PubMed Health⌕ Search

Biomedical subjects

L H Jiang

Publications and source records attributed to L H Jiang.

10 recordsLinked to original sources
PubMed1990

The effect of intraventricular administration of the 5-HT3 receptor agonist 2-methylserotonin on the release of dopamine in the nucleus accumbens: an in vivo chronocoulometric study.

In the present study we have examined the effects of the serotonin3 (5-HT3) agonist 2-methylserotonin (2-Me-5HT) on the dopamine (DA) release in the nucleus accumbens (NAc) of rats using in vivo chronocoulometric recording. The intraventricular (i.c.v.) administration of 2-Me-5HT dose-dependently increased the DA release in the NAc. This effect was blocked by the selective 5-HT3 antagonist BRL-43694 (granisetron), but not by the 5-HT1/5-HT2 antagonist metergoline. The i.c.v. injection of 8-hydroxydipropylaminotetraline (8-OHDPAT, a selective 5-HT1a agonist) or (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI, a 5-HT2/5-HT1c agonist) failed to alter the DA release in the NAc. The increase in the DA release produced by 2-Me-5HT was abolished in animals that had received acute bilateral injections of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our results suggest that the 2-Me-5HT-induced DA release in the NAc is mediated by 5-HT3 receptors. In addition, 2-Me-5HT induced effect is dependent upon the impulse flow of DA cells.

Animals↗
PubMed1990

Chronic BRL 43694, a selective 5-HT3 receptor antagonist, fails to alter the number of spontaneously active midbrain dopamine neurons.

In this study, we examined the effect of chronic administration of the selective 5-HT3 receptor antagonist BRL 43694 on the number of spontaneously active A9 (substantia nigra pars compacta) and A10 (ventral tegmental area) dopamine (DA) cells using the technique of extracellular single unit recording. Overall, chronic BRL 43694 (21 days, 5 mg/kg per day or 2.5 mg/kg q.i.d) failed to alter the number of spontaneously active DA cells in either area compared to saline-injected controls. Furthermore, the acute i.v. administration of BRL 43694 did not change A10 DA cell baseline firing rate. These data suggest that if BRL 43694 possesses antipsychotic activity, it is not the result of its action on midbrain DA neurons.

Animals↗
PubMed1990

One year of continuous treatment with haloperidol or clozapine fails to induce a hypersensitive response of caudate putamen neurons to dopamine D1 and D2 receptor agonists.

In a "blind" experimental design, the sensitivity of caudate-putamen (CPu) cells to the selective dopamine (DA) D1 receptor agonist SKF-38393 and D2 receptor agonist LY171555 (quinpirole) in rats treated with either haloperidol (HAL), clozapine or tap water for 1 year was compared using the techniques of single cell recording and microiontophoresis. Although the maximum binding value for D2 receptors was elevated in chronic HAL-treated rats, there was no sign of electrophysiological supersensitivity of CPu neurons to the selective DA D1 and D2 receptor agonists. CPu cells were subsensitive to LY-171555 in HAL-treated rats without a drug withdrawal period. This suggests that residual HAL in the rat brain actively blocked the D2 DA receptors. In contrast, in clozapine-treated rats with or without a drug withdrawal period, the sensitivity of CPu cells to either the D1 or D2 agonists was not altered. Coadministration of SKF-38393 and LY-171555 onto the CPu neurons primarily produced an additive effect and only two cells both from the HAL group showed a synergistic action. The majority of CPu cells failed to respond to iontophoretic application of CCK-8S in either the control or antipsychotic drug-treated rats. If these findings can be extended to humans, they do not support the view that tardive dyskinesia is the result of CPu DA receptor supersensitivity.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Electrophysiological characterization of 5-hydroxytryptamine2 receptors in the rat medial prefrontal cortex.

The aim of the present study was to characterize 5-hydroxytryptamine2 (5-HT2) receptors in the rat medial prefrontal cortex (mPFc) by single cell recording and microiontophoretic techniques. This was accomplished using 5-HT2 receptor agonists 1-[2,5-dimethoxy-4-iodophenyl]-2-aminopropane [(+/-)-DOI] and 1-[2,5-dimethoxy-4-bromophenyl]-2-aminopropane [(+/-)-DOB]. DOI ejected at a low current (0.5 nA) potentiates glutamate (GLU)-induced activation of mPFc neurons and this effect is blocked by spiperone. At higher currents. DOI invariably inhibits GLU-induced neuronal activity. The microiontophoretic ejection of both DOI and DOB predominantly inhibits spontaneously active mPFc cells. The inhibitory action of DOI on spontaneously active cells is dose-dependent and is blocked by putative 5-HT2 receptor antagonists, with a rank order of potency as follows: ritanserin greater than metergoline approximately LY-53857 greater than spiperone greater than mesulergine greater than mianserin approximately ketanserin. Interestingly, ketanserin and mianserin only weakly block the effect of DOI. The suppressant action of DOI is probably not related to its interaction with 5-HT10 sites as spiperone, which has low affinity for these sites, potently blocks the effect of DOI. The suppressant effect of DOI is not blocked by other receptor antagonists such as BRL-43694 (5-HT3), (+/-)-pindolol (5HT 1a,1b, beta adrenergic, beta), prazosin (adrenergic1, alpha-1), pyrilamine (histamine1, H1), l-sulpiride (dopamine2, D2) or SR 95103 (gamma-aminobutyric acid, GABAA). Overall our results indicate that DOI predominantly inhibits mPFc cells in a direct manner and this effect is mediated by 5-HT2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1988

