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Biomedical subjects

A Ally

Publications and source records attributed to A Ally.

At least 37 records · Page 2Linked to original sources
PubMed1997

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction.

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

Extracellular serotonin changes in VLM during muscle contraction: effects of 5-HT1A-receptor activation.

This study determined whether muscle contraction causes an increase in extracellular levels of serotonin (5-HT) in the rostral (rVLM) or caudal ventrolateral medulla (cVLM) in anesthetized rats. Muscle contraction, evoked by tibial nerve stimulation, increased mean arterial blood pressure (MAP) by 27 +/- 4 mmHg (n = 8). In addition, 5-HT levels in the rVLM were elevated by 65 +/- 9% during the contraction (n = 8). Results were similar over two repeated contractions. In contrast, muscle contraction increased MAP, but not 5-HT, levels in the cVLM (n = 6). Tibial nerve stimulation after muscle paralysis had no effect on either MAP or 5-HT levels in both rVLM and cVLM. Microdialysis of a 5-HT1A agonist, 8-OH-DPAT (10 mM), into the rVLM for 30 min (n = 6) blunted the MAP change and reduced 5-HT release during contraction. Administration of NAN-190, a 5-HT1A antagonist, into the rVLM had no effect on 5-HT release and cardiovascular responses during muscle contraction and blocked the changes in 5-HT, MAP, and heart rate to static contraction after subsequent microdialysis of 8-OH-DPAT. Results demonstrate that 5-HT levels in the rVLM increase during muscle contraction and that 5-HT1A-receptor activation in the rVLM blunts MAP response to muscle contraction via a decrease in the extracellular concentration of 5-HT.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

Central 5-HT1A modulation of cardiovascular responses to tibial nerve stimulation-evoked muscle contraction.

The effects of administering 8-hydroxy-2-(di-n-propylamine) tetralin [8-OH-DPAT, a serotonin 1A (5-HT1A) receptor agonist] into the rostral ventrolateral medulla (RVLM) on cardiovascular responses during tibial nerve stimulation-evoked muscle contraction were investigated using anesthetized rats. Stimulation of the tibial nerve (3 times motor threshold, 0.1 ms, 40 Hz) for 30 s increased mean arterial pressure (MAP), heart rate (HR), and muscle tension by 25 +/- 3 mmHg, 24 +/- 4 beats/min, and 299 +/- 35 g, respectively. Bilateral microdialysis of 8-OH-DPAT (10 mM) for 30 min attenuated the stimulation-evoked increases in MAP (8 +/- 2 mmHg) and HR (11 +/- 5 beats/min), without a change in muscle tension (292 +/- 30 g). However, administration of 1 mM 8-OH-DPAT had no effect on the cardiovascular responses. Thirty minutes of microdialysis of 8-OH-DPAT (10 mM) into the caudal ventrolateral medulla produced no effect on cardiovascular responses during muscle contraction. Prior administration of 10 mM 1-[2-methoxyphenyl]-4-[4-(2-phthalimido)-butyl]piperazine (NAN-190), a 5-HT1A receptor antagonist, for 30 min into the RVLM blocked the attenuating effects of subsequent microdialysis of 8-OH-DPAT (10 mM). Results suggest that activation of 5-HT1A receptors within the RVLM inhibit cardiovascular responses elicited during static muscle contraction.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

Central injection of physostigmine attenuates exercise-induced pressor response in conscious cats.

