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J L Martinez

Publications and source records attributed to J L Martinez.

At least 19 recordsLinked to original sources
PubMed1992

Differences in one-way active avoidance learning in mice of three inbred strains.

DBA/2J, C57BL/6J, and C3H/HeJ mice were given 10 one-way avoidance training trials per day, using an unconditioned stimulus intensity that provided equivalent motivation for learning to mice of all three strains, and were found to differ in their abilities to learn and retain the response. DBA/2J mice acquired the response in fewer days than did the mice of the other two strains, although C57BL/6J mice eventually reached a level of performance similar to that of DBA/2J mice. Both the rate of acquisition and the level at which avoidance performance stabilized were significantly lower in C3H/HeJ, than in DBA/2J or C57BL/6J, mice. In addition, DBA/2J mice showed a significantly greater task retention from one testing day to the next than did C57BL/6J or C3H/HeJ mice.

Animals↗
PubMed1992

Kappa opioid receptor activity modulates memory for peck-avoidance training in the 2-day-old chick.

To examine the role of kappa opioid receptors in memory formation, 2-day-old chicks were injected intracerebrally with either the endogenous opioid peptide dynorphin(1-13), the highly kappa selective agonist U-50,488 or the kappa selective antagonist nor-binaltorphimine (nor-BNI), given one-trial peck-avoidance training, and tested 24 h later. Dynorphin(1-13) impaired memory in a dose dependent manner at 24 h test. Injection of U-50,488 caused a biphasic dose-dependent effect on memory; low doses caused a trend toward enhanced memory and high doses caused significant impairment. Conversely, injection of low doses of nor-BNI caused a trend toward memory impairment, and higher doses caused significant memory enhancement. The results indicate that memory formation for one-trial peck-avoidance training may be modulated by kappa opioid receptor activity.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Cocaine enhances retention of avoidance conditioning in rats.

The effects of post-training cocaine administration were tested on retention of a one-way active avoidance task in rats. A 5.0 mg/kg IP dose of cocaine enhanced retention of the avoidance task, in three separate experiments, as indicated by an increase in the number of avoidances made when animals were tested 24 h after training, while both a lower (2.5 mg/kg) and a higher (7.5 mg/kg) cocaine dose had no effect. Lidocaine (4-8 mg/kg) administered post-training did not reliably affect retention in the same task. Cocaine's ability to enhance retention depended on the interval between training and drug injection such that only cocaine administered directly after training enhanced retention the following day. The results show that post-training cocaine administration enhances retention of an active avoidance task in rats, and that this effect is probably independent of the anesthetic properties of the drug.

Animals↗
PubMed1992

Roles of delta and mu opioid receptors in mediating the effects of enkephalins on avoidance conditioning.

The effects on one-way active avoidance conditioning of pre-training, systemic administration of the selective mu-receptor agonist [D-Ala2,N-Me-Phe4, Gly-ol]enkephalin (DAGO), and the selective mu-receptor antagonist (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP), were determined in Swiss-Webster mice. A low dose of DAGO (0.92 micrograms/kg) moderately enhanced avoidance acquisition, whereas a 100 micrograms/kg dose of CTOP more dramatically impaired acquisition. However, the avoidance-enhancing dose of DAGO significantly increased locomotor activity as measured in a separate group of mice in the avoidance chamber, and the avoidance-impairing dose of CTOP significantly decreased activity. Under these same training conditions, earlier studies (Schulteis et al. 1988; Schulteis and Martinez 1990) demonstrated that enkephalins impaired avoidance learning, and selective delta-receptor antagonists such as ICI 174,864 enhanced learning; in contrast to the present study, both of these effects were dissociated from performance effects such as alterations in locomotor activity. Taken together, the results suggested that the effects of enkephalins were mediated by the delta-, but not mu-, class of opioid receptor.

Amino Acid Sequence↗
PubMed1992

Peripheral modulation of learning and memory: enkephalins as a model system.

Extensive research on the effects of enkephalins on conditioning is reviewed and used as the basis for a model of peripheral modulation of learning and memory. An overall theme emphasized throughout our discussion is that these peptides can influence the strength with which a memory is acquired and stored by acting outside the blood-brain barrier. This assertion is supported by research on the behavioral effects of systemically administered enkephalins and opioid antagonists, the rapid hydrolysis of circulating enkephalins in vivo, and the limited ability of these peptides to penetrate the blood-brain barrier. A consideration of the extensive distribution of enkephalins throughout peripheral autonomic systems leads to the proposal that enkephalins may act to modulate learning and memory by altering peripheral autonomic function; autonomic afferents may then communicate with the memory trace in the CNS through a central modulatory pathway outlined herein. Evidence that some stressful experiences may lead to increases in circulating enkephalins also is discussed. The sites of action of these circulating enkephalins may involve peripheral autonomic sites, or additionally may involve the circumventricular organs. As a further regulatory mechanism, circulating enkephalin levels may be controlled by experience-dependent alterations of the activity of enzyme systems that participate in their breakdown. Finally, it is emphasized that the mechanisms of enkephalin action postulated herein may be applicable to the actions of other peripheral hormones, peptides, and neurotransmitters that participate in the modulation of learning and memory storage processes.

Animals↗
PubMed1992

Enkephalin hydrolysis by mouse plasma in vitro.

Hydrolysis of [Leu]- and [Met]enkephalin was determined in samples of pooled whole mouse plasma in vitro by using HPLC-ECD to measure accumulation of Tyr-containing metabolites. More Tyr-Gly-Gly accumulated from [Met]enkephalin than from [Leu]enkephalin hydrolysis, and [Met]enkephalin's half-life in mouse plasma was approximately half that of [Leu]enkephalin. Comparisons of metabolite formation in the presence versus the absence of inhibitors with high selectivity for various peptidases demonstrated that a bestatin-sensitive aminopeptidase, presumably aminopeptidase M, as well as enkephalinase and angiotensin converting enzyme, participate in the hydrolysis of enkephalin in mouse plasma.

Amino Acid Sequence↗
PubMed1992

[Leu]enkephalin and its metabolite, Tyr-Gly-Gly, impair active avoidance retention.

The current study examined the effects of [leu]enkephalin and its metabolite, Tyr-Gly-Gly, given immediately posttraining on active avoidance performance measured 24 h later. Initial experiments revealed that, in comparison to zero or one training trials, providing mice with two training trials significantly increased active avoidance performance measured 24 h later; this enabled us to examine the effects on retention of peptides administered immediately after the two training trials. It was found that Tyr-Gly-Gly (16 and 53 micrograms/kg) and [leu]enkephalin (30 and 100 micrograms/kg) administered in this fashion both significantly impaired retention; the dose-response functions for both peptides were U-shaped. Since the effects of enkephalins are most likely mediated by opioid delta-receptors, and Tyr-Gly-Gly has little or no activity at opioid receptors, the effects of the parent peptide(s) and metabolite are presumably pharmacologically distinct.

Amino Acid Sequence↗
PubMed1992

Cocaine and amphetamine facilitate retention of jump-up responding in rats.

The effects of cocaine and d-amphetamine administration on the acquisition of an automated jump-up active avoidance task were examined in two separate experiments. On days 1 and 2, male Sprague-Dawley rats received one escape-only training trial, followed immediately by the intraperitoneal injection of cocaine, amphetamine, or saline. On day 3, subjects received eight escape/avoidance trials. The posttraining administration of cocaine (2.75 and 5.55 mg/kg) and amphetamine (0.3 and 1.0 mg/kg) on days 1 and 2 facilitated jump-up avoidance performance on day 3. Importantly, both cocaine and amphetamine enhanced learning and memory under experimental conditions that allowed for drug-free training and testing.

Amphetamine↗
PubMed1992

Cocaine enhances one-way avoidance responding in mice.

We reported previously that posttraining cocaine injections enhance subsequent performance of an automated jump-up avoidance response and a trough avoidance response in rats. In the present study we examined the species generality of the cocaine enhancement by investigating the effects of posttraining cocaine injection on subsequent performance of a one-way active avoidance response in mice. Cocaine (30 mg/kg, IP) administered to mice immediately following completion of two escape-only trials on day 1 significantly enhanced avoidance response performance on day 2. Neither lidocaine nor cocaine methiodide, when administered in doses equimolar to the effective cocaine dose, altered performance on day 2. These data indicate that cocaine's enhancement of avoidance responding in mice probably is neither peripherally mediated nor attributable to its local anesthetic properties.

Animals↗
PubMed1992

Influences of changes in calcium concentration and verapamil on the cardiac depressant effect of ethanol in cat papillary muscle.

1. In isolated cat heart papillary muscle electrically driven at a constant rate the depressant effects of increasing concentrations of ethanol on peak tension developed (PTD) was studied in Ringer-Locke solution with different calcium concentrations and with the addition of verapamil. 2. Ethanol induced a concentration dependent decrease in PTD that was significantly greater for each concentration of ethanol in hypocalcic medium (1.1 mM) than in normocalcic medium (2.2 mM). 3. In normocalcic (2.2 mM) medium, verapamil (5.1 x 10(-4) mM) plus ethanol (48.6 and 97.2 mM) produced a decrease in PTD to values significantly greater than those obtained by the addition of ethanol and verapamil alone. Therefore a potentiation of the effects of ethanol by verapamil was observed when both drugs act simultaneously. 4. In hypercalcic medium (4.4 mM), verapamil plus ethanol (48.6 and 97.2 mM) produced a slight decrease in PTD that was significantly less than that observed in normocalcic and hypocalcic mediums. 5. In hypocalcic medium (1.1 mM) verapamil plus ethanol (48.6 and 97.2 mM) produced a decrease in PTD that was of the same relative magnitude (%) as that observed in normocalcic medium. However no potentiation of the combined effects of verapamil plus ethanol was observed in hypocalcic medium.

Animals↗
PubMed1992

Expression of actin isoforms in Artemia.