Cholecystokinin antagonist lorglumide reverses chronic haloperidol-induced effects on dopamine neurons.

Intravenous administration of the cholecystokinin (CCK) antagonist lorglumide (LORG) reversed chronic haloperidol (CHAL)-induced depolarization inactivation (DI) of dopamine (DA) cells in both the A9 and A10 areas. Moreover, microinjection of LORG, but not naloxone, directly into the medial nucleus accumbens (mNAc) dose-dependently reversed CHAL-induced effect. LORG injected into other brain regions was without effect. These results suggest that CCK receptors in the mNAc form an important link for maintaining CHAL-induced DI of DA cells and that CCK is involved in the therapeutic action of antipsychotic drugs.

Action Potentials↗
PubMed1988

Chronic treatment with high doses of haloperidol fails to decrease the time course for the development of depolarization inactivation of midbrain dopamine neurons.

Using extracellular single unit recording techniques, we investigated the effects produced by chronic treatment with high doses of haloperidol (CHAL, 5 mg/kg/day, s.c.) on midbrain dopamine (DA) neuronal activity. This regimen of HAL treatment produced a time-dependent reduction in the number of spontaneously active DA neurons. Additionally, this dose regimen induced an irregular firing pattern in many of the remaining active DA neurons in both the ventral tegmental area (A10) and substantia nigra pars compacta (A9) regions. These effects were comparable to those obtained previously in rats treated chronically with lower doses of HAL (0.5 mg/kg/day, s.c.). However, there was a greater decrease in the number of spontaneously active DA cells detected in rats treated with high doses of HAL for three weeks compared to those receiving the low doses. On the other hand, higher doses of apomorphine (200 micrograms/kg, i.v.) were required to reverse both the reduction of DA activity and irregular discharge pattern in rats treated chronically with high doses of HAL. In conclusion, the results of the present study substantiate the view that CHAL-induced depolarization inactivation (DI) of DA neurons is a time-dependent process and chronic treatment with high doses of HAL did not shorten the time course required for the development of DI on the majority of midbrain DA neurons.

Animals↗
PubMed1988

Effect of catecholamine-receptor antagonists on feeding-related neuronal activity in the central amygdaloid nucleus of the monkey: a microiontophoretic study.

1. Neuronal activity in the central amygdaloid nucleus (ACE) was recorded during a visually guided bar-press feeding task, and the modulatory effects of catecholaminergic blockers were investigated. 2. The feeding task had the following four phases: 1) a cue light to signal the start of bar press, 2) bar press, 3) a short cue tone followed by food delivery, and 4) ingestion reward. Of 278 cells observed, 176 (63%) increased or decreased their discharge rates in one or more phases of the feeding task. Of these, 60 (34%) responded to the cue light, 81 (46%) to the bar press, 66 (37%) to the cue tone, and 176 (100%) during the reward period. In the ingestion reward phase, firing of 128 (73%) increased and firing of 48 (27%) decreased. The reward-related response depended on the nature of food. In the trials with aversion food, some neurons increased firing (n = 6), whereas others showed opposite firing changes (n = 10). 3. The decreased firing rate during the reward period was greatly attenuated in the no-reward tasks (n = 29) and was blocked by electrophoretic application of a beta-adrenoceptive antagonist [sotalol (SOT), n = 26]. Noradrenaline (NA) application mimicked the inhibitory effect on the reward-related activity during extinction trial (n = 4). These results suggest that the decreased firing rate observed during the reward period was modulated by beta-adrenoreceptors. 4. Of 32 neurons tested, the activity of 8 (25%) and 14 (44%) were enhanced by the cue light or bar press, respectively. These effects were attenuated by electrophoretic application of a dopamine (DA) antagonist [spiperone (SPP)] but not by SOT. This indicates that dopaminergic inputs may be related to recognition of visual signals and to motor initiation during the monkey feeding paradigm.

Action Potentials↗