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B E Hunter

Publications and source records attributed to B E Hunter.

10 recordsLinked to original sources
PubMed1992

Chronic ethanol consumption reduces the neurotrophic activity in rat hippocampus.

The effect of chronic ethanol treatment (CET) for 21-26 weeks on the neurotrophic activity contained in the rat hippocampus (HPC) was determined with a bioassay in cultures of dissociated dorsal root ganglion cells (DRG) obtained from E7-8 chick embryos. Extracts of the HPC from CET or pair-fed control rats were used as experimental media, and neuronal survival and neurite-outgrowth of DRG cultures were determined. Both neuronal survival (-25%) and neurite-outgrowth (-50%) were reduced in the presence of HPC extracts from CET rats relative to controls. These data suggest that CET reduces the neurotrophic content of the HPC which may result in damage to septohippocampal neurons.

Animals↗
PubMed1992

Chronic ethanol treatment reduces inhibition in CA1 of the rat hippocampus.

The effect of chronic ethanol exposure on inhibition in the rat hippocampal slice was investigated using paired-pulse stimulation techniques with stimulation in stratum radiatum or stratum oriens of CA1. Experimental animals were fed ethanol in a liquid diet for 20 weeks and were withdrawn for at least 8 weeks prior to electrophysiological recording. Prior ethanol treatment had no effect on basic input-output relationships for the extracellular population spike. Ethanol treatment significantly reduced the recurrent inhibition produced by antidromic stimulation in a manner dependent upon stimulus intensity. In addition, with orthodromic paired-pulse stimulation of either stratum radiatum or oriens, a trend toward an augmentation of the facilitation of population spike amplitude was observed, suggesting that feedforward inhibition may also be reduced. These results are similar to those found with treatments that reduce inhibition. Therefore, we conclude that chronic ethanol exposure produces an enduring disruption of inhibitory neuronal function in the rat hippocampus.

Animals↗
PubMed1991

Chronic ethanol treatment differentially affects muscarinic receptor responses in rat hippocampus.

Sensitivity of hippocampal field potentials to local (iontophoretic) application of acetylcholine (ACh) was investigated in chronic ethanol treated (CET) and sucrose-fed (control) rats. CET and control rats were fed a liquid diet containing either ethanol or sucrose for 28 weeks. Five to six months after ethanol or sucrose was withdrawn, hippocampal slices were taken and ACh was applied in stratum pyramidale or stratum radiatum of CA1 to observe population spike facilitation or field EPSP inhibition, respectively. Population spikes were facilitated to a considerably lesser extent in CET slices relative to controls, while no treatment differences were observed for dendritic EPSP inhibition. These data suggest that ACh response properties in CA1 exhibit differential sensitivity to CET, and may reflect a distinct susceptibility of muscarinic receptor subtypes to the neurotoxic effects of ethanol.

Acetylcholine↗
PubMed1991

Binding of [125I]-insulin-like growth factor-1 (IGF-1) in brains of Alzheimer's and alcoholic patients.

Patients with chronic alcoholism and/or Alzheimer's disease suffer from degenerative changes in the cerebral cortex and hippocampus. To investigate possible changes in IGF-1 receptor binding sites in brain tissue of patients with these pathological conditions, the binding of [125I]-IGF-1 was determined in tissues obtained from control, Alzheimer's and/or patients with a history of alcoholism. The four experimental groups examined consisted of patients from similar age groups. Specific binding of [125I]-IGF-1 to cerebral cortical membranes from Alzheimer's patients had significantly more binding sites than age-matched controls, alcoholic patients and alcoholic patients with Alzheimer's disease. Regression analyses indicated that there were no significant differences in [125I]-IGF-1 binding in cerebral cortex with regard to age of patients (1.1% of total variance with a range of 52 to 92 years). Likewise, the time interval between death and autopsy contributed only 1.4% to the total variance in IGF-1 binding. No statistical differences in [125I]-IGF-1 binding were noted in hippocampal tissue from the various patient groups. Thus, human IGF-1 binding sites in cerebral cortex and hippocampus appear to be relatively stable for a number of variables. The increase in cerebral cortical [125I]-IGF-1 binding sites could be due to upregulation of IGF-1 receptors resulting from a decrease in IGF-1 levels in Alzheimer's patients.

Alcoholism↗
PubMed1978

Ethanol dependence in the rat: temporal changes in neuroexcitability following withdrawal.

Electrodes were chronically implanted in the dorsal hippocampus of rats. Pretreatment levels of neural excitability were assessed by determining the duration of direct hippocampal electrical stimulation sufficient to induce forelimb clonus in each rat. