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Revisiting Antagonist Effects in Hypoglossal Nucleus: Brainstem Circuit for the State-Dependent Control of Hypoglossal Motoneurons: A Hypothesis.

Fenik VB - Front Neurol (2015)

Bottom Line: We concluded that noradrenergic disfacilitation is the major mechanism that is responsible for approximately 90% of the depression of hypoglossal motoneurons, whereas the remaining 10% can be explained by serotonergic mechanisms that have net inhibitory effect on hypoglossal nerve activity during REM sleep-like state.We hypothesized that both noradrenergic and serotonergic state-dependent mechanisms indirectly control hypoglossal motoneuron excitability during REM sleep; their activities are integrated and mediated to hypoglossal motoneurons by reticular formation neurons.In addition, we proposed a brainstem neural circuit that can explain the new findings.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterans Affairs Greater Los Angeles Healthcare System , Los Angeles, CA , USA ; Websciences International , Los Angeles, CA , USA.

ABSTRACT
We reassessed and provided new insights into the findings that were obtained in our previous experiments that employed the injections of combined adrenergic, serotonergic, GABAergic, and glycinergic antagonists into the hypoglossal nucleus in order to pharmacologically abolish the depression of hypoglossal nerve activity that occurred during carbachol-induced rapid-eye-movement (REM) sleep-like state in anesthetized rats. We concluded that noradrenergic disfacilitation is the major mechanism that is responsible for approximately 90% of the depression of hypoglossal motoneurons, whereas the remaining 10% can be explained by serotonergic mechanisms that have net inhibitory effect on hypoglossal nerve activity during REM sleep-like state. We hypothesized that both noradrenergic and serotonergic state-dependent mechanisms indirectly control hypoglossal motoneuron excitability during REM sleep; their activities are integrated and mediated to hypoglossal motoneurons by reticular formation neurons. In addition, we proposed a brainstem neural circuit that can explain the new findings.

No MeSH data available.


Related in: MedlinePlus

Summary of hypoglossal nerve activity during carbachol- induced REM sleep-like episodes that were evoked before (baseline B0,C0) and at different times after (B1,C1 and B2,C2), the injections of the antagonist combinations into hypoglossal nucleus. (A) Combined injections of prazosin, methysergide, bicuculline and strychnine. (B) Combined injections of prazosin, methysergide and bicuculline. (C) Combined injections of prazosin and methysergide. (D) Injections of prazosin only. (E) Injections of methysergide only. Pz, prazosin, an α1-adrenoceptor antagonist; Me, methysergide, a broad-spectrum serotonergic antagonist; Bi, bicuculline, a GABAA antagonist; Str, strychnine, a glycinergic antagonist. B0 and C0, baseline hypoglossal nerve activity measured before and during carbachol, respectively; B1 and C1, hypoglossal nerve activity during “early” carbachol responses; B2 and C2, hypoglossal nerve activity during “late” carbachol responses. *p < 0.05, paired t-test [adapted from Fenik et al. (33–35)].
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Figure 2: Summary of hypoglossal nerve activity during carbachol- induced REM sleep-like episodes that were evoked before (baseline B0,C0) and at different times after (B1,C1 and B2,C2), the injections of the antagonist combinations into hypoglossal nucleus. (A) Combined injections of prazosin, methysergide, bicuculline and strychnine. (B) Combined injections of prazosin, methysergide and bicuculline. (C) Combined injections of prazosin and methysergide. (D) Injections of prazosin only. (E) Injections of methysergide only. Pz, prazosin, an α1-adrenoceptor antagonist; Me, methysergide, a broad-spectrum serotonergic antagonist; Bi, bicuculline, a GABAA antagonist; Str, strychnine, a glycinergic antagonist. B0 and C0, baseline hypoglossal nerve activity measured before and during carbachol, respectively; B1 and C1, hypoglossal nerve activity during “early” carbachol responses; B2 and C2, hypoglossal nerve activity during “late” carbachol responses. *p < 0.05, paired t-test [adapted from Fenik et al. (33–35)].

Mentions: The Figure 2 summarizes the effects of antagonists on the REM-HD that were obtained in our series of experiments (33–35). The amplitudes of moving average of hypoglossal nerve activity were measured before (B) and during carbachol (C) at baseline (B0,C0), right after (B1,C1) and at approximately 1 h after (B2,C2), the antagonist injections into hypoglossal nucleus. Additional episodes of REMSLS were elicited by carbachol at later times to observe the recovery process (not shown).


