Biomedical subjects

Y Anagnostakis

Publications and source records attributed to Y Anagnostakis.

6 recordsLinked to original sources

PubMed1998

Dizocilpine (MK-801) and tetrodotoxin influence accumbal dopamine release evoked by intrapallidal morphine.

It has been hypothesized that the intrapallidal morphine-induced dopamine release in the nucleus accumbens may be mediated by thalamocorticostriatal or mesolimbic pathways. In order to challenge the above hypothesis, we examined whether changes in accumbal dopamine and its metabolites produced by intrapallidal morphine a) are associated with local excitatory amino acid neurotransmission b) are determined by impulse propagation in dopamine neurons and c) are observed both ipsi- and contralateral to the morphine administration site. In vivo microdialysis was used to assess dopamine release and metabolism in the right and the left nucleus accumbens separately of awake, unrestrained rats. Vehicle or morphine hydrochloride (10 microliters/26.0 mM) was applied unilaterally into the pallidum alone or in combination with ipsilateral application of the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801) into the nucleus accumbens or the sodium channel blocker tetrodotoxin into the medial forebrain bundle. Drugs' application was performed via reverse dialysis. Concentrations of dopamine, 3,4-dihydroxyphenyl acetic acid (DOPAC) and homovanillic acid (HVA) in the collected dialysate were measured by high performance liquid chromatography with electrochemical detection. Morphine administration resulted in elevated levels of dopamine in the ipsilateral and of DOPAC and HVA in both the ipsi- and contralateral nucleus accumbens. Dizocilpine (MK-801) (0.3 mM) did not influence the basal levels of dopamine, DOPAC or HVA in the nucleus accumbens. Ipsilaterally, dizocilpine (MK-801) inhibited the effect of morphine on dopamine release, whereas it increased significantly the effect of the drug on DOPAC and HVA. Tetrodotoxin (3 microM) reversed the effect of intrapallidal morphine on dopamine, DOPAC or HVA in the ipsilateral nucleus accumbens. The results show that the intrapallidal morphine-induced dopaminergic activation in the ipsilateral nucleus accumbens is dependent upon both phasic and tonic activation of dopaminergic neurons. They suggest that both the thalamocorticostriatal and the mesolimbic dopamine pathways may mediate the investigated effect of morphine.

Animals↗

PubMed1996

Dopamine-somatostatin interactions in the rat striatum: an in vivo microdialysis study.

Dopamine-somatostatin interactions were investigated in the rat striatum using in vivo microdialysis. Somatostatin-14 and somatostatin-28 (10(-4), 10(-5), 10(-6) M) were infused, and the levels of dopamine and its metabolites DOPAC and HVA were assessed using high pressure liquid chromatography with electrochemical detection. Somatostatin-14 was more effective than somatostatin-28 in producing a dose-dependent increase in dopamine levels with no significant alterations in the levels of the metabolites. To assess the effect of dopamine on somatostatinergic neurons, dopaminergic agents were administered and somatostatin levels measured using a radioimmunoassay. The nonselective agonist apomorphine was administered subcutaneously (0.00, 0.05, 0.10, 0.50, 1.00 mg/kg) or directly infused (10(-4), 10(-5) M) in the striatum. The selective D1 and D2 dopamine antagonists SCH23390 and sulpiride, respectively, were also infused at concentrations of 10(-4) and 10(-5) M. None of these agents elicited any significant changes in the somatostatin release in the striatum, while altering dopamine release. This study provides for the first time evidence regarding dopamine-somatostatin interactions in the awake and freely moving animal. The results confirm that somatostatin modulates the function of dopaminergic neurons in the striatum and provide new evidence that somatostatin-14 may differentially regulate dopamine release. Furthermore, our findings suggest that dopamine does not play a major role in the regulation of somatostatin neurons.

Animals↗

PubMed1995

Ventral pallidum self-stimulation: a moveable electrode mapping study.

