltage (I-V) relation of the HOC and its reversal potential were shifted to the right. 3. In the presence of tetrodotoxin, the HH decreased. A low Ca(2+)-high Mg2+ medium depressed both the HH and PHH. Rauwolscine did not alter either response to hypoxia, while 8-cyclopentyl-1,3-dipropylxanthine decreased the PHH only. S-(p-Nitrobenzyl)-6-thioguanosine potentiated both HH and PHH. 4. Whereas tolbutamide markedly lowered the HH and PHH, glibenclamide was ineffective. Tetraethylammonium also failed to alter the hypoxic responses. Furthermore, ouabain or the removal of K+ from the superfusion medium, depressed PHH. 5. Pressure application of adenosine inhibited the spontaneous firing of LC neurons. DPCPX did not alter the firing, but antagonized the effect of adenosine. Tolbutamide also counteracted the inhibitory effect of adenosine and, additionally, facilitated the firing rate in some neurons. Moreover, tolbutamide abolished the adenosine-induced outward current. 6. Early hypoxic depolarization and PHH are mostly due to the blockade and subsequent reactivation of the K(+)-Na+ pump, respectively. The HH is caused by the opening of ATP-sensitive K+ (KATP) channels in response to the hypoxia-induced decline of intracellular ATP. Adenosine released by hypoxic stimuli may lead to an adenosine A1-receptor-mediated opening of (KATP) channels during the HH and more markedly during the PHH.

Adenosine↗
PubMed1994

Effects of somatostatin-28 on rat locus coeruleus neurons.

The effects of somatostatin-28 (SS-28) on rat locus coeruleus (LC) neurons were investigated with techniques of brain slice and intracellular recording. SS-28 was applied by micropressure ejection through a micropipette. SS-28 (500 microM, 10 or 20 psi, 1 msec - 5 sec) reversibly decreased the firing rate of all neurons of the locus coeruleus tested. In addition to inhibition of spontaneous firing, larger concentrations of SS-28 also hyperpolarized the neurons of the locus coeruleus and simultaneously decreased the input resistance. At the greatest concentration (20 psi x 5sec) applied, SS-28 produced complete inhibition of firing of all neurons tested; the inhibition was associated with a 11-mV hyperpolarization and decreased input resistance 9 percent. The voltage-current relationship of the resting cell revealed an inward-going rectification that became enhanced after the pressure application of SS-28. The reversal potential for the SS-28-induced hyperpolarization was -116 mV, which is approximately the potassium equilibrium potential. The results also showed that BaCl2 blocked the SS-28-induced hyperpolarization, but apamin did not. We conclude that the inhibitory actions of SS-28 are due to opening the inward-going rectification potassium channels and that SS-28 and somatostatin-14 exert similar electrophysiological actions on LC neurons.

Animals↗
PubMed2003

Attenuation of acute and chronic effects of morphine by the imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline in rat locus coeruleus neurons.

1 The aim of this study was to determine if 2-(2-benzofuranyl)-2-imidazoline (2-BFI) interacts with the opioid system in the rat locus coeruleus, using single-unit extracellular recordings. 2 In morphine-dependent rats, acute administration of the selective imidazoline receptor ligands 2-BFI (10 and 40 mg kg(-1), i.p. and 100 micro g, i.c.v.) or valldemossine (10 mg kg(-1), i.p.) did not modify the naloxone-induced hyperactivity of locus coeruleus neurons compared with that observed in the morphine-dependent control group. 3 After chronic administration of 2-BFI (10 mg kg(-1), i.p., three times daily, for 5 days) and morphine, naloxone-induced hyperactivity and tolerance to morphine were attenuated. This effect was not observed when a lower dose of 2-BFI (1 mg kg(-1), i.p.) or valldemossine (10 mg kg(-1), i.p.) were used. 4 Acute administration of 2-BFI (10 and 40 mg kg(-1), i.p. and 100 micro g, i.c.v.) but not valldemossine (40 mg kg(-1), i.p.) diminished the potency of morphine to inhibit locus coeruleus neuron activity in vivo (ED(50) values increased by 2.3, 2.9; and 3.1 fold respectively). Similarly, the potency of Met(5)-enkephalin to inhibit locus coeruleus neurons was decreased when 2-BFI (100 micro M) was applied to rat brain slices (EC(50) increased by 5.6; P<0.05). 5 The present data demonstrate that there is an interaction between 2-BFI and the opioid system in the locus coeruleus. This interaction leads to an attenuation of both the hyperactivity of locus coeruleus neurons during opiate withdrawal and the development of tolerance to morphine when 2-BFI is chronically administered. These results suggest that imidazoline drugs may prove to be useful agents for the management of opioid dependence and tolerance.

