ABSTRACT
<p><b>OBJECTIVE</b>To investigate the opioidergic mechanism of the central nucleus of the amygdala (CeA) for regulating sodium appetite in rats.</p><p><b>METHDOS</b>Using the elaborate invasive cerebral cannulation and brain microinjection method, we observed the effects of bilateral intra-CeA injections of DAMGO (a selective µ-opioid receptor agonist) and CTAP (a highly selective µ-opioid receptor antagonist), either alone or in combination, on NaCl solution (0.3 mol/L) and water intake by rats in different models of Naingestion.</p><p><b>RESULTS</b>In the two-bottle tests, bilateral injections of DAMGO at 1, 2, and 4 nmol into the CeA induced a dose-related increase of NaCl and water intake in rats treated with water deprivation with partial rehydration (WD-PR), and pretreatment with 0.5, 1, and 2 nmol CTAP injected into the CeA significantly suppressed DAMGO-induced NaCl and water intake in a dose-dependent manner: in the one-bottle tests, bilateral injections of DAMGO (2 noml) into the CeA had no effect on water intake of the rats. In rats with subcutaneous injection of furosemide (FURO) combined with captopril (CAP) (FURO+CAP), bilateral intra-CeA injections of DAMGO (2 nmol) caused increased NaCl and water intake in the two-bottle tests, but such effects were suppressed by pretreatment with CTAP injection into the CeA; in the one-bottle tests, bilateral intra-CeA injections of DAMGO had no effect on water intake of the rats.</p><p><b>CONCLUSION</b>µ-opioid receptors in the CeA are involved in the excitatory regulation of sodium appetite to mediate sodium intake. µ-opioid receptor antagonists are expected to be targets for developing inhibitors of sodium appetite.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the activity of pyramidal neurons in the medial prefrontal cortex (mPFC) of normal and 6-OHDA-lesioned rats and the responses of the neurons to 5-hydroxytryptamine-7 (5-HT(7)) receptor stimulation.</p><p><b>METHODS</b>The changes in spontaneous firing of the pyramidal neurons in the mPFC in response to 5-HT(7) receptor stimulation were observed by extracellular recording in normal and 6-OHDA-lesioned rats.</p><p><b>RESULTS</b>Both systemic and local administration of 5-HT(7) receptor agonist AS 19 resulted in 3 response patterns (excitation, inhibition and no change) of the pyramidal neurons in the mPFC of normal and 6-OHDA-lesioned rats. In normal rats, the predominant response of the pyramidal neurons to AS 19 stimulation was excitatory, and the inhibitory effect of systemically administered AS 19 was reversed by GABAA receptor antagonist picrotoxinin. In the lesioned rats, systemic administration of AS 19 also increased the mean firing rate of the pyramidal neurons, but the cumulative dose for producing excitation was higher than that in normal rats. Systemic administration of AS 19 produced an inhibitory effect in the lesioned rats, which was partially reversed by picrotoxinin. Local administration of AS 19 at the same dose did not change the ?ring rate of the neurons in the lesioned rats.</p><p><b>CONCLUSION</b>The activity of mPFC pyramidal neurons is directly or indirectly regulated by 5-HT7 receptor, and degeneration of the nigrostriatal pathway leads to decreased response of these neurons to AS 19.</p>