Disease relevance of Injections, Spinal

• Increased motoneuron survival and improved neuromuscular function in transgenic ALS mice after intraspinal injection of an adeno-associated virus encoding Bcl-2 [1].
• To examine the action(s) of 4-AP in demyelinating disorders, the drug was administered at clinical doses, both in vivo and in vitro, to rat dorsal column axons which had been experimentally demyelinated by the intraspinal injection of ethidium bromide [2].
• Adenosine analogs produce antinociception in normal animals and reduce allodynia and hyperalgesia following inflammation and nerve injury following spinal injection, yet none have been tested for clinical safety [3].
• Intradermal or spinal injection of intracellular calcium modulators (TMB-8 and Quin-2), which had no effect on nociception in control rats, significantly attenuated and together eliminated ddC and suramin-induced mechanical hypersensitivity [4].
• In contrast, intrathecal injections of glutamate receptor antagonists resulted in a dose-dependent depression of the strychnine evoked hyperesthesia with the ordering of activity being MK-801, AP-5, kynurenic acid, SKF10047 and ketamine [5].

Psychiatry related information on Injections, Spinal

• A single intrathecal injection of capsaicin depletes substance P from primary sensory neurons and causes a prolonged increase in the thermal and chemical pain thresholds of the rat but no apparent change in responses to noxious mechanical stimuli [6].
• The experiment is designed to demonstrate the changes in the tail-flick response latency after the intrathecal injection of serotonin [7].

High impact information on Injections, Spinal

• First, we performed a double-blind, randomized, controlled crossover trial of bolus intrathecal injections of 25, 50, and 75 microg of baclofen and placebo [8].
• We report that in SOD1(G93A) transgenic mice, a model for familial ALS, intraspinal injection of a lentiviral vector that produces RNAi-mediated silencing of SOD1 substantially retards both the onset and the progression rate of the disease [9].
• We now report that the intrathecal injection of morphine into female ovariectomized rats pretreated with oestradiol benzoate and progesterone inhibits sexual receptivity while injection of the opiate receptor antagonist naloxone enhances it [10].
• Low doses of D-Pro2-D-Phe7-D-Trp9-substance P, as specific substance P antagonist, depressed the scratching and biting behaviors elicited by intrathecal injections of substance P, and cutaneous application of algesic substances [11].
• These disruptions blocked pLTF, whereas intrathecal injection of BDNF elicited an effect similar to pLTF [12].

Chemical compound and disease context of Injections, Spinal

• To discover whether increasing PDGF expression increases the number of OPCs following demyelination and whether this enhances the efficiency of remyelination, we induced demyelination in GFAP-PDGF-A transgenic mice by intraspinal injection of lysolecithin or dietary administration of cuprizone [13].
• Five cases of presumed acute viral encephalitis with convulsions were examined with radioisotope (RI) cisternography six and 24 hours after an intrathecal injection of 1 mCi of pentetic acid labeled with either ytterbium 169 or indium 111 [14].
• RESULTS: Intrathecal injection of nociceptin, but not of NMDA antagonists, attenuated the level of thermal hyperalgesia in a dose-dependent manner at a dose of 0.17-17 nM (post-drug difference score: saline-treated rats, -4.9 +/- 2.2 s; 17 nM nociceptin-treated rats, -1.3 +/- 0.9 s) [15].
• RESULTS: In the standard diet group intrathecal injection of glycine prolonged the interval and decreased the amplitude of bladder contractions, decreased baseline urethral pressure and altered urethral activity during bladder contraction from a pattern of detrusor-sphincter dyssynergia to detrusor-sphincter synergy at 100 mug glycine [16].
• We have previously shown that intrathecal injection of the human immunodeficiency virus-1 (HIV-1) envelope glycoprotein, gp120, induces mechanical allodynia via the release of proinflammatory cytokines [17].

Biological context of Injections, Spinal

• The slow component of axonal transport was labeled by intraspinal injections of [35S] methionine [18].
• Using polyethylene glycol (PEG)-grafted PEI for DNA complexes, no attenuation of gene expression was detected after repeated intrathecal injections, even in those rats receiving three doses, administered 2 weeks apart [19].
• We demonstrate here that intracerebroventricular or spinal cord (intrathecal) injection of either plasmid DNA alone or cationic liposome: DNA complexes (CLDCs) produces significant levels of expression of both reporter genes and biologically relevant genes in nonparenchymal cells lining both the brain and the spinal cord [20].
• Compounds within this class were extremely effective inhibitors of lipid peroxidation in vitro and antagonized excitatory behavior coupled with peroxidative injury induced by spinal intrathecal injection of FeCl2 (mouse-FeCl2-it assay) in vivo [21].
• A dose-dependent decrease in blood pressure and heart rate was induced by intrathecal injections of clonidine (0.3-3 micrograms), at the T6-T7 level [22].

