Long-term decreases in spontaneous firing of caudate neurons induced by amphetamine in cats.
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Biomedical subjects
Publications and source records attributed to E Garcia-Rill.
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The effects of unilateral medial forebrain bundle ("MFB") lesions on the spontaneous firing patterns of caudate neurons on both sides of the brain in cats were studied 3 days, 7 days and more than 2 weeks postlesion. Our results indicate that: (1) the spontaneous firing of neurons in the caudate nucleus ipsilateral to the lesion slows significantly by 3 days postlesion and returns to control values by 7 days postlesion, (2) the spontaneous activity of contralateral caudate neurons slows progressively with postlesion time and (3) these changes in neural activity are not correlated with changes in dopamine concentrations in the caudate nucleus.
The projections to the striatum from two cytoarchitectonically and functionally distinct subdivisions of the cat precruciate motor cortex were studied using anatomical and electrophysiological techniques. Our results indicate that the medial precruciate cortex (stimulation of which leads to movements of the axial and proximal musculature) has a widespread projection to the lateral half of the caudate nucleus. The lateral precruciate cortex (stimulation of which leads to movements of the distal musculature) has a localized projection within the caudate nucleus adjacent to the internal capsule. Both medial and lateral precruciate areas project to the putamen. These results are discussed in relation to recent studies suggesting that the basal ganglia are involved in the enabling and sequencing of movements.
To assess the effects of partial deafferentation of the neostriatum on spontaneous neuronal activity in the basal ganglia and related thalamic nuclei, ablations of frontal cortex were carried out in adult cats. Postoperative measures of interspike intervals of single neurons in the caudate nucleus, globus pallidus and ventral anterior-ventral lateral complex of the thalamus revealed a slowing of neuronal firing in these structures as compared with non-lesioned controls. The fact that deafferentation by cortical damage produces changes in neuronal firing in target neurons of the striatum (globus pallidus) and in thalamic neurons at least two synapses removed from the striatum is noteworthy. The possible extent to which these results might have been influenced by reduction of cortical inputs to or denervation of the thalamus is discussed.
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Unilateral lesions interrupting striatal outputs and inputs (MFB lesions) produce a marked slowing of neuronal firing in the caudate nucleus contralateral to the side of the lesions without affecting neuronal firing in the ipsilateral caudate nucleus. Although the MFB lesion also interrupts the nigrostriatal pathway and depletes the ipsilateral striatum of dipamine and its associated enzymes, the slowing of unit firing rates is apparently due to interruption of striatal outputs rather than inputs. Unilateral thalamic lesions palced ipsilateral to MFB lesions in iether the ventral anterior-ventrolateral nuclei (VA-VL) or in the center median-parafascicular nuclei (CM-PF) prevent the MFB lesion-induced asymmetry in caudate neuronal firing rates. These thalamic lesions do not, however, restore the striatal dopamine content depleted by the MFB lesion. Unilateral CM-PF lesions in otherwise intact cats do not alter caudate unit firing rates nor do they affect striatal dopamine. VA-VL lesions in otherwise intact cats produce a bilateral slowing in the spontaneous firing of neurons in the caudate nuclei, again, whithout altering caudate dopamine concentrations. These results provide further evidence that caudate dopamine concentration per se does not appear to be a potent variable in controlling the spontaneous firing rates of striatal neurons.
The effects of changes in pCO2 in the development and resolution of normal (return to base line within 2 sec after S2) and abnormal (return to base line in more than 2 sec after S2) CNVs were studied. Decreased pCO2 produced by hyperventilation induced a significant reduction in the duration of the post-imperative negative variation (PINV) without significantly affecting the amplitude of the CNV. Increased pCO2, by inhalation of 5% CO2, on the contrary, produced prolongation of the PINV in two subjects. Control subjects with normal CNVs did not show significant changes in the amplitude or in the duration of the CNV wave when pCO2 was altered. The results are discussed in terms of the possible independence and higher sensitivity to metabolic changes of the PINV brain generators compared with the generators of the CNV wave per se.
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Following injections of retrograde tracers into the spinal cord enlargements, the mesencephalic locomotor region (MLR) was electrically stimulated to induce locomotion in decerebrate rats. MLR sites coincided with cholinergic pedunculopontine nucleus (PPN) neurons, which were selectively labelled using NADPH diaphorase histochemistry. Retrogradely labelled (spinal-projecting) PPN neurons were scattered among cholinergic PPN neurons. The absence of retrogradely labelled, NADPH diaphorase positive PPN neurons indicates that spinal enlargement projections are non-cholinergic.
Retrograde tracers were injected into the rat medioventral medulla (MED) and the injection site was identified as a locomotion- inducing area by electrical stimulation in the decerebrate preparation. Histological reconstructions showed that about 10% of cholinergic pedunculopontine (PPN) and laterodorsal tegmental (LDT) neurons project to the MED. Also, large numbers of non-cholinergic cells in and around the PPN and LDT were found to project to the MED.