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Autism Studies and Related Medical Conditions, January 2009 - TACA

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Reichelt K.L., Knivsberg A.M., Lind G., Nodl<strong>and</strong> M.: The probable etiology <strong>and</strong><br />

possible treatment of childhood autism. Brain Dysfunct. 1991, 4: 308-319. [No abstract<br />

available]<br />

Longoni R, Spina L, Mulas A, Carboni E, Garau L, Melchiorri P, Di Chiara G: (D-<br />

Ala2)deltorphin II: D1-dependent stereotypies <strong>and</strong> stimulation of dopamine release in<br />

the nucleus accumbens. J Neurosci 1991 Jun;11(6):1565-76.<br />

Abstract:<br />

Institute of Experimental Pharmacology <strong>and</strong> Toxicology, University of Cagliari, Italy.<br />

In order to investigate the relative role of central delta- <strong>and</strong> mu-opioid receptors in<br />

behavior, the effects of (D-Ala2)deltorphin II, a natural delta-opioid peptide, <strong>and</strong> PL017,<br />

a beta-casomorphin derivative specific for mu receptors, were compared after local<br />

intracerebral <strong>and</strong> intraventricular administration. Intracerebral infusion of the two<br />

peptides was done bilaterally in the limbic nucleus accumbens <strong>and</strong> in the ventral <strong>and</strong><br />

dorsal caudate putamen of freely moving rats through chronic intracerebral cannulas.<br />

After intra-accumbens infusion, the two peptides elicited marked but opposite<br />

behavioral effects: while (D-Ala2)deltorphin II evoked dose-dependent motor<br />

stimulation characterized by locomotion, sniffing, <strong>and</strong> oral stereotypies, PL017 elicited<br />

motor inhibition with rigidity <strong>and</strong> catalepsy. These effects were site specific because<br />

they could not be evoked from the ventral or from the dorsal caudate. Low doses of<br />

naloxone (0.1 mg/kg, s.c. ) blocked the effects of PL017 but not those of (D-<br />

Ala2)deltorphin II, which instead were reduced by high doses of naloxone (1.0 mg/kg)<br />

<strong>and</strong> by the putative delta-antagonist naltrindole; this drug failed to affect the catalepsy<br />

induced by PL017. Therefore, while (D-Ala2)deltorphin II effects were delta-mediated,<br />

PL017 effects were mu-mediated. Blockade of dopamine D1 receptors by SCH 23390<br />

abolished (D-Ala2)deltorphin II effects, while blockade of dopamine D2 receptors by<br />

raclopride or by haloperidol was without effect. Local application by reverse dialysis of<br />

(D-Ala2)deltorphin II (5 microM) to the accumbens resulted in a naloxone-sensitive<br />

increase of extracellular dopamine concentrations; these effects could not be evoked<br />

from the caudate, nor by PL017 in the accumbens. Intracerebroventricular<br />

administration of (D-Ala2)deltorphin II or of PL017 elicited behavioral effects<br />

qualitatively similar to those obtained from the accumbens.<br />

If deltorphin II is indeed present in the urine, this may explain why low doses of<br />

naloxone are often only moderately effective at reducing autistic behaviors.<br />

Fukudome S.-I. <strong>and</strong> Yoshikawa M.: Opioid peptides derived from wheat gluten:<br />

Their isolation <strong>and</strong> characterization. FEBS Letters 1991, 296: 107-111.<br />

Abstract: Four opioid peptides were isolated from the enzymatic digest of wheat<br />

gluten. Their structures were Gly-Tyr-Tyr-Pro-Thr, Gly-Tyr-Tyr-Pro, Tyr-Gly-Gly-Trp-Leu<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 167

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