Animals↗
PubMed1984

The effects of protein deprivation on the nucleus locus coeruleus: a morphometric Golgi study in rats of three age groups.

In a previous morphometric Golgi study of the nucleus locus coeruleus we identified in rats fed a 25% casein diet 3 cell types, fusiform, multipolar and ovoid, and compared their age-related changes from 30 to 90 days and 90 to 220 days. In the present study we investigated the effects of an 8% casein diet, initiated prenatally and continued postnatally in the pups, using the same morphometric parameters at the same 3 ages. In these rats the majority of significant age-related changes were in primary and secondary dendritic spine density. On all 3 cell types between 30 and 90 days there was a decreased spine density followed by an increase between 90 and 220 days. These age-related changes closely followed those in controls and, as a result, when the two diet groups were compared at each age they showed only 4 significant differences out of 18 comparisons. In control rats these age-related changes in dendritic spine density in the nucleus locus coeruleus were diametrically out-of-phase with those found in the nucleus raphe dorsalis in a previous study. This is consistent with the postulated mutual inhibitory relationship between the nucleus locus coeruleus and nucleus raphe dorsalis. Comparison of these same events in the nucleus locus coeruleus and nucleus raphe dorsalis in the 8% casein diet rats show no evidence of an out-of-phase relationship. Thus, the relationship between these two closely related nuclei appears to be fundamentally altered by the 8% casein diet. In these comparisons of dendrite spine density and other parameters the 8% casein diet rats have shown in both the nucleus locus coeruleus and nucleus raphe dorsalis deficits and increases as compared to controls. In contrast, in morphometric Golgi studies of pyramidal and Purkinje cells undernutrition generally results in deficits or little change in the various parameters. This suggests that the adaptation of the non-pyramidal neurons in the present study is different from that shown by pyramidal and Purkinje cells.

Age Factors↗
PubMed1989

In vivo degradation of noradrenaline by MAO A in locus coeruleus of the rat.

Depletion of noradrenaline in locus coeruleus neurons after reserpinization was prevented by clorgyline, a selective inhibitor of MAO A, but not by deprenyl, a selective inhibitor of MAO B. Only MAO A is therefore responsible for the degradation of homoneuronal noradrenaline in locus coeruleus nerve cells.

Animals↗
PubMed1986

Role of vasopressin in the cardiovascular response to stimulation of the locus coeruleus.

Hypothalamic vasopressin synthesizing nuclei (paraventricular and supraoptic) send vasopressin-containing projections to a number of neural target areas thought to be involved in cardiovascular regulation. One area known to receive vasopressinergic projections from the paraventricular nucleus is the pontine nucleus locus coeruleus. To examine the possible functional participation of vasopressin in central cardiovascular regulation, we examined mean arterial pressure (millimeters of Hg) and heart rate (beats per min) responses to electrical stimulation of the locus coeruleus in conscious, unrestrained vasopressin-deficient Brattleboro rats homozygous for diabetes insipidus (DI rats) and long Evans (LE) rats. Rats received chronic arterial and venous catheters and bipolar stimulating electrodes 3-5 days before experiment. Stimulation of the locus coeruleus (100 microA, 10-40 Hz) produced frequency-dependent increases in mean arterial pressure and heart rate in LE and DI, but the responses were significantly less in the latter group. The deficiency in mean arterial pressure and heart rate responses to locus coeruleus stimulation in DI rats was found to be centrally mediated in that responses to peripherally administered phenylephrine were the same as those for LE rats. Ganglionic blockade significantly attenuated responses to locus coeruleus stimulation in LE rats but had little effect in DI rats. Pretreatment of DI rats with chronic intracerebroventricular infusion of vasopressin (osmotic minipump) at a dose that had no effect peripherally increased the mean arterial pressure and heart rate responses to locus coeruleus stimulation. Our results suggest that vasopressin acts in the region of the locus coeruleus to exert a central action on sympathetic outflow.

Animals↗
PubMed1997

Carbon dioxide regulates the tonic activity of locus coeruleus neurons by modulating a proton- and polyamine-sensitive inward rectifier potassium current.

