C1 neurons excite locus coeruleus and A5 noradrenergic neurons along with sympathetic outflow in rats.
Abbott SB, Kanbar R, Bochorishvili G, Coates MB, Stornetta RL, Guyenet PG.
J Physiol 590(12):2897-2915, 2012.
C1 neurons are known to activate sympathetic tone and stimulate the hypothalamic-pituitary-adrenal axis. C1 activation is also reported to inhibit locus coeruleus (LC) neurons. Rats received 0.6 ng of SSP-SAP (Cat. #IT-11) injected under the caudal edge of the facial motor nucleus to destroy the retrotrapezoid nucleus, increasing the proportion of C1 ChR2-expressing neurons. Stimulation of C1 neurons resulted in activation of noradrenergic neurons that are involved in hypoxia and hypotension.
Immunogold Detection of L-glutamate and D-serine in Small Synaptic-Like Microvesicles in Adult Hippocampal Astrocytes.
Bergersen LH, Morland C, Ormel L, Rinholm JE, Larsson M, Wold JFH, Roe AT, Stranna A, Santello M, Bouvier D, Ottersen OP, Volterra A, Gundersen V.
Cereb Cortex 22(7):1690-1697, 2012.
Verifying the presence of D-serine in astrocyte vesicles would help resolve whether astrocytes produce rapid gliotransmitter exocytosis for the purpose of neuromodulation. In one of a series of experiments the authors looked at D-serine levels with anti-L-glutamate (Cat. #AB-T08). The results suggest that domains of astrocytes can acquire local Ca2+ increases that trigger glutamate and D-serine release.
Prior pathology in the Basal forebrain cholinergic system predisposes to inflammation-induced working memory deficits: reconciling inflammatory and cholinergic hypotheses of delirium.
Field RH, Gossen A, Cunningham C.
J Neurosci 32(18):6288-6294, 2012.
The authors lesioned the basal forebrain of mice with 0.08 μg or 0.4 μg icv injections of mu p75-SAP (Cat. #IT-16) to establish an early dementia-associated cholinergic loss model. The mice were then challenged with systemic inflammation using low-dose lipopolysaccharide (LPS). The mu p75-SAP lesion left hippocampal-dependent reference and working memory relatively intact. LPS-induced inflammation created acute working memory deficits; an aceytlcholinesterase inhibitor protected against this deficit.
Involvement of brain-derived neurotrophic factor and sonic hedgehog in the spinal cord plasticity after neurotoxic partial removal of lumbar motoneurons.
Gulino R, Gulisano M.
Neurosci Res 73(3):238-247, 2012.
In this work the authors created a motoneuron depletion with bilateral 6.0-μg injections of CTB-SAP (Cat. #IT-14) into the medial and lateral gastrocnemius muscles of rats. The results indicate BDNF and sonic hedgehog may collaborate in modulating synaptic plasticity after loss of motoneurons.
Adenosine inhibits glutamatergic input to basal forebrain cholinergic neurons.
Hawryluk JM, Ferrari LL, Keating SA, Arrigoni E.
J Neurophysiol 107(10):2769-2781, 2012.
Using patch-clamp recordings from mouse brain slices the authors demonstrate that adenosine not only directly inhibits cholinergic neurons in the basal forebrain, it also reduces excitatory inputs to these neurons as well. Cy3-anti-mu p75 (Cat. #FL-05, 40-60 ng) was injected into the lateral cerebroventricle.
c-Maf is required for the development of dorsal horn laminae III/IV neurons and mechanoreceptive DRG axon projections.
Hu J, Huang T, Li T, Guo Z, Cheng L.
J Neurosci 32(16):5362-5373, 2012.
The molecular mechanisms responsible for development of laminae III/IV neurons are not yet well understood. In this work the authors investigated the role of c-Maf, a basic leucine-zipper transcription factor from the AP-1 superfamily. Anti-TrkA (Cat. #AB-N03: 1:100) was used for immunohistochemistry.
Disrupted serotonergic system in patients with pulmonary hypertension may serve as novel biomarkers new therapeutic targets and to assess severity, progression and response to treatment.
Kirillova V, Prosviryakov E.
Cardiovasc Res 93 Suppl 1:P209, 2012.
At the Frontiers in Cardiovascular Biology meeting in London the authors presented work examining the role serotonin and serotonin transporters play in pulmonary hypertension. Anti-SERT (Cat. #AB-N09 discontinued, 1:500) was used in immunohistochemistry to detect the serotonin transporter in the myocardium. The data demonstrate that serotonin levels in the blood and serotonin transporter levels in the myocardium are both increased in patients with pulmonary hypertension.
TrkA gene ablation in basal forebrain results in dysfunction of the cholinergic circuitry.
Sanchez-Ortiz E, Yui D, Song D, Li Y, Rubenstein JL, Reichardt LF, Parada LF.
J Neurosci 32(12):4065-4079, 2012.