The effects of intracerebroventricular administration of physostigmine, a cholinesterase inhibitor, on the cardiovascular responses evoked by static voluntary exercise were investigated using conscious cats. Four cats were trained to press a bar (200-650 g) with one forelimb for at least 20 s. The changes in mean arterial pressure (MAP), heart rate (HR), and developed force during the first five trials in 30 min by each individual cat were averaged, and a mean of the four values was then calculated. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or physostigmine (5 micrograms) was administered intracerebroventricularly. Before physostigmine, exercise trials by the cats increased MAP and HR by 17 +/- 3 mmHg and 42 +/- 4 beats/min, respectively. Administration of physostigmine did not alter the resting MAP and HR but attenuated the MAP and HR responses to exercise (5-30 min postphysostigmine: MAP = 8 +/- 3 mmHg, HR = 25 +/- 7 beats/min; 30-60 min postphysostigmine: MAP = 4 +/- 3 mmHg, HR = 19 +/- 8 beats/min). Intracerebroventricular administration of CSF had no effect on the cardiovascular responses to static exercise. Pretreatment with the muscarinic antagonist, atropine (25 micrograms icv), blocked the attenuating effects of subsequent intracerebroventricular administration of physostigmine. These results demonstrate that stimulation of central muscarinic receptors attenuates the cardiovascular responses to static exercise by conscious cats. In addition, the present study suggests that there is no tonic effect of central muscarinic receptors on the cardiovascular responses to voluntary exercise.

Analysis of Variance↗
PubMed1997

Effects of central nervous stimulants on spino-bulbo-spinal reflex potentials in cats.

Effects of central nervous stimulants on the spino-bulbo-spinal reflex potential were evaluated in anesthetized intact cats, and compared with those on segmental spinal reflex potentials in anesthetized spinal cats. In spinal cats, strychnine augmented polysynaptic reflex potential, picrotoxin inhibited dorsal root reflex potential, aminopyrine potentiated mono- and poly-synaptic reflex potentials but inhibited dorsal root reflex potential, and 4-aminopyridine potentiated all the three types of segmental reflex potentials. A combination of fenbufen, a non-steroidal antiinflammatory agent, and enoxacin, a new quinolone antimicrobial, inhibited all the three types of segmental reflex potentials. In contrast, all these drugs consistently produced an augmentation of the spino-bulbo-spinal reflex potential in anesthetized intact cats. From these findings, we suggest that the spino-bulbo-spinal reflex potential may be used as an electrophysiological parameter for the evaluation of central nervous stimulants.

Action Potentials↗
PubMed1996

Cardiovascular responses to static exercise in conscious cats: effects of intracerebroventricular injection of clonidine.

1. Static exercise elicits increases in arterial blood pressure and heart rate (HR) in humans and conscious animals. In this study, the effects of intracerebroventricular (I.C.V.) administration of clonidine, an alpha 2-adrenergic agonist, on these cardiovascular responses were investigated using conscious cats. Four cats were operantly trained to extend a forelimb and press a bar (200-650 g) for 15-60 s. A stainless-steel cannula was inserted into the right lateral ventricle for I.C.V. injection of drugs, and a common carotid artery was catheterized to measure mean arterial pressure (MAP) and HR. The number of exercise trials and changes in MAP, HR and force were pooled for 30 min periods. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or clonidine (2 or 5 micrograms) were administered intracerebroventricularly. 2. Before clonidine injection, fifty-two exercise trials increased MAP and HR by 15 +/- 3 mmHg and 41 +/- 5 beats min-1, respectively. Administration of clonidine (2 micrograms) did not alter the resting MAP and HR, but attenuated the increases in MAP and HR in response to exercise (0-30 min post-clonidine: n = 81; delta MAP, 6 +/- 3 mmHg; delta HR, 20 +/- 6 beats min-1; 30-60 min post-clonidine: n = 71; delta MAP, 4 +/- 4 mmHg; delta HR, 17 +/- 8 beats min-1). Administration of artificial CSF I.C.V. had no effect on the cardiovascular responses to static exercise. 3. An increased dose of clonidine (5 micrograms) decreased resting MAP and HR by 31 +/- 7 mmHg and 37 +/- 7 beats min-1, respectively, and markedly blunted the cardiovascular responses to exercise (pre-clonidine: n = 52; delta MAP, 17 +/- 3 mmHg; delta HR, 38 +/- 5 beats min-1; post-clonidine 0-30 min: n = 66; delta MAP, 4 +/- 2 mmHg; delta HR, 15 +/- 5 beats min-1; post-clonidine 30-60 min: n = 60; delta MAP, 4 +/- 2 mmHg; delta HR, 14 +/- 6 beats min-1). Pretreatment with the alpha 2-adrenergic antagonist, yohimbine (8 micrograms, I.C.V.), blocked the attenuating effects of I.C.V. administration of clonidine (5 micrograms). 4. These results show that stimulation of central alpha 2-adrenoceptors by clonidine attenuates the cardiovascular responses to static exercise in conscious cats. In addition, this study suggests that alpha 2-adrenoceptors blocked by yohimbine injected I.C.V. do not appear to have a tonic influence on HR and blood pressure.

