Comparative Effect of Some Neurotropic Agents on Balance Compensation After Unilateral and Bilateral (Two-Staged) Labyrinthectomy in Squirrel Monkeys

Igarashi, Makoto; Ishii, Masanori; Ishikawa, Kazuo; Himi, Tetsuo

doi:10.1007/978-3-642-73849-4_55

Cited by 7 publications

(3 citation statements)

References 31 publications

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“…They presume that general stimulation of CNS activity promotes functional recovery. Also the peptide-facilitated compensation ofother brain regions after lesions (Igarashi et al, 1988;Gilchrist et al, 1990) may be induced by a modulatory action of the peptide on the behavioral state and subsequently the synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

The ACTH(4-9) analog Org2766 modulates the behavioral changes induced by NMDA and the NMDA receptor antagonist AP5

et al. 1994

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In studies on aged and brain-lesioned rats the chronic administration of the ACTH(4–9) analog Org2766 has been demonstrated to improve the behavioral performance. Those results suggest that maintenance of hippocampal functioning in senescence and facilitation of functional recovery after brain damage are not due to facilitated reinnervation of denervated structures as suggested in previous studies concerning regeneration of the PNS. Alternative explanations may refer to either the neuroprotective properties of the peptide as demonstrated when chronic treatment immediately follows the damage, or a peptide-induced general change in attention that indirectly may contribute to functional recovery. The behavioral effects after acute treatment with ACTH-like peptides have been previously associated with sustained attention by enhanced neuronal excitability of limbic structures. Now, a hypothesis accounting for both neuroprotection and enhanced attention is forwarded by supposing that the peptide exerts its influence by modulation of NMDA receptor activation. Therefore, the acute effects and interactions between the peptide and the NMDA receptor antagonist AP5 (D,L-2-amino-5-phosphonopentanoic acid), and the peptide and NMDA were studied in a water maze and an open field. Impaired water maze performance induced by an acute intracerebroventricular administration of AP5 was counteracted by the ACTH(4–9) analog Org2766, whereas the peptide alone did not affect spatial orientation. NMDA induced extreme locomotor activity at the periphery of the open field. Interestingly, the ACTH(4–9) analog strongly suppressed NMDA-induced enhanced locomotor activity and normalized the pattern of exploratory behavior.

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Section: Discussionmentioning

confidence: 99%

The ACTH(4-9) analog Org2766 modulates the behavioral changes induced by NMDA and the NMDA receptor antagonist AP5

et al. 1994

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“…Other actions of TRH that might promote recovery include improvement of blood flow, reversing or attenuating physiological effects of endogenous opioids, and attenuating the effects of platelet-activating factor [17,20]. Alternatively, it has been suggested that TRH, as well as other drugs which facilitate vestibular compensation, do so by increasing general motor activity or arousal, thus providing more opportunity to learn new sensory-motor relationships [23].…”

Section: Discussionmentioning

confidence: 99%

“…TRH causes excitation of motoneurons in the spinal cord [20,21] and increases locomotor activity in the rat [22]. TRH also improves locomotor balance after bilateral labyrinthectomy [23], and is a neurotrophic factor in cultured spinal motor neurons [24].…”

Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Hypergravity Affects Thyrotropin-Releasing Hormone Levels in Rat Brainstem and Cerebellum

Daunton

Tang²,

Corcoran³

et al. 1998

Neurosignals

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In studies to determine the neurochemical mechanisms underlying adaptation to altered gravity we have investigated changes in neuropeptide levels in brainstem, cerebellum, hypothalamus, striatum, hippocampus, and cerebral cortex by radioimmunoassay. Fourteen days of hypergravity (hyperG) exposure resulted in significant increases in thyrotropin-releasing hormone (TRH) content of brainstem and cerebellum, but no changes in levels of other neuropeptides (β-endorphin, cholecystokinin, met-enkephalin, somatostatin, and substance P) examined in these areas were found, nor were TRH levels significantly changed in any other brain regions investigated. The increase in TRH in brainstem and cerebellum was not seen in animals exposed only to the rotational component of centrifugation, suggesting that this increase was elicited by the alteration in the gravitational environment. The only other neuropeptide affected by chronic hyperG exposure was met-enkephalin, which was significantly decreased in the cerebral cortex. However, this alteration in met-enkephalin was found in both hyperG and rotation control animals and thus may be due to the rotational rather than the hyperG component of centrifugation. Thus it does not appear as if there is a generalized neuropeptide response to chronic hyperG following 2 weeks of exposure. Rather, there is an increase only of TRH and that occurs only in areas of the brain known to be heavily involved with vestibular inputs and motor control (both voluntary and autonomic). These results suggest that TRH may play a role in adaptation to altered gravity as it does in adaptation to altered vestibular input following labyrinthectomy, and in cerebellar and vestibular control of locomotion, as seen in studies of ataxia.

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Molecular mechanisms of Brainstem plasticity

1991

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Vestibular compensation is the process of behavioral recovery that occurs following unilateral deafferentation of the vestibular nerve fibers (unilateral labyrinthectomy, UL). Since UL results in a permanent loss of vestibular input from the ipsilateral vestibular (VIIIth) nerve, vestibular compensation is attributed to CNS plasticity and has been used as a general model of lesion-induced CNS plasticity. Behavioral recovery from the ocular motor and postural symptoms of UL is correlated with a partial return of resting activity to neurons in the vestibular nucleus (VN) on the deafferented side (the "deafferented VN"), and lesions to the deafferented VN prevent compensation; therefore, the regeneration of resting activity within the deafferented VN is believed to have a causal role in vestibular compensation. The biochemical mechanisms responsible for the adaptive neuronal changes within the deafferented VN are poorly understood. Neuropeptide hormone fragments, such as adrenocorticotrophic hormone (ACTH)-4-10, have been shown to accelerate vestibular compensation and can act directly on some VN neurons in vitro. Antagonists for the N-methyl-D-aspartate (NMDA) receptor have been shown to inhibit vestibular compensation if administered early in the compensation process. Biochemical studies in frog indicate marked alterations in the phosphorylation patterns of several proteins during compensation, and the in vitro phosphorylation of some of these proteins is modulated by ACTH-(1-24), calcium (Ca2+), and calmodulin or protein kinase C. It is therefore possible that ACTH fragments and NMDA antagonists (via their effects on NMDA receptor-mediated Ca2+ channels) modulate vestibular compensation through their action on Ca(2+)-dependent pathways within VN neurons. Recent studies have shown that some Ca2+ channel antagonists and the Ca(2+)-dependent enzyme inhibitor calmidazolium chloride facilitate vestibular compensation. How the regulation of Ca2+ may be related to the neuronal changes responsible for vestibular compensation is unclear at present.

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Comparative Effect of Some Neurotropic Agents on Balance Compensation After Unilateral and Bilateral (Two-Staged) Labyrinthectomy in Squirrel Monkeys

Cited by 7 publications

References 31 publications

The ACTH(4-9) analog Org2766 modulates the behavioral changes induced by NMDA and the NMDA receptor antagonist AP5

The ACTH(4-9) analog Org2766 modulates the behavioral changes induced by NMDA and the NMDA receptor antagonist AP5

Chronic Exposure to Hypergravity Affects Thyrotropin-Releasing Hormone Levels in Rat Brainstem and Cerebellum

Molecular mechanisms of Brainstem plasticity

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