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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

Theoretical examples of sleep-induced inhibitory (A–C) and disfacilitatory (D–F) effects on the magnitude of a parameter value measured during wakefulness (W) and sleep (S) before (baseline W0,S0) and after applications of antagonists (Cases 1 and 2), which supposedly remove either state-dependent inhibitory (A) and facilitatory (D) inputs, or tonic state-independent inhibitory (B) and facilitatory (E) inputs or simultaneously state-dependent and state-independent inhibitory (C) and facilitatory (F) inputs. W0 and S0 – the parameter value measured during baseline wakefulness and sleep, respectively; W1 and S1 – the Case 1 after an antagonist application during wakefulness and sleep, respectively; W2 and S2 – the Case 2 after an antagonist.
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Figure 1: Theoretical examples of sleep-induced inhibitory (A–C) and disfacilitatory (D–F) effects on the magnitude of a parameter value measured during wakefulness (W) and sleep (S) before (baseline W0,S0) and after applications of antagonists (Cases 1 and 2), which supposedly remove either state-dependent inhibitory (A) and facilitatory (D) inputs, or tonic state-independent inhibitory (B) and facilitatory (E) inputs or simultaneously state-dependent and state-independent inhibitory (C) and facilitatory (F) inputs. W0 and S0 – the parameter value measured during baseline wakefulness and sleep, respectively; W1 and S1 – the Case 1 after an antagonist application during wakefulness and sleep, respectively; W2 and S2 – the Case 2 after an antagonist.

Mentions: Since effects of the applied antagonists on the activity of motoneurons during wakefulness, NREM, and REM sleep are heterogeneous and sometimes difficult to interpret, we would like to theoretically summarize and provide interpretations of the most common outcomes of antagonist applications on a parameter value that is measured during, e.g., sleep and wakefulness (Figure 1). The parameter is either the amplitude of membrane potential, or frequency of neuronal firing rate, or amplitude of moving average of nerve activity, etc. In these theoretical examples, sleep has a depressant influence on the magnitude of the measured parameter and, therefore, its value is decreased during sleep as compared to wakefulness due to either direct inhibition of motoneurons (Figures 1A–C) or the removal of excitatory inputs from motoneurons, i.e., disfacilitation (Figures 1D–F). In addition, applied antagonists may block receptors that are relevant to the effect of sleep and, thereby, reduce the sleep effects (Figures 1A,D), or they may block some other receptors that do not mediate the sleep effects but that mediate tonic excitatory or inhibitory drives that affect motoneuronal excitability (Figures 1B,E).


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

Fenik VB - Front Neurol (2015)

Theoretical examples of sleep-induced inhibitory (A–C) and disfacilitatory (D–F) effects on the magnitude of a parameter value measured during wakefulness (W) and sleep (S) before (baseline W0,S0) and after applications of antagonists (Cases 1 and 2), which supposedly remove either state-dependent inhibitory (A) and facilitatory (D) inputs, or tonic state-independent inhibitory (B) and facilitatory (E) inputs or simultaneously state-dependent and state-independent inhibitory (C) and facilitatory (F) inputs. W0 and S0 – the parameter value measured during baseline wakefulness and sleep, respectively; W1 and S1 – the Case 1 after an antagonist application during wakefulness and sleep, respectively; W2 and S2 – the Case 2 after an antagonist.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 1: Theoretical examples of sleep-induced inhibitory (A–C) and disfacilitatory (D–F) effects on the magnitude of a parameter value measured during wakefulness (W) and sleep (S) before (baseline W0,S0) and after applications of antagonists (Cases 1 and 2), which supposedly remove either state-dependent inhibitory (A) and facilitatory (D) inputs, or tonic state-independent inhibitory (B) and facilitatory (E) inputs or simultaneously state-dependent and state-independent inhibitory (C) and facilitatory (F) inputs. W0 and S0 – the parameter value measured during baseline wakefulness and sleep, respectively; W1 and S1 – the Case 1 after an antagonist application during wakefulness and sleep, respectively; W2 and S2 – the Case 2 after an antagonist.
Mentions: Since effects of the applied antagonists on the activity of motoneurons during wakefulness, NREM, and REM sleep are heterogeneous and sometimes difficult to interpret, we would like to theoretically summarize and provide interpretations of the most common outcomes of antagonist applications on a parameter value that is measured during, e.g., sleep and wakefulness (Figure 1). The parameter is either the amplitude of membrane potential, or frequency of neuronal firing rate, or amplitude of moving average of nerve activity, etc. In these theoretical examples, sleep has a depressant influence on the magnitude of the measured parameter and, therefore, its value is decreased during sleep as compared to wakefulness due to either direct inhibition of motoneurons (Figures 1A–C) or the removal of excitatory inputs from motoneurons, i.e., disfacilitation (Figures 1D–F). In addition, applied antagonists may block receptors that are relevant to the effect of sleep and, thereby, reduce the sleep effects (Figures 1A,D), or they may block some other receptors that do not mediate the sleep effects but that mediate tonic excitatory or inhibitory drives that affect motoneuronal excitability (Figures 1B,E).

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