Effects of D-amphetamine and phencyclidine on behavior and extracellular concentrations of neurotensin and dopamine in the ventral striatum and the medial prefrontal cortex of the rat

Neurotensin: role in psychiatric and neurological diseases.

The role of neurotensin in the pathophysiology of schizophrenia and the mechanism of action of antipsychotic drugs.

- 5,7-Bis(trifluoroacetyI)-8-quinolylamine (1) reacted with various aliphatic and aromatic aldehydes in the presence of aqueous ammonia to afford fluorine-containing 1,2-dihydropyridoI3.2-hlquinazolines (2) and pyrido[3,2-h]quinazoline-6-methanoIs (3) in moderate to high yields. Dehydrogenation of 2 with DDQ gave the corresponding pyndo-[3,2-h]quinazolines (4) in excellent yields. Conversion of alcohols (3) into hydrates (4) with DDQ was also successful.

A Facile and Convenient Synthetic Method for Fluorine-containing 1,2-Dihydropyrido[3,2-h]quinazolines and Pyrido[3,2-h]quinazolines

Brain neurotensin, psychostimulants, and stress--emphasis on neuroanatomical substrates.

In order to further characterize the pharmacologic mechanisms that mediate the antipsychotic drug-induced increase in neurotensin (NT) in nucleus accumbens and striatum, the effects of three weeks treatment with psychotherapeutic levels of lithium alone or in conjunction with haloperidol were compared to the ability of haloperidol alone to alter NT and neuromedin N (NMN) regional brain concentrations in rats. A separate experiment examined the ability of a selective dopamine D2 receptor agonist, quinelorane, to alter NT/NMN regional concentrations after three weeks of treatment as compared to haloperidol, a D2 receptor antagonist. Haloperidol (1 mg/kg) increased both NT and NMN concentrations in several brain regions and these parallel peptide increases were highly correlated. Lithium chloride (0.4 mM) had no effect, either alone or with haloperidol, on NT/NMN concentrations. Quinelorane (1 mg/kg), however, effectively increased both NT and NMN concentrations in the caudate nucleus and nucleus accumbens, as did haloperidol (2 mg/kg). These data indicate that the induction of NT and NMN, whose adjacent sequences are contained in a pro-hormone product of a single gene, occurs in tandem and remains proportional, as well as demonstrating that putative D2 receptor agonists can produce effects on NT/NMN systems that are similar to D2 receptor antagonists. © 1994 Wiley-Liss, Inc.

Effects of haloperidol, quinelorane, and lithium on regional neurotensin/neuromedin N concentrations: further evidence for neurotensin/neuromedin N-dopamine interactions.

An accumulation of behavioral, physiological, and neurochemical evidence indicates that the brain tridecapeptide neurotensin (NT) has a number of selective interactions with brain dopamine (DA) systems.' Because of the purported involvement of DA in the behavioral and addictive properties of cocaine,2 it is of interest to evaluate whether alterations in the balance between NT and DA systems may be at least one neurochemical mechanism underlying the behavioral properties of cocaine. To investigate this question, we have used a radioimmunoassay (RIA) to quantitate NT concentrations in cell extracts from specific DA cell body and terminal regions 24 hours after a single dose of cocaine. Adult male Sprague-Dawley rats were killed by decapitation 24 hours after a subcutaneous injection of 40 mg/kg cocaine or saline vehicle, and the brain was removed and rapidly frozen. The frontal cortex, nucleus accumbens, caudate nucleus, substantia nigra, and ventral tegmental area were subsequently dissected. Using a sensitive and specific RIA,3 the concentration of neurotensin-like immunoreactivity (NT-LI) was measured in the supernatant after extraction of the brain tissue in cold 1 M HCI. Extracted pellets were assayed for protein content using the method of Lowry et aL4 As shown in FIGURE 1, NT-LI was increased by 44% in the substantia nigra and by 91% in the nucleus accumbens 24 hours after the injection of 40 mg/kg cocaine. NT-LI in the frontal cortex and ventral tegmental area was not altered by cocaine administration. In the caudate nucleus, there was a trend toward a cocaine-induced increase in NT-LI, but this difference did not reach statistical significance. These results demonstrate that acute treatment with the psychostimulant cocaine alters the concentration of NT within the nucleus accumbens and substantia nigra. Our results are consistent with those of Hanson et aL5 These investigators also found increased NT-LI in the substantia nigra up to 8 hours after a single dose of cocaine as well as a trend toward an increase in striatal NT-LI 24 hours after cocaine administration. In future studies, it will be of interest to determine the functional relevance of the anatomically specific, cocaine-induced changes in NT concentrations and the possible involvement of NT systems in the behavioral response to cocaine.

Cocaine effects on central nervous system neurotensin concentrations.

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Effects of haloperidol, quinelorane, and lithium on regional neurotensin/neuromedin N concentrations: further evidence for neurotensin/neuromedin N-dopamine interactions.

Cocaine effects on central nervous system neurotensin concentrations.