The electrophysiological effects of CO2 on locus coeruleus noradrenergic neurons were investigated in rat brain slices. Under control conditions, when slices were perfused with artificial cerebrospinal fluid containing 24 mM NaHCO3/5% CO2 (pH approximately 7.34, 33 degrees C) and exposed to 5% CO2/95% O2 arriving through an interface chamber, locus coeruleus neurons discharged spontaneously at approximately 1 Hz. Extracellular recordings showed that lowering CO2 that arrived through the chamber below 5% resulted in reductions in firing rate, often with a complete cessation of activity when exogenous CO2 was removed completely. Intracellular recordings revealed that lowering CO2 produced an outward current with an increase in slope conductance and a reversal potential near the potassium equilibrium potential; doubling the concentration of external potassium shifted the reversal potential of the current activated by CO2 removal by approximately +20 mV. Raising CO2 above 5% induced an increase in firing rate, an inward current, a decreased slope conductance at potentials near resting membrane voltage, and an increased slope conductance at more negative potentials. These effects of CO2 were mimicked by other manipulations that are known to affect intracellular pH. For example, NH4Cl, which acutely induces intracellular alkalinization, caused a marked reduction in firing rate, an outward current and an increased slope conductance that reversed near the potassium equilibrium potential. Bath-applied barium blocked the effects induced by removal of CO2 or addition of NH4Cl. The polyamine spermine (tetrahydrochloride) applied via intracellular micropipettes blocked the outward current induced by removal of CO2 or addition of NH4Cl. Spermine (free base) or an equivalent concentration of putrescine failed to alter the CO2 (0%)- or NH4Cl-induced effects. We conclude that CO2 maintains the tonic activity of locus coeruleus neurons by decreasing intracellular pH which, in turn, closes inward rectifier potassium channels, an effect that may be mediated by a protonated polyamine. According to this model, when there is alkalinization of locus coeruleus cells through removal of CO2 or addition of NH4Cl, endogenous spermine or a similar polyamine becomes partially deprotonated, releasing the channel block and allowing the cell to hyperpolarize. The possible implications of these results for the physiological effects of CO2 in the locus coeruleus are discussed.

Ammonium Chloride↗
PubMed1985

Catecholamine inhibition of calcium action potentials in rat locus coeruleus neurones.

Intracellular recordings were made from neurones in the nucleus locus coeruleus in a slice of tissue cut from the rat pons. Clonidine (100 nM-10 microM), noradrenaline (10 microM-1 mM) and adrenaline (10 microM-1 mM) all reduced the duration of the spontaneously occurring action potential of the neurones. This effect was also observed on the action potential in the presence of tetrodotoxin, which results from calcium entering the cell. These concentrations of clonidine, noradrenaline and adrenaline always hyperpolarized the membrane. This hyperpolarization was prevented by two procedures which block potassium currents--intracellular caesium and extracellular barium. In conditions of potassium current blockade, noradrenaline (100 microM-1 mM) and adrenaline (20 microM-1 mM) shortened the calcium action potential but clonidine was ineffective even at 10 microM. Adrenaline and noradrenaline also suppressed inward calcium and barium currents measured under voltage clamp. This action of noradrenaline and adrenaline was not prevented by yohimbine (10 microM), propranolol (20 microM) or prazosin (1 microM); it was reduced by a concentration of phentolamine about 100 times higher than its Ke for alpha 2-adrenoceptors on locus coeruleus neurones. It is concluded that noradrenaline and adrenaline can directly inhibit calcium action potentials in locus coeruleus neurones when applied in high concentrations, but that this does not involve an alpha 2-adrenoceptor.

Action Potentials↗
PubMed2000

Pharmacological inactivation of the vesicular monoamine transporter can enhance 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration of midbrain dopaminergic neurons, but not locus coeruleus noradrenergic neurons.