The authors created a conditional trkA knockout mouse line. Anti-trkA (Cat. #AB-N03) was used for immunohistochemistry (1:1000) and western blots (1:4000). The data demonstrate the importance of trkA in the establishment of basal forebrain cholinergic circuitry, and choline acetyltransferase expression.
Cholinergic denervation attenuates phencyclidine-induced c-fos responses in rat cortical neurons.
Savage S, Mattsson A, Olson L.
Neuroscience 216:38-45, 2012.
Phenylcyclidine (PCP) has been used to model aspects of schizophrenia in animals. 81 ng of 192-IgG-SAP (Cat. #IT-01) was injected into the nucleus basalis magnocellularis of rats to assess the effects of low dose PCP in a cholinergically-deprived system. Saporin (Cat. #PR-01) was used as a control. Results demonstrate basalocortical cholinergic neurons are necessary for PCP to have full effect.
Brainstem facilitations and descending serotonergic controls contribute to visceral nociception but not pregabalin analgesia in rats.
Sikandar S, Bannister K, Dickenson AH.
Neurosci Lett 519(1):31-36, 2012.
Neurons in the rostral ventromedial medulla (RVM) are classified as ON, OFF, or NEUTRAL based on firing patterns in response to noxious somatic stimulation. ON cells express μ-opioid receptors, and are therefore a target for dermorphin-SAP (Cat. #IT-12). The authors injected the RVM of rats with 3 pmol of dermorphin-SAP; Saporin (Cat. #PR-01) was used as a control. Results show the μ-opioid receptor population is not needed for the function of analgesics through the serotonergic system.
Effects of noradrenergic alpha-2 receptor antagonism or noradrenergic lesions in the ventral bed nucleus of the stria terminalis and medial preoptic area on maternal care in female rats.
Smith CD, Holschbach MA, Olsewicz J, Lonstein JS.
Psychopharmacology (Berl) 224(2):263-276, 2012.
The authors investigated the function of norepinephrine in mothering. Lesioned animals received 55-ng infusions of anti-DBH-SAP (Cat. #IT-03) into the ventral bed nucleus of the stria terminalis. Mouse-IgG-SAP (Cat. #IT-18) was used as a control. The results demonstrate that downregulated noradrenergic activity is necessary for postpartum maternal behavior, but is not enough to elicit maternal behavior in nulliparous females.
Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells.
Tai SK, Leung LS.
Behav Brain Res 232(1):174-182, 2012.
It is known that vestibular stimulation induces acetylcholine release in the hippocampus. The authors hypothesized that this stimulation enhances long-term potentiation (LTP) in CA1 and depends on the activation of septohippocampal cholinergic neurons. Rats received 105-ng bilateral infusions of 192-IgG-SAP (Cat. #IT-01) into the medial septum. The data suggest that LTP enhancement during vestibular stimulation is mediated by cholinergic septohippocampal cells.
Sudden Death and Myocardial Lesions after Damage to Catecholamine Neurons of the Nucleus Tractus Solitarii in Rat.
Talman WT, Dragon DN, Jones SY, Moore SA, Lin LH.
Cell Mol Neurobiol 32(7):1119-1126, 2012.
Previous work has shown that elimination of neurons expressing the neurokinin-1 receptor (NK1r) from the nucleus tractus solitarii (NTS) causes various circulatory system dysfunctions, often leading to sudden death. The authors injected the brainstem of rats with 42 ng anti-DBH-SAP (Cat. #IT-03). to eliminate catecholaminergic neurons in the NTS that express tyrosine hydroxylase. This elimination had similar cardiac and cardiovascular effects to the elimination of NK1r-expressing neurons.
Consequences of the ablation of nonpeptidergic afferents in an animal model of trigeminal neuropathic pain.
Taylor AM, Osikowicz M, Ribeiro-da-Silva A.
Pain 153(6):1311-1319, 2012.
The authors used IB4-SAP (Cat. #IT-10; 3.2 μg injected into the mental nerve) to eliminate C-fibers in the lower lip of rats to see if this was enough to induce the sprouting of autonomic fibers. Saporin alone (Cat. #PR-01) was used as a control. Only parasympathetic fibers sprouted in these animals, but after nerve ligation surgery both sympathetic and parasympathetic fibers sprouted.
Analgesia Targeting IB4-Positive Neurons in Cancer-Induced Mechanical Hypersensitivity.
Ye Y, Dang D, Viet CT, Dolan JC, Schmidt BL.
J Pain 13(6):524-531, 2012.
DOR (δ opioid receptor) agonists produce minimal side effects and do not lead to tolerance, making them potential alternatives to the widely used μ opioid receptor agonists. Utilizing the fact that DOR’s are expressed by IB4-positive neurons, the authors injected the subarachnoid space between the L4 and L5 vertebrae of rats with 2.4 μg of IB4-SAP (Cat. #IT-10). 3 μg of saporin (Cat. #PR-01) was used as a control. The results indicate that pharmacological agents targeting IB4-positive neurons may have use in cancer pain treatment.