Complementary DNA clones have been isolated from the crustacean Artemia that code for four different actin isoforms. The nucleotide sequence of these clones has been determined. The four clones are about 80% identical in their translated regions but unrelated in their untranslated regions. The cloned Artemia actins are very similar in their deduced amino acid sequences to other invertebrate actins, especially in the amino terminal region. The analyses of the steady-state levels of actin mRNAs during Artemia development has shown a parallel increase in the levels of all four mRNAs between five and ten hours of development. Whole-mount embryo hybridizations have shown that one of the clones codes for a muscular actin isoform while the other three clones code for cytoplasmic isoforms.

Actins↗
PubMed1992

Mu opioid receptors are associated with the induction of hippocampal mossy fiber long-term potentiation.

We assessed the effects of antagonists selective for mu (mu), delta (delta) or kappa (kappa) opioid receptors on the induction of long-term potentiation (LTP) and short-term potentiation (STP) at the rat hippocampal mossy fiber-CA3 synapse in vivo. The mu opioid receptor-selective antagonist Cys2,Tyr3,Orn5,Pen7 amide (CTOP, 1 or 3 nmol) did not alter either mossy fiber-CA3 responses evoked at low frequencies or previously potentiated mossy fiber-CA3 responses, but it attenuated the induction of mossy fiber LTP in a dose-dependent manner. By contrast, LTP of CA3 responses evoked by stimulation of commissural afferents to the CA3 region was unaffected by CTOP. Neither the delta opioid receptor-selective antagonist naltrindole hydrochloride (0.3-10 nmol) or the kappa opioid receptor-selective antagonist nor-binaltorphimine hydrochloride (3-10 nmol) altered the induction of mossy fiber LTP. Thus, a role for delta or kappa opioid receptors in the induction of mossy fiber LTP could not be demonstrated. CTOP, in quantities that attenuated mossy fiber LTP induction, also attenuated the magnitude of mossy fiber STP measured 5 sec after delivery of conditioning trains. Further examination of the component of STP corresponding to post-tetanic potentiation (PTP) revealed that CTOP selectively attenuated the estimated magnitude and time constant of decay of mossy fiber PTP. These results suggest that the frequency-dependent activation of mu opioid receptors by endogenous opioid peptides is required for the induction of LTP at hippocampal mossy fiber synapses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Do bacteria have sex?

Explore the source record for details and available documents.

Bacterial Physiological Phenomena↗
PubMed1991

Further characterization of the in vitro hydrolysis of [Leu]- and [Met]enkephalin in rat plasma: HPLC-ECD measurement of substrate and metabolite concentrations.

Hydrolysis of [Leu]- and [Met]enkephalin was determined in whole rat plasma in vitro by using HPLC-ECD to measure Tyr, Tyr-Gly and Tyr-Gly-Gly formation. Although [Leu]- and [Met]enkephalin did not differ in Tyr or Tyr-Gly accumulation, the amount of Tyr-Gly-Gly resulting from [Met]enkephalin hydrolysis was greater than that resulting from [Leu]enkephalin hydrolysis, and [Met]enkephalin's half-life in plasma was slightly shorter than that of [Leu]enkephalin. By comparing metabolite formation in the presence and absence of peptidase inhibitors with high selectivity for their respective enzymes, these studies demonstrated that aminopeptidase M and angiotensin converting enzyme are the major peptidases that hydrolyze enkephalins in rat plasma.

Amino Acids↗
PubMed1991

Hydrolysis of [Leu]enkephalin by chick brain in vitro.

Using high-performance liquid chromatography with electrochemical detection to measure substrate disappearance and metabolite accumulation following addition of [Leu]enkephalin to samples prepared from chick brain in vitro, the following were found: 1. [Leu]enkephalin hydrolysis by whole forebrain homogenates is almost solely attributable to aminopeptidase MII activity. 2. [Leu]enkephalin hydrolysis by whole forebrain P2 membrane fractions is attributable to both aminopeptidase MII and dipeptidyl carboxypeptidase activity. 3. Differences are apparent in both [Leu]enkephalin disappearance and Tyr-Gly-Gly accumulation in P2 membrane fractions, but not in homogenate fractions, prepared from several regions of the chick brain.

Aminopeptidases↗
PubMed1991

Opioid receptors are involved in an NMDA receptor-independent mechanism of LTP induction at hippocampal mossy fiber-CA3 synapses.

Long-term potentiation (LTP) of mossy fiber responses in area CA3 of the rat hippocampus in vivo is blocked by naloxone, an opioid receptor antagonist, in a stereospecific and dose-dependent manner. LTP of commissural afferents to the same population of CA3 pyramidal cells is not attenuated by naloxone. This suggests that opioid receptors are involved in a mechanism of LTP induction that is specific to mossy fiber synapses, and that endogenous opioid receptors are involved in a mechanism of LTP induction that is specific to mossy fiber synapses, and that endogenous opioid peptides, presumably released as a result of mossy fiber stimulation, may be necessary for the induction of mossy fiber LTP. The naloxone sensitivity is limited to the induction phase of LTP, since naloxone does not reverse previously established LTP. These data suggest that LTP at the mossy fiber-CA3 synapse constitutes an NMDA receptor-independent, opioid receptor-dependent, form of hippocampal synaptic plasticity.

Animals↗