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Biomedical subjects

C Schmauss

Publications and source records attributed to C Schmauss.

34 records · Page 2Linked to original sources
PubMed1989

A comparison of snRNP-associated Sm-autoantigens: human N, rat N and human B/B'.

N is a tissue-specific, Sm-epitope bearing, snRNP-associated protein found predominantly in brain. The cDNA sequence encoding human N is compared to those for rat N and human B/B'. The amino acid sequences of human and rat N are 100% conserved. Although the amino acid sequences of N and B/B' are very similar to each other, B/B' contains 50 amino acids which are not present in N. On Northern blots the cDNAs encoding N and B/B' recognize two different RNA species. A comparison of the codon usage, as specified by the open reading frames of N and B/B' as well as results from Southern blots, show that N and B/B' are derived from different genes.

Amino Acid Sequence↗
PubMed1987

Spinal kappa-opioid receptor-mediated antinociception is stimulus-specific.

The intrathecal injection of a variety of selective kappa-opioid receptor ligands did not result in significant inhibition of thermal nociceptive tail flick responses in rats. In contrast, these compounds dose dependently inhibited pressure nociceptive responses. Cross-tolerance studies revealed that the kappa-opioid receptor ligands tifluadom, U-50488H and dynorphin-(1-17) act upon a receptor distinguishable from the receptor through which morphine exerts its inhibition of mechanical nociceptive responses. The less selective kappa-opiate receptor ligands bremazocine and ethylketocyclazocine (EKC), however, blocked both tail flick and tail pressure nociceptive responses and their effect showed marked cross-tolerance to morphine in the tail flick nociceptive test, but not for the pressure nociceptive responses. We suggest that EKC and bremazocine act upon the spinal kappa-opioid receptor to block mechanical nociceptive responses but that the analgesic effect of EKC and bremazocine on thermal nociceptive responses is probably mediated via spinal micron- and/or delta-, and delta-opioid receptors, respectively.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1987

Intrathecally administered dynorphin-(1-17) modulates morphine-induced antinociception differently in morphine-naive and morphine-tolerant rats.

The intrathecal (i.t.) administration of morphine, but not of dynorphin-(1-17), dose dependently inhibited thermal nociceptive responses to radiant heat. In morphine-naive rats, i.t. dynorphin-(1-17) slightly antagonized morphine analgesia but potentiated it in morphine-tolerant rats. These data provide further evidence that dynorphin-(1-17) modulates the effects of exogenously administered opiates differently, depending upon whether the animals are opiate-naive or opiate-tolerant.

Analgesics↗
PubMed1987

Characterization of benzodiazepine withdrawal in high- and low-dose dependent psychiatric inpatients.

Fourteen patients with high- (n = 7) and low-dose (n = 7) benzodiazepine (BDZ) dependency presented predominantly with anxious and depressive neurotic symptoms which caused long-term BDZ medication. Their BDZ dependency was characterized by giving preference to the abuse of benzodiazepines with long elimination half-life. Significant enlargement of CSF spaces was only found in high-dose dependent patients. Withdrawal after long-term BDZ medication revealed no differences between high- and low-dose BDZ dependency with respect to onset of withdrawal reaction and the correlation between onset of withdrawal and peak fall of BDZ serum level. The peak of withdrawal was reached 3-4 days later in high-dose BDZ dependent patients compared with those with a low-dose dependency. The peak withdrawal in high-dose dependent patients appeared when the serum BDZ metabolite nordiazepam dropped significantly. No such concomitant appearance of peak withdrawal and drop of serum nordiazepam level could be found in low-dose dependent patients. Specificity and intensity of BDZ withdrawal symptoms were the same for those dependent upon high doses of BDZs and those dependent upon low doses, but a protracted withdrawal was only observed in low-dose BDZ-dependent patients. During the withdrawal period psychopathometric measurements consistently revealed parallel changes in the scores for physical withdrawal symptoms, anxiety and depression. It is not clear whether anxiety and depression are "typical" BDZ withdrawal reactions or represent a "reactivated" state of the psychopathological disturbance which lead to the BDZ dependency. Possible implications for the therapeutical management of BDZ-dependent patients are discussed.

Adult↗
PubMed1987

Enlargement of cerebrospinal fluid spaces in long-term benzodiazepine abusers.