The vesicular monoamine transporter in the brain can sequester the neurotoxin 1-methyl-4-phenylpyridinium into synaptic vesicles and protect catecholamine-containing neurons from degeneration. Mouse nigrostriatal dopaminergic neurons, and to a lesser extent locus coeruleus noradrenergic neurons, are vulnerable to toxicity produced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. The present study sought to determine whether pharmacological inactivation of the vesicular monoamine transporter in the brain would enhance the degeneration of substantia nigra dopaminergic neurons and locus coeruleus noradrenergic neurons in 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine-treated animals. Mice were treated subacutely with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine alone, or in combination with vesicular monoamine transporter inhibitors (tetrabenazine or Ro4-1284), and 10-24 days later striatal dopamine and cortical norepinephrine levels were measured using chromatographic methods. In the same animals, substantia nigra and locus coeruleus catecholaminergic neurons were counted using tyrosine hydroxylase immunohistochemical staining with computer imaging techniques. Mice in which pharmacological blockage of the vesicular monoamine transporter enhanced the effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity in the depletion of striatal dopamine concentrations also exhibited enhanced degeneration of substantia nigra dopaminergic neurons. In the same animals, however, vesicular monoamine transporter blockade did not enhance the effects of 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine in the locus coeruleus noradrenergic system. These data are consistent with the hypothesis that the vesicular monoamine transporter can protect catecholamine-containing neurons from 1-methyl-4-phenylpyridinium-induced degeneration by sequestration of the toxin within brain vesicular monoamine transporter-containing synaptic vesicles. Since the amount of vesicular monoamine transporter in locus coeruleus neurons is more than in substantia nigra neurons, and because 1-methyl-4-phenylpyridinium is sequestered within locus coeruleus neurons to a far greater extent than within substantia nigra neurons, it may be that a greater amount of vesicular monoamine transporter inhibition is required for 1-methyl-4-phenylpyridinium to be toxic to locus coeruleus neurons than to substantia nigra dopaminergic neurons.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1983

Fetal locus coeruleus transplanted into the transected spinal cord of the adult rat.

Locus coeruleus tissue from 16-day-old fetal rats has been successfully transplanted into the transected spinal cord of the young adult female rat. During development, the solid tissue implant (approximately equal to 1.2 mm3) always breaks up into smaller cell clusters. Fluorescent axons from the fetal neurons invaded the host tissue, and grew for several millimeters away from the cell-body region. The damaged rostral noradrenergic axons in the ventral horn (projecting from the locus coeruleus) exhibited an intense proliferation in response to a neurotrophic factor produced by the fetal implant. Finally, in 2/8 cases, the axons of the fetal, noradrenergic locus coeruleus neurons remained confined to the fetal nuclear tissue. The results are discussed in the context of recent attempts to reconstruct the damaged mammalian spinal cord.

Animals↗
PubMed1984

Anatomical alterations in locus coeruleus neurons in the adult spontaneously hypertensive rat.

A golgi-Cox examination of the locus coeruleus in the spontaneously hypertensive rat (SHR) has shown an increase in the number of primary dendritic branches, in the number of secondary branch points, in the mean length of the dendritic branches from the soma to the outer extent of the secondary branches, and in the longest extent of the dendritic domain in comparison with the locus coeruleus in the Wistar-Kyoto normotensive rats at sixteen weeks of age. We suggest that the anatomical changes may provide a substrate for altered afferent relationships in the neurochemical regulation of neurons of the locus coeruleus, although it remains to be shown whether such alterations are related in any way to blood pressure. It appears evident that the altered mechanisms resulting in hypertension in this genetic model are more complex than an anatomical or neurochemical modification in one of the central autonomic nuclei. However, the present finding that anatomical alterations in the dendritic arborizations of a key nucleus such as the locus coeruleus occur, points towards a need for further examination of the interrelationships of specific neurotransmitter systems in this nucleus.

Animals↗
PubMed1996

Precipitated kappa-opioid receptor agonist withdrawal increase glutamate in rat locus coeruleus.

Extracellular fluid levels of excitatory amino acids (glutamate, Glu; and aspartate, Asp) in the locus coeruleus and the behavioral signs during naloxone-precipitated withdrawal from kappa-opioid receptor agonists, butorphanol and (5 alpha, 7 alpha, 8 beta) -(+)-N-methyl-N-[7-(1-pyrrolidinyl)-1-oxaspiro[4,5]dec-8-yl]-be nzaneacetamide (U-69,593), were investigated by in vivo microdialysis. Increases in levels of Glu, but not of Asp, were noted after naloxone (12 or 48 nmol/5 microliters, locus coeruleus)-precipitated withdrawal in the rats which had been intracerebroventricularly infused with butorphanol (26 nmol/1 microliters/h) or U-69,593 (26 nmol/10 microliters/h) for 3 days. The Glu levels in the locus coeruleus increased following administration of naloxone before and during the first 15-min sample after the precipitation of withdrawal in the butorphanol- or U-69,593-dependent rats. Furthermore, behavioral evidence of withdrawal (teeth-chattering, wet-dog shakes, etc.) was detected following the naloxone challenge in the butorphanol- and U-69,593-infused rats, but not in saline-infused controls. These results provide direct evidence to support the role of excitatory amino acids within the locus coeruleus in butorphanol or U-69,593 withdrawal.

