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M Güemes

Publications and source records attributed to M Güemes.

6 recordsLinked to original sources
PubMed1998

Socio-sexual behavior in male rats after lesions of the dorsolateral tegmentum.

The medial preoptic area of the anterior hypothalamus (MPOA/AH) and the dorsolateral tegmentum (DLT) play an important role in the control of sexual behavior. Unilateral lesions of the MPOA/AH (medial preoptic area of the anterior hypothalamus) combined with unilateral lesions of the contralateral DLT result in deficits in male sexual behavior, while bilateral electrolytic lesions of the DLT have similar effects. In the present study, coital and socio-sexual interactions were recorded before and after bilateral electrolytic DLT lesions. Coital behavior was monitored for 15 weeks after surgery and socio-sexual interactions one 1 and 3 weeks after lesion. DLT-lesioned animals showed reduced copulatory behavior throughout the 15 weeks postlesion. This inhibition was associated with changes in exploratory (sniffing), precopulatory (pursuit and genital exploration), and postcopulatory behaviors (self-grooming). No differences were found in the weights of the testicles, prostate and seminal vesicles. These results indicate that lesions of the DLT produced permanent deficits in sexual behavior associated with a generalized modification of sociosexual behavior. These deficits indicate reduced sexual motivation possibly due to the disruption of the output pathway from the MPOA/AH (medial preoptic area of the anterior hypothalamus) to the DLT.

Animals↗
PubMed1990

Purinergic and cyclic AMP modulation of noradrenaline release in cat femoral arteries.

1. Adenosine, AMP, ATP (5 x 10(-4) M), 5'-N-ethylcarboxamide adenosine (NECA) and N6-L-phenylisopropyl adenosine (L-PIA) (10(-4) M) decreased tritium release elicited by electrical stimulation (ES) or 50 mM K+ in cat femoral arteries preincubated with [3H]noradrenaline (NA). 2. This effect was antagonized by 1-methyl-3-isobutylxanthine (MIX, 5 x 10(-5) M). 3. The release induced by ionophore X-537A (10(-5) M) was unaffected by adenosine and AMP. 4. The increase of intracellular cAMP levels caused by dibutyryl cAMP (5 x 10(-4) M), Ro-20 1724 (10(-4) M), forskolin (5 x 10(-6) M), NaF (2 x 10(-3) M) reduced, but MIX (5 x 10(-5) M) increased tritium release elicited by ES and K+. 5. Dipyridamole (5 x 10(-5) M) and erythro-9-2-hydroxy-3 nonyl adenosine (EHNA) (10(-4) M) also reduced tritium release. 6. Dipyridamole decreased both the uptake of [3H]NA and [3H]adenosine. 7. These data indicate: (a) the existence of A1 and A2 subtypes of purinoceptors situated presynaptically, which modulates NA release, (b) the intracellular increase of cAMP negatively modulates this secretion, and (c) these arteries possess an active system for incorporating and degrading adenosine.

Adenine Nucleotides↗
PubMed1990

Role of presynaptic purinoceptors and cyclic AMP on the noradrenaline release in cat cerebral arteries.

Field electrical stimulation (ES), K+ (50 mM) or ionophore X-537A (0.01 mM) induced tritium release from cat cerebral arteries preincubated with [3H]noradrenaline (NA). Adenosine and AMP (0.5 mM) did not modify tritium release caused by ionophore X-537A, but these agents and ATP (0.5 mM) significantly reduced that elicited by ES and K+; this reduction was antagonized by 1-methyl-3-isobutylxanthine (MIX; 0.05 mM). Inosine (0.5 mM) and the agonist of purinergic A2-receptors, 5'N-ethyl-carboxamide adenosine (NECA; 0.5 mM) had no effect, but the agonist of purinergic A2-receptors L-N6-phenylisopropyl adenosine (L-PIA; 0.1 mM) diminished tritium efflux caused by ES and K+. The adenosine inhibition of ES-induced radioactivity release was not affected by indomethacin (0.05 mM). MIX (0.05 mM) increased tritium release evoked by ES and K+. Agents that increase intracellular cyclic (c)AMP levels, such as dibutyryl cAMP (0.5 mM), the phosphodiesterase inhibitor Ro 20-1724 (0.1 mM), and the activators of adenylate cyclase, forskolin (0.005 mM) and NaF (2 mM) reduced tritium secretion elicited by ES and K+. However, the intracellular increase of cyclic GMP (cGMP) caused by 8-Br-cGMP did not affect this secretion. Dipyridamole (0.05 mM) and the adenosine deaminase inhibitor erythro-9-2-hydroxy-3 nonyl adenosine (EHNA; 0.1 mM) also produced inhibition of tritium secretion elicited by ES and K+. Dipyridamole reduced both the uptake of [3H]NA and [3H]adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine↗