Animals↗
PubMed1996

NMDA receptor blockade in cat dorsal horn blunts reflex pressor response to muscle contraction and stretch.

The role of N-methyl-D-aspartate (NMDA) receptors in the reflex pressor response to static muscle contraction and passive stretch was examined by microdialyzing the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (AP-5) into the L7 or L6 and S1 levels of the dorsal horn of anesthetized cats. Contraction, elicited by electrical stimulation of the cut L7 and S1 ventral roots, increased mean arterial pressure (MAP) and heart rate (HR). Passive stretch at tensions similar to those generated by contraction also increased these variables. These cardiovascular changes were unaffected by dialyzing AP-5 (10 mM) into the dorsal horn at L7. Increasing the syringe concentration of AP-5 to 100 mM attenuated the pressor and HR responses from 62 +/- 8 to 31 +/- 6 mmHg and 18 +/- 4 to 12 +/- 4 beats/min, respectively. AP-5 blunted the increase in MAP (59 +/- 10 vs. 41 +/- 10 mmHg) evoked by muscle stretch. Simultaneously microdialyzing AP-5 (10 or 100 mM) into the dorsal horn at the L6 and S1 spinal levels also blunted the MAP and HR responses to contraction and stretch. These results suggest that NMDA receptors play a role in mediating the MAP and HR responses to static muscle contraction at the spinal level of the central nervous system. Furthermore, these data demonstrate that collaterals from muscle afferents partially mediate the reflex cardiovascular responses evoked by muscle contraction and stretch.

2-Amino-5-phosphonovalerate↗
PubMed1995

Cardiovascular effects elicited by central administration of physostigmine via M2 muscarinic receptors in conscious cats.

The cardiovascular effects of an intracerebroventricular (i.c.v.) injection of physostigmine were studied using conscious cats. Physostigmine (5-25 micrograms: 5 microliters) caused a dose-dependent increase in mean arterial pressure (MAP) and heart rate (HR). The highest dose (25 micrograms) increased MAP and HR by 32 +/- 3 mmHg and 45 +/- 5 beats/min, respectively (n = 5). Pre-administration of the muscarinic receptor antagonist, atropine (25 micrograms; i.c.v.) blocked the effects of physostigmine (25 micrograms; i.c.v.). Also, the pre-administration of the M2 muscarinic antagonist, methoctramine (25 micrograms; i.c.v.), antagonized the cardiovascular effects of physostigmine without altering the baseline variables. However, the M1 muscarinic antagonist, pirenzepine (100 micrograms; i.c.v.) did not alter baseline MAP or HR, and also failed to inhibit the cardiovascular responses to physostigmine. Similarly, the M3 muscarinic blocker, 4-diphenyl-acetoxy-N-methylpiperidine methiodide (50 micrograms; i.c.v.), neither changed baseline cardiovascular variables nor blocked the effects of physostigmine. When the same cats were anesthetized with intravenous injection of sodium pentobarbital (25-30 mg/kg), physostigmine (25 micrograms; i.c.v.) evoked a decrease in MAP and HR of 13 +/- 6 mmHg and 15 +/- 6 bpm, respectively (n = 5). These results demonstrate that the increases in MAP and HR to the i.c.v. administration of physostigmine in conscious cats are possibly mediated through stimulation of central M2 muscarinic receptors. In addition, anesthesia reverses the effects elicited by the central administration of physostigmine to a decrease in MAP and HR.

Animals↗
PubMed1995

Modulation of reflex pressor response to contraction and effect on substance P release by spinal 5-HT1A receptors.