Anatomical context of Injections, Spinal

• Activation by intrathecal injection of receptors on spinal C fiber terminals (mu,/delta opiate, alpha2 adrenergic, neuropeptide Y) prevents release of primary afferent peptides and spinal amino acids and blocks acute and facilitated pain states [23].
• To examine this issue, the dorsal columns of the adult rat spinal cord were demyelinated by x-irradiation and intraspinal injections of ethidium bromide [24].
• A single intrathecal injection of Depo/Ara-C can maintain a therapeutic drug concentration in the cerebrospinal fluid for a very prolonged period [25].
• To identify differences in the electrophysiological response of specific fiber types to the application of 4-AP, rat ventral and dorsal spinal roots, demyelinated by intrathecal injections of lysophosphatidylcholine, were examined in vitro before and during potassium-channel blockade [26].
• A single intraspinal injection of complement proteins plus antibodies to galactocerebroside (the major myelin sphingolipid) resulted in demyelination followed by oligodendrocyte remyelination [27].

Associations of Injections, Spinal with chemical compounds

• Nociceptive responses, to a hindpaw injection of 50 microliters of 2.5% formalin, and flexion reflex thresholds, to mechanical stimulation (Randall-Selitto test) in the hindpaw contralateral to a thermal injury (15 sec immersion in water at 55 degrees C), were assessed following intrathecal injection of PKC inhibitors (GF 109203X or chelerythrine) [28].
• Substance P (SP) and the excitatory amino acid (EAA) agonists NMDA, kainic acid (KA), or quisqualic acid (Quis) each produce a transient, caudally directed biting and scratching response (CBS) in mice after their intrathecal injection [29].
• PATIENTS AND METHODS: Treatment consisted of two cycles of MBVP (MTX 3 g/m2 days 1 and 15, teniposide 100 mg/m2 days 2 and 3, carmustine 100 mg/m2 day 4, methylprednisolone 60 mg/m2 days 1 to 5, and two intrathecal injections of MTX 15 mg, cytarabine 40 mg, and hydrocortisone 25 mg) followed by 40 Gy of RT [30].
• Spinal intrathecal injections of the nonsteroidal antiinflammatory analgesics (NSAIAs) indomethacin and acetylsalicylic acid, which inhibit prostaglandin synthesis, cause dose-dependent hypoalgesia in the rat [31].
• Seven days later, rats received ganciclovir for 14 days by daily i.p. injections (30 mg/kg/ml) or intrathecal injections (25 micrograms/kg or 600 micrograms/kg) for 14 days [32].

Gene context of Injections, Spinal

• First, intrathecal injection of the COX inhibitor indomethacin, which exerted pronounced antinociceptive effects in wt mice, was completely ineffective in iNOS-/- mice [33].
• Intrathecal injection of the MEK (ERK kinase) inhibitor PD98059 on Day 2, 10 or 21 reduces SNL-induced mechanical allodynia [34].
• Intrathecal injection of ET-1 depressed the phase 1 and 2 flinching behavior in a dose-dependent manner and this ET-1 effect was antagonized by FR139317 [35].
• Intrathecal injection of either ET-3 or Sarafotoxin S6c enhanced the phase 2a flinching behavior in a dose-dependent manner [35].
• Nociceptive behavior after intrathecal injections of substance P, neurokinin A and calcitonin gene-related peptide in mice [36].

Analytical, diagnostic and therapeutic context of Injections, Spinal

• Vitamin E was also effective in producing analgesia by intrathecal injection, suggesting the importance of spinal mechanisms [37].
• Thirty-four male rats, implanted with chronic indwelling intrathecal catheters, received a subcutaneous injection of either morphine sulfate or an equal volume of saline, followed by an intrathecal injection of clonidine HCl or an equal volume of vehicle [38].
• To characterize the pharmacological profile of these peptidase inhibitors, we compared electroacupuncture antinociception with and without intrathecal injections of captopril and bestatin [39].
• Measurements were obtained under control conditions, 15 min after lumbar intrathecal injection of 10 microl artificial cerebrospinal fluid containing the CAIs acetazolamide or ethoxyzolamide, and during the 55 min after intraperitoneal injection of three sedative drugs: 30 mg/kg pentobarbital, 50 mg/kg propofol, or 1.9 mg/kg midazolam [40].
• Microinjection of substance P near A7 neurons also produces antinociception that is blocked by intrathecal injection of alpha2-adrenoceptor antagonists [41].

References