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Biomedical subjects

E G Anderson

Publications and source records attributed to E G Anderson.

At least 19 recordsLinked to original sources
PubMed1992

Serotonin preferentially hyperpolarizes capsaicin-sensitive C type sensory neurons by activating 5-HT1A receptors.

The effects of serotonin (5-HT) were investigated by intracellular recording from 179 dorsal root ganglion (DRG) cells classified by conduction velocity. Bath applied 5-HT depolarized 82% and hyperpolarized 4% of the A-type cells. In C-type cells, 5-HT depolarized only 41%, but hyperpolarized 39% of the cells. The depolarizing responses were of two types; an increase or decrease in R(in), mediated by 5-HT2or3 receptors, respectively. These receptors were observed in both A- and C-type cells. Hyperpolarizing responses were largely confined to A(delta)- and C-type cells. Carboxamidotryptamine and 8-OH-dipropylamino-tetralin were full agonists in eliciting hyperpolarization, and metitepin, spiperone and spiroxitrine behaved as competitive antagonists. This indicated that hyperpolarization was mediated by a 5-HT1A receptor. A 5-HT1A&3 receptor were found co-localized on some C-type cells. A strong depolarizing response to capsaicin was observed in the subgroup of C-type neurons that were also hyperpolarized by 5-HT. Thus a co-localization of capsaicin and 5-HT1A receptors was also observed.

Animals↗
PubMed1991

Traumatic epidermal inclusion cysts due to shoe impingement: a report of two cases.

Two cases are presented of bilateral traumatic inclusion cysts occurring on the dorsum of the first metatarsophalangeal joint. Both cases were women who wore high-heeled fashion shoes and the cysts occurred where the edge of the shoe impinged on a particularly prominent extensor hallucis longus tendon. Inclusion cysts have not previously been reported on the dorsum of the foot and their occurrence where impingement exists confirms a traumatic etiology. The importance of identifying the causative factor in such cases is emphasized.

Adult↗
PubMed1990

5-HT1 receptor agonists reduce the Ca+ component of sensory neuron action potentials.

Serotonin (5-HT) agonists, selective for 5-HT1, 5-HT2 or 5-HT3 receptor subtypes, were tested for their ability to mimic 5-HT in narrowing the tetraethylammonium-induced calcium-dependent plateau of action potentials recorded from frog sensory neurons. 5-Carboxamidotryptamine, 5-HT, alpha-methyl 5-HT and 5-methoxy-tryptamine possessed full agonist activity, with EC50S of 19 nM, 210 nM, 3.7 microM and 1.7 microM, respectively. 2-Methyl 5-HT was inactive. This agonist profile indicates that the calcium-dependent plateau in these sensory somata is modulated by a 5-HT1-like receptor.

5-Methoxytryptamine↗
PubMed1990

5-HT2 and 5-HT3 receptors mediate two distinct depolarizing responses in rat dorsal root ganglion neurons.

The effects of serotonin (5-HT) were studied on transmembrane potentials in 188 rat dorsal root ganglion cells (150 A-type, 16 C-type and 22 unidentified neurons). 5-HT produced a concentration-dependent depolarization in 88% of these neurons. Membrane input resistance (Rin), determined from the slope of current-voltage displacement curves, was increased in 51% and decreased in 41% of the responding neurons. Both responses occurred in 8% of the neurons. No differences in these responses were observed between A- and C-type neurons. Norepinephrine (NE) depolarized 75% (n = 20) of the neurons tested while increasing the Rin. In cells where 5-HT decreased Rin, 2-methyl 5-HT, but not alpha-methyl 5-HT, mimicked the response. The selective 5-HT3 antagonist, ICS 205-930, blocked this response, but ketanserin and methiothepin did not affect it. The 5-HT-induced increase in Rin was blocked by 5-HT2 antagonists (ketanserin, methiothepin and spiperone); mimicked by alpha-methyl 5-HT, but not affected by 2-methyl 5-HT. The selective 5-HT3 antagonist, ICS 205-930, did not antagonize this response. The action of NE but not 5-HT was blocked by the selective alpha 1 antagonist, prazosin. These data indicate that the 5-HT induced depolarization with decreased Rin is mediated by 5-HT3 receptors and the depolarization with increased Rin is mediated by 5-HT2 receptors. Furthermore, these two receptors can occur on the same cell.

Animals↗
PubMed1990

5-HT3 receptors modulate spinal nociceptive reflexes.

The selective 5-HT3 receptor agonist 2-methyl-serotonin (2-Me-5-HT) mimicked the antinociceptive activity of 5-HT when intrathecally administered to rats. Two hundred micrograms (i.t.) doses of these agonists produced similar increases in tail flick latency. However, equal doses of 2-Me-5-HT and 5-HT doubled and tripled, respectively, the mean response latency as measured by the hot plate test. The potent and selective 5-HT3 receptor antagonists ICS 205-930 (3-tropanyl-indole-3-carboxylate) and MDL 72222 (3-tropanyl-3,5-dichlorobenzoate) antagonized the antinociceptive effects of both 5-HT and 2-Me-5-HT. However, there were differences in the efficacy of these antagonists. Thus, intrathecal pretreatment with ICS 205-930 (0.05 micrograms) or MDL 72222 (0.1 micrograms) blocked the antinociceptive effects of 5-HT (200 micrograms, i.t.) as measured by the tail flick test, however, higher doses (0.1 and 1.0 micrograms, respectively) were required in the hot plate test. Pretreatment with ICS 205-930 (0.1 microgram) or MDL 72222 (0.1 microgram) blocked the effects of 2-Me-5-HT (200 micrograms, i.t.) in both analgesiometric tests. It is concluded that 5-HT3 receptors are intimately involved in the modulation of spinal nociceptive responses.

Animals↗