Revisiting Antagonist Effects in Hypoglossal Nucleus: Brainstem Circuit for the State-Dependent Control of Hypoglossal Motoneurons: A Hypothesis.

Fenik VB - Front Neurol (2015)

Summary of hypoglossal nerve activity during carbachol- induced REM sleep-like episodes that were evoked before (baseline B0,C0) and at different times after (B1,C1 and B2,C2), the injections of the antagonist combinations into hypoglossal nucleus. (A) Combined injections of prazosin, methysergide, bicuculline and strychnine. (B) Combined injections of prazosin, methysergide and bicuculline. (C) Combined injections of prazosin and methysergide. (D) Injections of prazosin only. (E) Injections of methysergide only. Pz, prazosin, an α1-adrenoceptor antagonist; Me, methysergide, a broad-spectrum serotonergic antagonist; Bi, bicuculline, a GABAA antagonist; Str, strychnine, a glycinergic antagonist. B0 and C0, baseline hypoglossal nerve activity measured before and during carbachol, respectively; B1 and C1, hypoglossal nerve activity during “early” carbachol responses; B2 and C2, hypoglossal nerve activity during “late” carbachol responses. *p < 0.05, paired t-test [adapted from Fenik et al. (33–35)].
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664632&req=5

Figure 2: Summary of hypoglossal nerve activity during carbachol- induced REM sleep-like episodes that were evoked before (baseline B0,C0) and at different times after (B1,C1 and B2,C2), the injections of the antagonist combinations into hypoglossal nucleus. (A) Combined injections of prazosin, methysergide, bicuculline and strychnine. (B) Combined injections of prazosin, methysergide and bicuculline. (C) Combined injections of prazosin and methysergide. (D) Injections of prazosin only. (E) Injections of methysergide only. Pz, prazosin, an α1-adrenoceptor antagonist; Me, methysergide, a broad-spectrum serotonergic antagonist; Bi, bicuculline, a GABAA antagonist; Str, strychnine, a glycinergic antagonist. B0 and C0, baseline hypoglossal nerve activity measured before and during carbachol, respectively; B1 and C1, hypoglossal nerve activity during “early” carbachol responses; B2 and C2, hypoglossal nerve activity during “late” carbachol responses. *p < 0.05, paired t-test [adapted from Fenik et al. (33–35)].
Mentions: The Figure 2 summarizes the effects of antagonists on the REM-HD that were obtained in our series of experiments (33–35). The amplitudes of moving average of hypoglossal nerve activity were measured before (B) and during carbachol (C) at baseline (B0,C0), right after (B1,C1) and at approximately 1 h after (B2,C2), the antagonist injections into hypoglossal nucleus. Additional episodes of REMSLS were elicited by carbachol at later times to observe the recovery process (not shown).

Bottom Line: We concluded that noradrenergic disfacilitation is the major mechanism that is responsible for approximately 90% of the depression of hypoglossal motoneurons, whereas the remaining 10% can be explained by serotonergic mechanisms that have net inhibitory effect on hypoglossal nerve activity during REM sleep-like state.We hypothesized that both noradrenergic and serotonergic state-dependent mechanisms indirectly control hypoglossal motoneuron excitability during REM sleep; their activities are integrated and mediated to hypoglossal motoneurons by reticular formation neurons.In addition, we proposed a brainstem neural circuit that can explain the new findings.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterans Affairs Greater Los Angeles Healthcare System , Los Angeles, CA , USA ; Websciences International , Los Angeles, CA , USA.

ABSTRACT
We reassessed and provided new insights into the findings that were obtained in our previous experiments that employed the injections of combined adrenergic, serotonergic, GABAergic, and glycinergic antagonists into the hypoglossal nucleus in order to pharmacologically abolish the depression of hypoglossal nerve activity that occurred during carbachol-induced rapid-eye-movement (REM) sleep-like state in anesthetized rats. We concluded that noradrenergic disfacilitation is the major mechanism that is responsible for approximately 90% of the depression of hypoglossal motoneurons, whereas the remaining 10% can be explained by serotonergic mechanisms that have net inhibitory effect on hypoglossal nerve activity during REM sleep-like state. We hypothesized that both noradrenergic and serotonergic state-dependent mechanisms indirectly control hypoglossal motoneuron excitability during REM sleep; their activities are integrated and mediated to hypoglossal motoneurons by reticular formation neurons. In addition, we proposed a brainstem neural circuit that can explain the new findings.

No MeSH data available.


Related in: MedlinePlus