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C Prasad

Publications and source records attributed to C Prasad.

189 records · Page 11Linked to original sources

Identification and characterization of cyclo(His-Pro)-like immunoreactivity in amniotic fluid.

Amniotic fluid (AF) from 25 term pregnancies was analyzed for cyclo(His-Pro)-like immunoreactivity (CHP-LI). CHP-LI was detected in all AF samples and was indistinguishable from synthetic CHP by immunoidentity, by gel chromatography on Sephadex G-25, and by high pressure liquid chromatography. The mean concentration of CHP-LI in AF was 13,622 +/- 1288 pg/ml (+/- SE) and concentrations were not altered by maternal labor. Plasma concentrations of CHP-LI were similar in 4 pregnant and 4 control subjects [2260 +/- 432 pg/ml vs. 2162 +/- 419 pg/ml (+/- SE), respectively]. We conclude that 1) CHP-LI is readily detected in AF from term pregnancies and is indistinguishable from synthetic CHP, and 2) concentrations of CHP-LI in human AF are significantly higher than concentrations of maternal plasma CHP-LI, suggesting CHP AF originates by mechanisms other than diffusion from maternal plasma.

Amniotic Fluid↗

Neuropeptide-dopamine interactions. IV. Effect of thyrotropin-releasing hormone on striatal dopaminergic neurons.

Many biologic effects of TRH seem to be mediated via a dopaminergic mechanism. The present study examined the effects of chronic TRH administration on the properties of nigrostriatal dopaminergic neurons. Ten days, continuous subcutaneous TRH administration via an osmotic minipump led to a significant rise in striatal level of 3,4-dihydroxyphenylacetic acid, but not of homovanillic acid or dopamine. These treatments also did not elicit any significant changes in the maximal binding capacity (Bmax) or affinity (KD) of either D1- or D2-dopamine receptor. By contrast, TRH administration led to a significant increase in both Bmax and KD of striatal mazindol binding. This effect of TRH, however, was not observed in in vitro studies. In conclusion, these data suggest that in vivo administration of TRH may modulate dopaminergic activities by altering, directly or indirectly, dopamine release and reuptake.

3,4-Dihydroxyphenylacetic Acid↗

Neuropeptide-dopamine interactions. V. Cyclo(His-Pro) regulation of striatal dopamine transporter complex.

Cyclo(His-Pro) (CHP) is a cyclic dipeptide that is ubiquitously distributed through the central nervous system, including striatum. Many biologic effects of CHP seem to be mediated through a dopaminergic mechanism. To further examine the mechanism of action of this peptide, we have studied effects of chronic CHP treatment on the properties of nigro-striatal dopaminergic neurons in rats. Chronic CHP administration elicited significant increase in both KD and Bmax of striatal mazindol-binding sites (labelling DA transporter complex), but no change in either D1- or D2-type DA receptors. Chronic treatment with DA uptake blockers (e.g., benztropine, GBR 12909, bupropion, and mazindol) also produced changes in striatal mazindol-binding sites that were similar to that of chronic CHP. Furthermore, CHP led to a dose-dependent inhibition of [3H]-DA uptake by striatal synaptosomes, reaching to maximal inhibition of uptake (30%) at CHP dosage of 10 nM. The dose-response curve for CHP inhibition of DA uptake, unlike DA uptake blockers that led to a total inhibition, was partial and V-shaped. Again unlike DA uptake blockers, CHP did not inhibit the binding of [3H]-mazindol to striatal membranes. On the basis of these data we hypothesize that while CHP may inhibit DA uptake by modifying mazindol-binding locus at DA transporter complex, its primary action may be at a site other than mazindol-binding site.

Analysis of Variance↗

Bidirectional changes in striatal D2-dopamine receptor density during chronic ethanol intake.

Results of previous studies on the effects of ethanol consumption for a single fixed period on the properties of D2 dopamine receptors appear contradictory and inconclusive. In this study, we have examined the time course of the effects of dietary ethanol on the properties of striatal D2 dopamine receptor. Ethanol intake led to a significant decrease in the maximum number (Bmax) after 1 (35% of control) and 2 weeks (48% of control), but not after 3 (93% of control) or 4 weeks (97% of control) of treatment. However, there was a significant increase in Bmax after 6 (118% of control) and 10 weeks (123% of control) of ethanol consumption. The affinity (Kd) of the receptor, however, remained unaltered in all cases. In conclusion, these data show that the duration of ethanol exposure may be an important determinant regulating D2-dopamine receptor density.

Animals↗

Can dietary macronutrient preference profile serve as a predictor of voluntary alcohol consumption?

A diet rich in protein has been shown to increase voluntary alcohol consumption (VAC) in a variety of animal species. Macronutrient preference (MP) profile varies widely among different outbred rats of the same strain. Using outbred Sprague-Dawley rats and two inbred selected strains of rats (P and NP) that are known for large differences in alcohol preference, we have examined whether 1) there is a relationship between MP profile and VAC and 2) MP profile can be a predictor of VAC. Results of these studies show 1) wide animal-to-animal variations in both the MP and VC and 2) the presence of an association between MP profile and VAC in P and NP but not Sprague-Dawley rats. Therefore, we conclude that MP profile may not serve as a reliable predictor of VAC in a nonselected population.

Alcohol Drinking↗

A relationship between increased voluntary alcohol preference and basal hypercorticosteronemia associated with an attenuated rise in corticosterone output during stress.

Some of the multiple biological effects of stress include activation of a variety of neuroendocrine systems, resulting in enhanced secretion of many hormones, including corticosterone, as well as facilitation of drug-seeking behavior. Therefore, we have examined the potential relationship between voluntary alcohol consumption (VAC) and corticosterone output profile using: (1) selectively bred alcohol-preferring (P) and nonpreferring (NP) rats; and (2) outbred male Holtzman Sprague-Dawley rats selected for (a) low basal corticosterone (< 2 micrograms/mg Cr) and high stimulation (> 250%) (L-H rats), and (b) high basal corticosterone (> 4 micrograms/mg Cr) and low stimulation of corticosterone output on 24-hour fasting stress (< 125%) (H-L rats). The results of this study show: (a) the corticosterone output profiles of P and NP rats were similar to those of H-L and L-H rats, respectively; and (b) the H-L rats exhibited significantly higher VAC than the L-H rats. In conclusion, these data suggest that basal hypercorticosteronemia associated with attenuated rise in corticosterone output during stress may be associated with increased VAC.

Alcohol Drinking↗

Neuropeptide-dopamine interactions. III. Cyclo(His-Pro) and persistence of dopaminergic supersensitivity on withdrawal from one year continuous neuroleptic treatment.

When rats are given dopaminergic antagonists (neuroleptics) continuously for several days behavioral supersensitivity to dopaminergic agonists results. This supersensitivity, however, declines rapidly on neuroleptic withdrawal. The data presented here, however, are the first to show that the supersensitivity persists for a longer duration (greater than 100 days) if the neuroleptic is administered continuously for 1 year. Oral administration of 0.76 +/- 0.13 mg/kg/day cyclo(His-Pro), a peptide exhibiting dopaminergic agonist-like properties, during neuroleptic withdrawal did not change the course of dopaminergic supersensitivity reversal.

Animals↗