In 17 benzodiazepine (BDZ) dependent in-patients a CT scan was performed before initiation of withdrawal therapy. The evaluation of the ventricular to brain ratio (VBR) by standardized and computerized measurements revealed significantly higher mean VBRs for both high- and low-dose BDZ-dependent patients compared to the mean VBR of an age- and sex-matched control group. In addition, the mean VBR of high-dose BDZ-dependent patients (N = 8) was significantly higher than the mean VBR of low-dose BDZ-dependent patients (N = 9). This difference could not be accounted for by the age of the patients or duration of BDZ-dependency and, therefore, suggests a dose-dependent effect of BDZs on the enlargement of internal CSF-spaces. On the other hand, higher values for the width of external CSF-spaces were found to be related to increasing age of the patients and duration of BDZ-dependency.

Adult↗
PubMed1987

Antipsychotic effect of buprenorphine in schizophrenia.

The antipsychotic potency of the partial opiate agonist buprenorphine was evaluated in 10 neuroleptic-free schizophrenic patients suffering from frequent hallucinations, delusions, and severe formal thought disorders. Buprenorphine had a pronounced antipsychotic effect, which lasted about 4 hours, in patients with schizophreniform disorders (N = 4) and paranoid schizophrenia (N = 3).

Adult↗
PubMed1985

Studies on spinal opiate receptor pharmacology. III. Analgetic effects of enkephalin dimers as measured by cutaneous-thermal and visceral-chemical evoked responses.

D-Ala2-D-Leu5-enkephalin (DADL) along with dimers formed from tetra(DTE: des-Leu5-enkephalin)- or pentapeptide (DPE: Leu5-enkephalin) coupled by methylene bridges of various lengths (n) have been shown in in vitro systems to possess varying degrees of mu/delta-receptor selectivity. In the present studies we have systematically compared the intrathecal effect of these agents and morphine on the cutaneous stimuli (hot plate (HP) and tail flick (TF) and visceral-chemical (writhing) tests in the rat. The following observations were made. (1) Dimers with high delta-receptor selectivity were active in the TF(DPE2 greater than or equal to DADL greater than or equal to DTE2 greater than or equal to morphine greater than DPE12 much greater than DTE12 = 0) and HP(DPE2 greater than or equal to DTE2 greater than or equal to DADL greater than or equal to morphine greater than DPE12 greater than or equal to DTE12 greater than 0. To examine cross-tolerance, the intrathecal ED50 for morphine, DPE and DADL were determined in rats rendered tolerant by subcutaneous morphine pellets. The TF ED50 tolerant/TF ED50 naive was 18.4, 5.4 and 1.3, respectively. The ratio of activity on the HP was 14.0, 4.7 and 2.2 (2) On the visceral-chemical test, only morphine was active. The dimers or DADL in doses which totally blocked the TF or HP are at higher doses which were just below those producing motor dysfunction had no effect on the writhing response. (3) At high intrathecal doses (40 X TF ED50), morphine produced a motor rigidity which blocked the placing and stepping reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1985

Dopamine and the action of opiates: a reevaluation of the dopamine hypothesis of schizophrenia. With special consideration of the role of endogenous opioids in the pathogenesis of schizophrenia.

It is suggested that the antipsychotic efficacy of opioids in patients suffering from schizophrenia may result from an interaction of opioids with the dopaminergic system. The modulatory effect of opioids on dopaminergic functions has already been demonstrated in basic experiments: Anatomical and biochemical data reveal an interaction between opioid receptors and dopamine (DA) actions on dopaminergic nerve terminals, cell bodies, and afferent nerve endings. Endogenous enkephalin levels correlate well with the endogenous dopamine content in various brain areas. Systemic or iontophoretic administration of morphine alters the spontaneous activity of ventral tegmental dopaminergic neurons. Morphine and enkephalin effectively enhance pituitary prolactin release, whereas dopamine inhibits it. Opioid agonists effectively alter DA release, DA reuptake, and DA metabolism in the striatum and substantia nigra. In reverse, chronic neuroleptic treatment enhances the synthesis and release of pituitary beta-endorphin. Opioids affect contralateral rotation elicited by dopamine agonists in animals with unilateral lesions of the nigrostriatal pathway. Phencyclidine, a psychotropic drug that shares certain pharmacological characteristics with the putative sigma-opioid receptor ligand SKF 10,047, indirectly mimics the effects of dopamine agonists on prolactin release, release of acetylcholine, etc. It is suggested that an imbalance of opiate-DA interaction might be involved in the pathogenesis of schizophrenia. Consequently, clinical studies on the effects of opioids on psychotic symptoms should also examine opioid influence on dopaminergic functions in these patients.

Brain↗
PubMed1984

Vasopressin and oxytocin in the rat spinal cord: analysis of their role in the control of nociception.

