Biomedical subjects

M A Ashworth-Preece

Publications and source records attributed to M A Ashworth-Preece.

4 recordsLinked to original sources

PubMed1999

Visualisation of AMPA binding sites in the brain stem of normotensive and hypertensive rats.

The present study has employed in vitro receptor autoradiography with (S)-[(3)H]-5-fluorowillardiine (10 nM) to visualise the presence of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) binding sites in the brain stems of adult (16-18 weeks) normotensive (Wistar-Kyoto (WKY) and Don Ryu (DRY)) and Spontaneously Hypertensive (SHR) rats. Similar topographic distribution and density of (S)-[(3)H]-5-fluorowillardiine binding was observed in the nucleus tractus solitarius (NTS) of all three strains. Specific (S)-[(3)H]-5-fluorowillardiine binding sites were also visualised in sections of nodose ganglion from adult WKY rats, demonstrating that vagal afferent perikarya possess AMPA binding sites. However, while unilateral vagal deafferentation did not result in a significant decrease in binding site density in the caudal half of the rat NTS, the visualisation of AMPA binding sites on the nodose ganglion is consistent with the existence of a population of binding sites on vagal afferent terminals. In the caudal half of the rat NTS, AMPA binding sites appear to be predominantly postsynaptic in nature.

Alanine↗

PubMed1998

Nicotinic acetylcholine receptor mediated modulation of evoked excitatory amino acid release in the nucleus tractus solitarius of the rat: evidence from in vivo microdialysis.

In vivo microdialysis was used to measure release of endogenous l-glutamate and l-aspartate in the nucleus tractus solitarius of the anaesthetised rat evoked by baroreceptor loading. Aortic constriction, the method of loading, elicited a reproducible increase in extracellular levels of l-glutamate to 322+/-139% of basal levels, which could be attenuated by concomitant local administration of the nicotinic acetylcholine receptor antagonist mecamylamine (100 microM).

Animals↗

PubMed1995

5-Hydroxytryptamine3 receptor modulation of excitatory amino acid release in the rat nucleus tractus solitarius.

In vivo microdialysis was employed to measure release of endogenous L-glutamate (GLU) and L-aspartate (ASP) in the medial nucleus tractus solitarius of urethane anaesthetised rats. Basal extracellular levels of these amino acids were stable following a 90 min equilibration period (6.3 +/- 0.24 and 3.4 +/- 0.6 pmol/20 microliters sample of GLU and ASP, respectively). Basal levels of endogenous extracellular GLU and ASP were increased over 2-fold and 3-fold, respectively, following local administration of the selective 5-hydroxytryptamine (5-HT3) receptor agonist phenylbiguanide (300 microM). Intracerebral administration of the selective 5-HT3 receptor antagonist ondansetron (30 microM) blocked the effect of phenylbiguanide on GLU release whilst the effect on ASP was variable and complex. These data suggest that 5-HT3 receptor activation in the rat nucleus tractus solitarius can affect excitatory amino acid neurotransmission in this region of the medulla oblongata.

Animals↗

PubMed1995

Differential effects of WAY-100135 on the decrease in 5-hydroxytryptamine release induced by buspirone and NAN-190.

1-(2-Methoxyphenyl)-4-[(phthalimido)butyl] piperazine (NAN-190) and 8-[4-[4-(2-pyrimidinyl)-1-piperazinyl]butyl]-8-azaspiro[4.5] decane-7,9-dione (buspirone) are 5-HT1A receptor partial agonists which decrease 5-hydroxytryptamine (5-HT) release in vivo. In order to assess whether these ligands decrease 5-HT release by stimulating 5-HT1A receptors we examined the ability of the selective 5-HT1A receptor antagonist N-tert-butyl 3-4-(2-methoxyphenyl) piperazin-1-yl-2-phenylpropanamide dihydrochloride (WAY-100135) to block their inhibitory effects on 5-HT. NAN-190 (0.1 mg/kg s.c.) and buspirone (1.0 mg/kg s.c.) significantly decreased extracellular levels of 5-HT in hippocampal dialysates. WAY-100135 (10.0 mg/kg s.c.) attenuated the effect of buspirone but had no significant effect on the NAN-190-induced decreased in 5-HT release. These data demonstrate that buspirone is an agonist at the somatodendritic 5-HT1A receptor but that the inhibitory effects of NAN-190 on 5-HT release may be mediated via a mechanism other than, or in addition to, 5-HT1A receptor agonism.

Animals↗