Analgesics↗
PubMed1999

Nitrergic stimulation of the locus coeruleus modulates blood pressure and heart rate in the anaesthetized rat.

To investigate whether nitric oxide is involved in the cardiovascular responses mediated via the locus coeruleus, the effects of microinjections of L-arginine and L-glutamate into the locus coeruleus on blood pressure and heart rate were investigated in sodium pentobarbitone-anaesthetized rats. Unilateral microinjection of L-arginine (25, 50 nmol) elicited dose-related depressor (-17 +/- 4, -25 +/- 4 mmHg) and bradycardic (13 +/- 3, 24 +/- 6 b.p.m.) effects. Furthermore, these effects were attenuated by prior local microinjection of N(G)-nitro-L-arginine (40 nmol). Peripheral muscarinic receptor blockade with atropine methyl nitrate (1 mg/kg, i.v.) attenuated the bradycardic but not the depressor responses to L-arginine. L-Glutamate (2 nmol) microinjections also mediated depressor (-27 +/- 6 mmHg) and bradycardic (53 +/- 23 b.p.m.) effects that were attenuated by microinjections of dizocilpine maleate (1 nmol) into the locus coeruleus. In addition, pretreatment with N(G)-nitro-L-arginine (40 nmol) also significantly attenuated the depressor response elicited by L-glutamate. These results suggest that nitrergic and glutamatergic pathways are operative within the locus coeruleus to modulate cardiovascular function, and also that a functional interaction may exist between the nitrergic and glutamatergic systems within the rat locus coeruleus.

Anesthesia, General↗
PubMed1989

Evidence that dorsal locus coeruleus neurons can maintain their spinal cord projection following neonatal transection of the dorsal adrenergic bundle in rats.

In adult rats, locus coeruleus neurons which extend axons to the spinal cord are found only at mid-rostrocaudal levels of the nucleus, where they are essentially confined to its ventral, wedge-shaped half (Satoh et al. 1980; Westlund et al. 1983; Loughlin et al. 1986). However, during early postnatal development, coeruleospinal cells are found throughout the locus coeruleus (Cabana and Martin 1984; Chen and Stanfield 1987). This developmental restriction of the distribution of coeruleospinal neurons is due to axonal elimination rather than to cell death, since neurons retrogradely labeled through their spinal axons perinatally are still present in the dorsal portion of the locus coeruleus at survival periods beyond the age at which these cells lose their spinal projection (Chen and Stanfield 1987). I now report that if axons ascending from the locus coeruleus are cut by transecting the dorsal adrenergic bundle on the day of birth, a more widespread distribution of coeruleospinal neurons is retained beyond the perinatal period. These results not only indicate that the absence of the normally maintained collateral of a locus coeruleus neuron is sufficient to prevent the elimination of a collateral which would otherwise be lost, but also may imply that during normal postnatal development the presence of the maintained collateral is somehow causally involved in the elimination of the transient collateral.

Adrenergic Fibers↗
PubMed1983

Decreased activity of locus coeruleus neurons in the rat after DSP-4 treatment.

The activity of noradrenergic neurons of the rat locus coeruleus was investigated at 10 and 50 days after the administration of DSP-4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzyl-amine), a selective noradrenergic neurotoxin. The mean neuronal firing rate in control animals was 2.4 Hz. In contrast, DSP-4 animals had lower rates of 1.2 Hz at 10 days and 1.7 Hz at 50 days. Histological examinations revealed no morphological changes of locus coeruleus cell bodies at either the 10- or 50-day time points. These results suggest that DSP-4 can impair neuronal activity of the locus coeruleus without altering the structural appearance of locus coeruleus perikarya.

Action Potentials↗
PubMed1996

Do amphibians have a true locus coeruleus?

Much controversy surrounds the identity of a locus coeruleus in amphibians because although previous studies on the isthmic region of the brain of anurans and urodeles revealed the presence of noradrenergic cell bodies they failed to demonstrate their projection to the telencephalon or the spinal cord. In the present study applications of Texas Red-conjugated dextran amines to the basal telencephalon or to the spinal cord in combination with tyrosine hydroxylase immunohistochemistry revealed that the noradrenergic cell bodies in the isthmic region of anuran (Rana perezi) and urodele (Pleurodeles waltl) amphibians project to the telencephalon as well as to the spinal cord. On the basis of location, neurotransmitter content and efferent projections, the isthmic noradrenergic cell group of amphibians is, therefore, considered homologous to the locus coeruleus of amniotes.

Animals↗