Lesions of the hypothalamic paraventricular nucleus depleted immunoreactive (ir)-vasopressin (VP) and -oxytocin (OT) from rat spinal cord but failed to modify nociceptive thresholds. Further, intrathecal introduction of VP and OT into the cord failed either to influence nociceptive thresholds or to modify the antinociceptive action of morphine. However, doses of VP as low as 20 ng caused, in contrast to OT, a hind-limb muscular flaccidity and respiratory disturbances. Rats suffering from chronic arthritis did not, finally, reveal any alterations in levels or ir-VP or ir-OT in the spinal cord. Is is concluded that spinal pools of VP and OT are derived from the paraventricular nucleus and do not play a major role in nociceptive processes in the spinal cord. A role of spinal VP in motor and, possibly autonomic control is, nevertheless, indicated.

Animals↗
PubMed1984

In vivo studies on spinal opiate receptor systems mediating antinociception. II. Pharmacological profiles suggesting a differential association of mu, delta and kappa receptors with visceral chemical and cutaneous thermal stimuli in the rat.

The intrathecal administration of mu (morphine) and delta (D-Ala2-D-Leu5-enkephalin) but not kappa agonists (ethylketocyclazocine, bremazocine and U50488H) or partial agonists (nalbuphine and buprenorphine) produced a dose-dependent inhibition of all cutaneous thermal (hot plate and tail-flick) responses in the rat. In contrast, on visceral chemical tests (writhing), mu and kappa agonists but not delta agonists exerted a powerful suppression of the response. Whereas the ED50 of morphine on the cutaneous thermal tests did not differ from that observed on the visceral chemical test, agents with significant mu and delta activity (metkephamid and beta-endorphin) showed a prominent reduction in activity on the writhing as compared with the hot plate and tail-flick. Systemic naloxone resulted in a dose-dependent antagonism of the effect of all intrathecal agents. Estimation of the pA2 of mu agents indicated no difference on the hot plate/tail-flick and writhing (pA2 approximately 7). Kappa ligands were selectively resistant to antagonism with naloxone pA2 values for those agonists ranging from 5.9 to 6.6. These observations suggest that there are three discriminable populations of receptors in the spinal cord whose activation results in a selective modulation of the response of the animal to noxious stimuli. In addition, the selective effects of the delta agonists on cutaneous thermal and kappa agonists on visceral chemical suggest a differential coding of spinal afferents through which these stimuli are transmitted.

Animals↗
PubMed1983

Differential association of spinal mu, delta and kappa opioid receptors with cutaneous thermal and visceral chemical nociceptive stimuli in the rat.

The intrathecal administration of several mu (morphine), delta (d-ala2-d-leu5-enkephalin, dimeric leu-enkephalin) and mixed mu/delta (beta-endorphin) agonists produced a dose-dependent inhibition of all cutaneous thermal (Tail Flick/Hot Plate) nociceptive responses in the rat. The kappa agonist U50488H had no analgesic potency in thermal nociceptive tests. On a visceral chemical test (writhing) and agonists exerted a powerful suppression of the response. In contrast at doses 10 to 50 times the ED50 on cutaneous thermal tests, delta agonists had no effect on the writhing response. At higher intrathecal doses, delta ligands produced flaccidity. These observations suggest the existence of three discriminable populations of opioid receptors in the spinal cord whose activation has different effects on the animals response to noxious stimuli.

Animals↗
PubMed1982

The analgetic effects of an intrathecally administered partial opiate agonist, nalbuphine hydrochloride.

Nalbuphine (0.1-200 micrograms), unlike morphine (0.1-10 micrograms) administered intrathecally had no effect on the tail flick or hot plate response latencies. In contrast, both intrathecal nalbuphine and morphine inhibited, in a monotonic, dose dependent fashion, the writhing evoked by intraperitoneally administered acetic acid (ED50 = 38 nmol and 1.12 nmol, respectively.) The effects of intrathecal nalbuphine and morphine was antagonized by an equal dose of naloxone administered systemically. Co-intrathecal administration of morphine and nalbuphine revealed that a maximum inhibition of writhing could be obtained with low doses of either drug, while the effects of higher doses of either drug were attenuated as compared to the effects produced by the high dose of either drug alone. These data are consistent with the suggestion that nalbuphine exerts its agonistic effect through a mechanism that is pharmacologically distinct from that of morphine, and the likelihood of two populations of opioid receptors associated with the pain response evoked by thermal and visceral afferents, respectively is considered.

Analgesics↗