Differential control of aggression by the midbrain

The Journal of Physiology

Takahashi

Saitoh

et al. 2005

103

Orexinergic neurones in the perifornical lateral hypothalamus project to structures of the midbrain, including the substantia nigra and the mesopontine tegmentum. These areas contain the mesencephalic locomotor region (MLR), and the pedunculopontine and laterodorsal tegmental nuclei (PPN/LDT), which regulate atonia during rapid eye movement (REM) sleep. Deficiencies of the orexinergic system result in narcolepsy, suggesting that these projections are concerned with switching between locomotor movements and muscular atonia. The present study characterizes the role of these orexinergic projections to the midbrain. In decerebrate cats, injecting orexin-A (60 µM to 1.0 mM, 0.20-0.25 µl) into the MLR reduced the intensity of the electrical stimulation required to induce locomotion on a treadmill (4 cats) or even elicit locomotor movements without electrical stimulation (2 cats). On the other hand, when orexin was injected into either the PPN (8 cats) or the substantia nigra pars reticulata (SNr, 4 cats), an increased stimulus intensity at the PPN was required to induce muscle atonia. The effects of orexin on the PPN and the SNr were reversed by subsequently injecting bicuculline (5 mM, 0.20-0.25 µl), a GABA A receptor antagonist, into the PPN. These findings indicate that excitatory orexinergic drive could maintain a higher level of locomotor activity by increasing the excitability of neurones in the MLR, while enhancing GABAergic effects on presumably cholinergic PPN neurones, to suppress muscle atonia. We conclude that orexinergic projections from the hypothalamus to the midbrain play an important role in regulating motor behaviour and controlling postural muscle tone and locomotor movements when awake and during sleep. Furthermore, as the excitability is attenuated in the absence of orexin, signals to the midbrain may induce locomotor behaviour when the orexinergic system functions normally but elicit atonia or narcolepsy when the orexinergic function is disturbed.

Section: Discussionmentioning

confidence: 99%

Orexinergic projections to the cat midbrain mediate alternation of emotional behavioural states from locomotion to cataplexy

The Journal of Physiology

Takahashi

Saitoh

et al. 2005

103

“…Emotional signals via the limbic and hypothalamic structures (Derryberry and Tucker, 1992;Smith, DeVito, 1984) to the midbrain may increase muscle tone and induce emotional locomotor behavior (Garcia-Rill et al, 2004;Shaikh et al, 1984) (Fig.2C). In the absence of orexin (Fig.2D), the excitability of both the locomotor system and the muscle tone excitatory system would be reduced.…”

Section: Implications Of Pathophysiological Mechanisms Of Narcolepsymentioning

confidence: 99%

Forebrain control of locomotor behaviors

2008

Brain Research Reviews

131

120

Activation of different areas in the forebrain evokes different types of goal directed adaptive behaviors. An important component of these different patterns of behavior is the locomotion that brings the animal to or away from a particular location.Here I review the role of projections from forebrain structures to the mesopontine tegmentum of the brainstem where neural mechanisms for initiation of locomotion and regulation of postural muscle tone are located that are activated during locomotor behavior. It is interesting is to understand how signals that converge from the forebrain structures to the mesopontine tegmentum control locomotor behavior, because the mesopontine tegmentum receives inhibitory efferents from the basal ganglia and excitatory efferents from the limbic-hypothalamic system and the neocortex. Here I hypothesize that the mesopontine tegmentum has functional gating mechanisms that determine whether the subject will initiate and select volitionally-guided or emotionally-triggered locomotor behaviors, depending on the behavioral context.

“…8A). Emotional signals via the limbic and hypothalamic structures (Derryberry and Tucker, 1992;Smith and Devito, 1984) to the midbrain may thus increase muscle tone and induce emotional locomotor behavior Shaikh et al, 1984;Sinammon;Skinner et al, 2004).…”

Section: -2 Pathophysiology Of Narcolepsymentioning

confidence: 99%

Neurobiological basis of state-dependent control of motor behaviors

Sleep and Biological Rhythms

Saitoh

Nonaka³

et al. 2006

We note the importance of an appropriate combination of excitability for the higher (neocortex, basal ganglia, and limbic system) and lower (brainstem-spinal cord) motor systems could be necessary for normal behavior during wakefulness and REM sleep.Neurotransmitters such as acetylcholine, the monoamines, GABA, and the orexins, would regulate the background excitability of the higher and lower motor systems so that an interaction of these systems could be appropriately maintained. Pathophysiological mechanisms of sleep deficiency may be induced by not only an organic disturbance of brain structures (hardware) but also by dysfunction of the neurotransmitter systems (software). From these considerations, we provide a hypothetical model for "state-dependent interaction of the higher and lower motor systems" for understanding normal behavior and pathophysiological mechanisms of sleep-related disorders such as narcolepsy and the REM-sleep behavioral syndrome.2