This study investigated whether activation of serotonin1A [5-hydroxytryptamine (5-HT)1A] receptors in the dorsal horn of the spinal cord attenuates the reflex pressor response to static contraction and passive muscle stretch. In addition, we determined if the attenuation of the response to contraction is mediated by inhibiting substance P (SP) release in the dorsal horn. Static contractions of the triceps surae muscle of chloralose-anesthetized cats were induced by stimulating the cut L7 and S1 ventral roots. Microdialysis (10 mM) of a selective 5-HT1A agonist [8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT)] into the L7 dorsal horn region produced a reversible attenuation of the reflex pressor response to a 1-min contraction (in mmHg: control = 36 +/- 3; 8-OH-DPAT = 17 +/- 3; recovery = 31 +/- 8; P = 0.013; n = 6) or passive stretch (in mmHg: control = 36 +/- 6; 8-OH-DPAT = 15 +/- 2; recovery = 32 +/- 6; P = 0.002; n = 6). However, a 5-HT1B agonist, 1-[3-(trifluoromethyl)-phenyl]piperazine, had no effect on the reflex pressor response. During 5-min contractions (n = 8), 8-OH-DPAT (10 mM) also blunted the pressor response but had no effect on the levels of SP-like immunoreactivity (in fmol/100 microliters: control = 0.492 +/- 0.026; 8-OH-DPAT = 0.501 +/- 0.034). These results suggest that activation of 5-HT1A receptors in the dorsal horn attenuates the reflex pressor response to contraction through a mechanism other than inhibition of SP release.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Attenuation of the exercise pressor reflex. Effect of opioid agonist on substance P release in L-7 dorsal horn of cats.

Using alpha-chloralose-anesthetized cats, we studied blood pressure and heart rate responses to static contraction and passive stretch of the triceps surae muscle before and after microdialyzing the mu-opioid agonist [D-Ala2]-methionine enkephalinamide (DAME, 200 mumol/L) into the L-7 dorsal horn of the spinal cord. In addition, we measured contraction-induced substance P release in the dorsal horn before and after drug delivery. After 92 +/- 3 minutes of dialyzing the opioid agonist, contraction-induced increases in mean arterial pressure and heart rate were attenuated from control values of 58 +/- 7 mm Hg and 17 +/- 3 beats per minute to postdrug values of 27 +/- 7 mm Hg and 10 +/- 2 beats per minute, respectively. A similar attenuation was observed for the passive muscle stretches after 97 +/- 5 minutes of dialysis (control, 38 +/- 4 mm Hg and 8 +/- 2 beats per minute; after drug, 23 +/- 4 mm Hg and 5 +/- 1 beats per minute). Prior microdialysis of naloxone (300 mumol/L), a mu-antagonist, blocked this effect, suggesting that the opioid agonist has a specific receptor action. Naloxone alone had no effect on the pressor or tachycardiac responses. The contraction-induced increase in substance P-like immunoreactivity was reduced from a control value of 0.119 +/- 0.024 to 0.047 +/- 0.010 fmol/100 microL by DAME. Time-control experiments revealed no decrease in the release of substance P-like immunoreactivity. Thus, activation of opioid receptors modulates the transmission of group III and IV muscle afferent nerve activity through the L-7 dorsal horn.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Large-scale genomic sequencing: optimization of genomic chemical sequencing reactions.

We have developed a streamlined, reproducible method for performing genomic chemical sequencing reactions on the genomic DNA of Mycoplasma capricolum, which has a genome size of about 750,000 base pairs and whose composition is 75% AT. The general modifications that ensure reproducibility and allow the processing of multiple samples can be widely adopted to other large-scale sequencing projects, while the specific modifications to the chemical reactions are applicable to the sequencing of other DNAs with a high AT content.

Adenine↗
PubMed1994

Intracellular and extracellular spaces and the direct quantification of molar intracellular concentrations of phosphorus metabolites in the isolated rat heart using 31P NMR spectroscopy and phosphonate markers.

To quantify metabolite and cation concentrations using NMR spectroscopy, the volumes of intracellular and extracellular spaces must be known. We describe a simple 31P NMR spectroscopic method that employs dimethyl methylphosphonate (DMMP) as a marker of total water space and phenylphosphonate (PPA) as a marker of extracellular space to determine intracellular and extracellular space volumes in the isolated, perfused rat heart. In vivo and in vitro radiolabel studies were used to verify this method. The difference between the total and extracellular water spaces, determined as milliliters/heart, gave the intracellular volume and allowed direct calculation of myocardial creatine phosphate, ATP, and inorganic phosphate concentrations, which were 13.4 mM, 10.1 mM, and 3.4 mM, respectively, for the glucose-perfused rat heart. The extracellular volume decreased by 84% in hearts subjected to 28 min total, global ischemia and increased by 15% during reperfusion. The method described allows the determination of intracellular energy metabolite concentrations in perfused rat heart directly from a single, fully relaxed 31P NMR spectrum.

Animals↗
PubMed1994

Central cholinergic modulation of the exercise pressor reflex in anesthetized cats.

Effects of central administration of a cholinesterase inhibitor, physostigmine, on cardiovascular responses to static contraction and passive stretch of the triceps surae were studied using anesthetized cats. Contraction increased mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) by 44 +/- 5 mmHg, 18 +/- 1 beats/min, and 86 +/- 6%, respectively. MAP, HR, and RSNA increased during stretch by 44 +/- 5 mmHg, 15 +/- 1 beats/min, and 61 +/- 4%, respectively. Administration of physostigmine (100 micrograms; 5 microliters) into the third ventricle decreased resting MAP by 22 +/- 3 mmHg and RSNA by 32 +/- 4%, with no effect on HR. Physostigmine attenuated the contraction-evoked responses as MAP, HR, and RSNA increased by 17 +/- 2 mmHg, 3 +/- 1 beats/min, and 31 +/- 6%, respectively. Also, physostigmine blunted MAP, HR, and RSNA responses to stretch (16 +/- 2 mmHg, 4 +/- 1 beats/min, and 9 +/- 6%, respectively). Posterior hypothalamic stimulation increased MAP by 39 +/- 3 mmHg, which was unaffected by physostigmine, despite a lower baseline. Cardiovascular and RSNA responses to contraction and stretch returned to control 90-120 min after physostigmine. Preadministration of the muscarinic antagonist, atropine sulfate (100 micrograms; 5 microliters), blocked the effects of physostigmine. Results suggest central cholinergic stimulation can inhibit the exercise pressor reflex in anesthetized cats.

Anesthesia↗
PubMed1994

Effects of clonidine on the reflex cardiovascular responses and release of substance P during muscle contraction.

The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48 +/- 6 mm Hg, 18 +/- 2 beats per minute, and 66 +/- 5%, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51 +/- 6 mm Hg, 17 +/- 2 beats per minute, and 50 +/- 3%, respectively. Microdialysis of clonidine (380 mumol/L) blunted the contraction-evoked responses: MAP, HR, and RSNA increased by 19 +/- 4 mm Hg, 7 +/- 1 beats per minute, and 24 +/- 5%, respectively. The increases elicited by passive stretch were also attenuated (MAP, 22 +/- 4 mm Hg; HR, 6 +/- 1 beats per minute; and RSNA, 15 +/- 4%). This attenuation by clonidine was dose dependent (3.8 mumol/L, 38 mumol/L, 380 mumol/L, and 3.8 mmol/L). Preadministration of the alpha 2-adrenergic antagonist yohimbine (3 mmol/L) blocked the effect of clonidine (380 mumol/L) on the cardiovascular and RSNA responses to muscle contraction. Clonidine (380 mumol/L) did not alter the release of SP in the dorsal horn during contraction (before clonidine, 0.380 +/- 0.018 fmol/100 microL; after clonidine, 0.356 +/- 0.012 fmol/100 microL).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Cardiovascular effects of central administration of cholinomimetics in anesthetized cats.