The distribution of electrical self-stimulation (ESS) foci within the ventral pallidum (VP) was mapped using moveable electrodes in rats. The function relating ESS bar-pressing rate to the frequency of cathodal rectangular pulses (0.4 mA and 0.1 ms) was obtained for several positions of a moveable electrode in the VP and in the various adjacent to VP nuclei. The rate-frequency functions were fitted to a sigmoid model to obtain the asymptotic rate and threshold frequency. ESS was found in almost all (98%) VP sites tested and to a lesser degree (66%) in the surrounding areas (namely globus pallidus and caudate). Depending on the VP site, maximum rates varied from 14 to 85 bar presses/min, whereas threshold frequencies varied from 10.2 to 36.4 pulses/train; no correlation between these two aspects of ESS was found. Extra-pallidal areas contained less low-frequency threshold sites compared to VP. The lowest threshold found in the VP was slightly higher than that usually obtained for the most rewarding brain areas (VTA, dorsal raphé, LH, amygdala), which suggests that the VP represents an important structure for reward. Furthermore the threshold frequencies were found to decline along the rostrocaudal axis of the VP which supports the view that the VP is heterogeneous in regard to reward related functions.

Amygdala↗

PubMed1994

Effect of morphine applied by intrapallidal microdialysis on the release of dopamine in the nucleus accumbens.

The effect of morphine, administered intrapallidally, on extracellular concentrations of DA, DOPAC, and HVA in the nucleus accumbens and striatum was studied in the behaving rat using the in vivo microdialysis technique. Unilateral application of morphine hydrochloride was performed through microdialysis probes into the rat ventral pallidum (10 microliters of 0, 2.6, 4.0, 13.0, and 26.0 mM) or globus pallidus (10 microliters of 0 and 26.0 mM). The levels of DA, DOPAC, and HVA were measured using the HPLC with EC detection in dialysates collected from the nucleus accumbens, anteromedial, and anterolateral striatum. Samples were taken every 45 min over 3 h before and over 5 h after morphine or vehicle administration. Administration of morphine into the ventral pallidum resulted in increased DOPAC and HVA concentrations in the nucleus accumbens. Pretreatment with naloxone (1 mg/kg, SC) abolished this effect of morphine. Administration of morphine into the globus pallidus resulted in increased DA, DOPAC, and HVA concentrations in the nucleus accumbens and DA in the anteromedial striatum. The levels of DA and metabolites in anterolateral striatum remained rather unchanged following morphine administered into the ventral pallidum or the globus pallidus. The changes in DA neurotransmission into the nucleus accumbens induced by morphine application into the ventral pallidum and globus pallidus are reminiscent of a phasic and tonic release of DA respectively. The results show that intrapallidal morphine increases DA neurotransmission in nucleus accumbens and suggest that the effect of morphine is mediated by ventral pallidum/mesolimbic and globus pallidus/thalamocortical pathways, depending on the site of injection.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Analgesia induced by morphine injected into the pallidum.

Bilateral microinjections of morphine hydrochloride (10; 20; 30 micrograms/0.5 microliter/side) or saline were aimed at three different regions of the rat globus pallidus: dorsal, medial, ventral. Before and at various intervals after intrapallidal morphine (15; 30; 60; 90; 180 min), estimation of pain threshold was made by the hot plate procedure. Dose-dependent morphine analgesia was elicited from all three regions injected. Differences between the pallidal areas as to the intensity and duration of the drug's effect were noticed. Pretreatment with subcutaneous naloxone (1 mg/kg, s.c.) inhibited the morphine (20 micrograms) analgesia elicited from the medial and dorsal pallidum; it decreased and delayed the effect of morphine injected into the ventral pallidum. The results suggest that the three pallidal areas tested are involved to a different degree (medial/dorsal greater than ventral) in the morphine analgesia mediated by opiate receptors.

Animals↗

PubMed1992

Pallidal substrate of morphine-induced locomotion.

Bilateral microinjections of morphine hydrochloride (5.0; 7.5; 10.0 micrograms/0.5 microliters/side) or saline were infused into 3 different regions (dorsal, medial, ventral) of the rat globus pallidus, to examine their effects on locomotor activity. Locomotor activity of each rat was measured 45 min before and 90 min after saline or morphine pallidal microinjections. Morphine induced a dose-dependent increase in locomotion. This increase in locomotion was also significantly different between the 3 pallidal regions. Pretreatment with naloxone (1 mg/kg, sc) inhibited the morphine (7.5 micrograms) hyperlocomotion elicited from all three pallidal areas. The results suggest that the entire pallidum serves as substrate of morphine hyperlocomotion mediated by opiate receptors.

Animals↗