Lesions of the pedunculopontine tegmental nucleus increase sucrose consumption but do not affect discrimination or contrast effects.
Mary C. OlmsteadWendy L. InglisChris P. BordeauxEmily J ClarkeNick P. WallumBarry J. EverittTrevor W. Robbins
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Pedunculopontine Tegmental Nucleus
Pedunculopontine nucleus
The pedunculopontine nucleus is composed of cholinergic and non-cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post-mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man.
Pedunculopontine nucleus
Pedunculopontine Tegmental Nucleus
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Pedunculopontine Tegmental Nucleus
Pedunculopontine nucleus
Subthalamic Nucleus
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The pedunculopontine tegmental nucleus (PPN) is anatomically connected with dopaminergic cells in the ventral mesencephalon, which are known to participate in the regulation of various adaptive appetitive behaviours. In the present experiment we studied a possible involvement of PPN in feeding elicited by stimulation of the ventral tegmental area (VTA). It was found that bilateral electrolytic lesioning of the PPN affected VTA-elicited feeding. However, the effects were diverse and showed dependence on the localization of the lesion within the PPN area. Lesions localized anteriorly in the PPN impaired VTA feeding whereas those involving the middle portion of the nucleus facilitated electrically elicited food ingestion. A precise alignment of the lesion and the area activated at the site of stimulation appeared crucial for the effect of the lesion. The results indicate that PPN belongs to the central feeding circuitry and it contains both activating and inhibiting elements directed to the ventral tegmental area.
Pedunculopontine Tegmental Nucleus
Pedunculopontine nucleus
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Although gait ataxia is usually associated with cerebellar lesions, we review a less familiar cause. We present three patients with dorsal midbrain lesions and correlate these presentations with recent findings in the functional anatomy of the midbrain.We suggest that these lesions involve a well-studied but generally unfamiliar area of the dorsal midbrain known as the mesencephalic locomotor region. More specifically, we hypothesize that involvement of the pedunculopontine nucleus, a major component of the mesencephalic locomotor region, may be at least partially responsible for producing midbrain ataxia.
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To observe the protein expression of growth associated protein-43 (GAP-43) in midbrain ventral tegmental area in morphine withdrawal rats at different time, and to evaluate the effect of GAP-43 on morphine withdrawal memory.Rat models of morphine dependent 1 week, 2 weeks and 4 weeks were established by morphine hydrochloride intraperitoneal injection with increasing doses to establish natural withdrawal. The protein expression of GAP-43 in midbrain ventral tegmental area was observed by immunohistochemical staining and the results were analyzed by Image-Pro Plus 5.1 image analysis system.With prolongation of dependent time, the expression of GAP-43 was decreased then increased in midbrain ventral tegmental area.GAP-43 could play a role in morphine withdrawal memory in midbrain ventral tegmental area.
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Objective To observe the protein expression of growth associated protein-43(GAP-43) in midbrain ventral tegmental area in morphine withdrawal rats at different time, and to evaluate the effect of GAP-43 on morphine withdrawal memory. Methods Rat models of morphine dependent 1 week, 2 weeks and 4 weeks were established by morphine hydrochloride intraperitoneal injection with increasing doses to establish natural withdrawal. The protein expression of GAP-43 in midbrain ventral tegmental area was observed by immunohistochemical staining and the results were analyzed by Image-Pro Plus 5.1 image analysis system. Results With prolongation of dependent time, the expression of GAP-43 was decreased then increased in midbrain ventral tegmental area. Conclusion GAP-43 could play a role in morphine withdrawal memory in midbrain ventral tegmental area.
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Pedunculopontine nucleus
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Pedunculopontine Tegmental Nucleus
Diencephalon
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Pedunculopontine Tegmental Nucleus
Pedunculopontine nucleus
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