The cardiovascular effects of central administration of cholinomimetics were investigated in anesthetized cats, to identify the site and mechanism of their action. Physostigmine, 10-100 micrograms, given by intracerebroventricular administration (i.c.v.) caused a dose-dependent reduction in blood pressure and renal sympathetic nerve discharges and no change in heart rate, which were antagonized by intravenous injection (i.v.) of atropine but not by methscopolamine or pirenzepine, given intravenously. Carbachol 3-30 micrograms (i.c.v.) reduced blood pressure and renal sympathetic nerve discharges and caused no change in heart rate. The M1 muscarinic agonist, McN-A-343, 100-1000 micrograms (i.c.v.) did not affect blood pressure, heart rate or renal sympathetic nerve discharges. Bilateral application of physostigmine, 10-100 micrograms/site on the ventral medullary surface, decreased blood pressure and renal sympathetic nerve discharges but not heart rate. Carbachol, 3-30 micrograms/site, caused reductions in blood pressure and renal sympathetic nerve discharges and no change in heart rate. Atropine, but not pirenzepine or methscopolamine, reversed the effects of physostigmine or carbachol. Treatment with McN-A-343, 100-1000 micrograms/site, did not alter blood pressure, heart rate or renal sympathetic nerve discharges. Under pretreatment with atropine into the ventral medulla but not pirenzepine, physostigmine, given intravenously, did not influence blood pressure. It is concluded that a cholinergic mechanism, concerned with a depressor response, is located on the ventral medulla. Muscarinic receptors of the non-M1 subtype, possibly M2, are related to this mechanism.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1993

Effects of methylmercury and trimethyltin on cardiac, platelet, and aorta eicosanoid biosynthesis and platelet serotonin release.

The effects of two organometals on heart, platelet, and aorta prostaglandin biosynthesis were examined in vitro. Methylmercuric chloride (MMC, 39-796 nM) increased the biosynthesis of thromboxane A2 (TxA2) and prostacyclin (PGI2) in the heart and stimulated the biosynthesis of PGI2 in incubates of aorta rings. The aorta biosynthesis of PGI2 was monitored by its inhibition of platelet aggregation and serotonin [5-hydroxytryptamine (5-HT)] secretion, while the metabolites 6-keto-PGF1a and TxB2 were quantified by radioimmunoassay. In platelet experiments, low concentrations of MMC (5 microM) enhanced aggregation to adenosine diphosphate (ADP) and at high concentrations MMC (50-100 microM) directly stimulated aggregation and 5-HT secretion. These effects of MMC were inhibited by nonsteroidal antiinflammatory drug, thromboxane synthetase, and phospholipase A2 inhibitors. Trimethyltin (TMT), another highly toxic organometal, had no effect on prostaglandin biosynthesis in either heart or aorta incubates. TMT did not increase platelet aggregation responses to ADP, nor did it directly trigger aggregation. At moderate concentrations, TMT (20-45 microM) slightly depressed ADP aggregation; however, this was paradoxically associated with increased 5-HT secretion. In platelets pretreated with either NDGA or ASA, TMT in the absence of aggregation enhanced 5-HT secretion in response to ADP. TMT, unlike MMC, did not stimulate platelet TxB2 biosynthesis from exogenous [3H]arachidonic acid, whereas MMC stimulates heart, vascular, and platelet eicosanoid biosynthesis. TMT, unlike MMC, does not directly activate the arachidonic acid cascade.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Enriched environment primes forebrain choline acetyltransferase activity to respond to learning experience.

Weanling rats were raised in an enriched or an impoverished environment. The enriched rats subsequently learned the Morris water maze faster than their impoverished counterparts. The enriched rats, both maze-trained and untrained, showed higher choline acetyltransferase (ChAT) activity in the caudate than did the impoverished, untrained rats. Maze training increased caudate ChAT in impoverished rats. Enriched but not impoverished rats showed increased hippocampal and anterior cortical ChAT activity after maze training. Thus, enrichment causes a long-lasting increase in caudate acetylcholine (Ach) synthesis and it also primes cortex and hippocampus to respond to a training experience with increased Ach synthesis.

Animals↗