Changes in taste reactivity to intra-oral hypertonic NaCl after lateral parabrachial injections of an α2-adrenergic receptor agonist

Abstract

Bilateral injections of moxonidine, an α2-adrenoceptor and imidazoline receptor agonist, into the lateral parabrachial nuclei (LPBN) enhance sodium appetite induced by extracellular dehydration. In the present study, we examined whether LPBN moxonidine treatments change taste reactivity to hypertonic NaCl solution administered into the mouth by intra-oral (IO) cannula. Male Holtzman rats prepared with IO and bilateral LPBN cannulas received subcutaneous injections of furosemide (FURO; 10 mg/kg) and captopril (CAP; 5 mg/kg) to induce hypovolemia with mild hypotension and an accompanying salt appetite and thirst before testing the taste reactivity to oral infusions of 0.3 M NaCl (1.0 ml/min). In the first experiment 45 min after subcutaneous injections of FURO+CAP or vehicle, moxonidine was bilaterally injected into the LPBN, and then 15 min later both bodily and oral-facial ingestive and rejection responses to 0.3 M NaCl delivered through the IO cannula were assessed. Both LPBN vehicle and moxonidine treated rats showed increased ingestive and decreased rejection responses to the IO hypertonic solution. The IO 0.3 M NaCl infusion-evoked ingestive and rejection taste related behaviors were comparable in the LPBN vehicle- vs. the LPBN moxonidine-injected groups. In a second experiment, rats received the same FURO+CAP treatments and LPBN injections. However, beginning 15 min after the LPBN injections, they were given access to water and 0.3M NaCl and were allowed to consume the fluids for most of the next 60 min with the free access intake being interrupted only for a few minutes at 15, 30 and 60 min after the fluids became available. During each of these three brief periods, a taste reactivity test was conducted. On the three taste reactivity tests rats that received LPBN vehicle injections showed progressive declines in ingestive responses and gradual increases in rejection responses. However, in contrast to the LPBN vehicle treated rats, animals receiving bilateral injections of LPBN moxonidine maintained a high number of ingestive responses and a low number of rejection responses throughout the test period even in spite of evidencing substantial water and 0.3 M NaCl consumption during the periods of free access. The results suggest that after α2-adrenoceptor agonist delivery to the LPBN the acceptance of 0.3 M NaCl is sustained and the negative attributes of the solution are minimized. The maintained positive rewarding qualities of 0.3 M NaCl are likely to account for why LPBN moxonidine treated rats show such a remarkable salt appetite when assayed by the volume of hypertonic 0.3 M NaCl consumed.

Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α2-adrenergic activation in the lateral parabrachial nucleus

“…Injections centered in the ventral lateral and external lateral portions, as well as in the Kölliker-Fuse nucleus observed in some rats were also considered as correctly placed in the LPBN. The sites of the injections in the present study were similar to those of previous studies that showed the effects of moxonidine, muscimol or opioids injected into the LPBN on NaCl and water intake [19][20][21]24,27].…”

“…In conclusion, the present and previous studies [19,34,35,38] suggest that moxonidine acting in ␣ 2 -adrenoceptors in the LPBN increases the release of GABA and opioids and blocks serotonin action, reducing the activity of the inhibitory mechanisms, which might enhance ingestive reactions and reduces rejection responses caused by the ingestion of 0.3 M NaCl and water, increasing the intake.…”

“…From the LPBN, the signals may reach integrative areas that also receive facilitatory signals from forebrain areas involved in the control of sodium and water intake like, SFO, OVLT and other hypothalamic areas [37]. As a consequence of the activation of the inhibitory mechanisms, fluid depleted rats that ingest water and hypertonic NaCl show reduced ingestive reactions and increased rejection responses to an intraoral infusion of 0.3 M NaCl [19]. However, a previous study demonstrated that rats treated with moxonidine into the LPBN continue to show enhanced ingestive reactions and reduced rejection responses to an intraoral infusion of 0.3 M NaCl even after consuming large volumes of 0.3 M NaCl and water [19].…”

“…As a consequence of the activation of the inhibitory mechanisms, fluid depleted rats that ingest water and hypertonic NaCl show reduced ingestive reactions and increased rejection responses to an intraoral infusion of 0.3 M NaCl [19]. However, a previous study demonstrated that rats treated with moxonidine into the LPBN continue to show enhanced ingestive reactions and reduced rejection responses to an intraoral infusion of 0.3 M NaCl even after consuming large volumes of 0.3 M NaCl and water [19]. These results suggest that moxonidine in the LPBN possibly reduces some type of inhibitory signals produced as a consequence of the ingestion of NaCl and water.…”

“…Studies that have investigated the involvement of the LPBN in the control of fluid-electrolyte balance demonstrated that different neurotransmitters like serotonin, cholecystokinin, glutamate and corticotrophin releasing factor (CRF) or receptors like ␣ 2 -adrenoceptors, GABAergic, opioid or purinergic receptors in the LPBN are involved with the control of sodium intake [1,3,5,[18][19][20][21][22][23][24][25][26][27][28]. The activation of the ␣ 2 -adrenoceptors with bilateral injections of noradrenaline or moxonidine into the LPBN increases 0.3 M NaCl and water intake induced by the treatment with the diuretic furosemide (FURO) combined with low dose of the angiotensin converting enzyme inhibitor captopril (CAP) injected subcutaneously.…”