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R W Hamill

Publications and source records attributed to R W Hamill.

65 records · Page 4Linked to original sources
PubMed1981

Effects of spinal cord transection on synapse numbers and biochemical maturation in rat lumbar sympathetic ganglia.

The effects of interruption of descending central pathways on the morphological and biochemical ontogeny of peripheral sympathetic ganglia were examined in the sixth lumbar (L6) sympathetic rat ganglia. Previous studies defined the normal maturation of presynaptic choline acetyltransferase (CAT) activity, postsynaptic tyrosine hydroxylase (T-OH) activity, and total protein in the L6 ganglion. In the present investigations ganglion synapse numbers and adrenergic neuron numbers were examined in transected and sham-operated littermate controls 6 weeks after surgery at 10 days of age and correlative biochemical studies were performed. Spinal transection resulted in a reduction in synapse number on ganglion cell bodies (53.5% reduction) and neuronal processes (55.8% reduction). This abnormality in synapse number was associated with a reduction of CAT activity to 56% of control. Although T-OH activity also failed to develop normally and was 25% of control, there was no associated alteration in adrenergic neuron number. These studies suggest that descending central pathways regulate the maturation of presynaptic cholinergic terminals (and hence synapse number) in sympathetic ganglion and that CAT activity serves as an accurate marker for these terminals. Additionally, the ontogeny of ganglion T-OH activity is altered by central lesions and this effect is not secondary to a decrease in adrenergic neuron number.

Animals↗
PubMed1976

Central regulation of sympathetic neuron development.

The sixth lumbar (L-6) ganglion has been used to study the central regulation of peripheral sympathetic neuron development. During post-natal ontogeny, tyrosine hydroxylase [tyrosine 3-monooxygenase, L-tyrosine, tetrahydropteridine: oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] activity increased 60-fold, while total protein rose 10-fold in the ganglion. Transection of the spinal cord at the fifth thoracic (T-5) segment in neonatal rats prevented the normal developmental increase in tyrosine hydroxylase activity of the L-6 ganglion. However, spinal transection did not alter the ontogeny of tyrosine hydroxylase in the superior cervical ganglion, which derives its innervation from spinal segments rostral to the surgical lesion. Thus, spinal transection interfered with the maturation of sympathetic neurons distal to, but not proximal to, the lesion. The effect of transection on the L-6 ganglion persisted for at least one month, the longest time tested. Our observations suggest that trans-synaptic regulation of adrenergic maturation in the periphery is governed by suprasegmental mechanisms in the central nervous system.

Animals↗
PubMedDate not supplied

The amygdala in Alzheimer's disease: neuropathology and Alz 50 immunoreactivity.

Patients with Alzheimer's disease (AD) often show emotional, motivational, and memory disturbances which may have morphological substrates that include the amygdaloid complex. Neuropathological studies in other limbic areas have recently been enhanced by immunocytochemical studies with Alz 50 antibody. Therefore, we examined the distribution of Alz 50 immunoreactive (Alz 50-IR) neuritic plaques (NP) and neurofibrillary tangles (NFT) in the amygdala in AD cases, in one aged patient with Down's syndrome, and in controls of similar ages. In all AD cases numerous NP and variable numbers of NFT were observed and a distinctive subregional anatomical distribution of NP and Alz 50-IR neuropil in the amygdala existed, whereas no similar selective topography for NFT or Alz 50-IR neurons was found. A high density of NP was demonstrated in the ventromedial aspects of the basolateral and corticomedial nuclear regions. There was no correlation with the pattern of cholinergic innervation. There was, however, a correspondence between intraamygdaloid- and amygdaloid-hippocampal connections and regions of high NP density. Our findings support the concept that the disease process may occur along anatomically defined pathways, and the amygdala may be a central participant in this process.

Acetylcholinesterase↗
PubMedDate not supplied

Characterization of brain samples in studies of aging, Alzheimer's, and other neurodegenerative diseases.

We review current understanding of the clinical and pathologic information needed for the determination of optimal brain tissue samples for the conduct of studies of Alzheimer's disease (AD). Characteristics that may distinguish AD from other dementing disorders are discussed. Selected considerations in the conduct of basic neurobiological studies are also outlined. Although the 28 NIA-funded Alzheimer's Centers can provide excellent clinical and neuropathological data, studies conducted outside these centers should also strive to gather the information suggested here. Clinical and neuropathological data should be used not only to classify subjects as control or AD, but also as variables that may significantly contribute to the analysis of neurobiological data obtained in the laboratory.

Aging↗
PubMedDate not supplied

Tardive dyskinesia in Alzheimer's disease: clinical features and neuropathologic correlates.

Medical record review was conducted on 14 patients with neuropathologically confirmed Alzheimer's disease, all of whom had been treated with antipsychotic medications, to determine the relationship between neuropathology and the development of tardive dyskinesia. Four cases were found to have chart descriptions of hyperkinetic movement disorders consistent with tardive dyskinesia. When the group with tardive dyskinesia was compared to the group without tardive dyskinesia, there were no statistically significant differences regarding gender, age of onset of dementia, duration of dementia, age at death, or duration of antipsychotic treatment. Neuropathologic comparisons revealed greater degenerative changes in the substantia nigra in those patients with tardive dyskinesia. These preliminary observations suggest that patients with Alzheimer's disease and significant coexisting substantia nigra pathologic changes may be at higher risk for developing tardive dyskinesia when treated with antipsychotic medication.

Aged↗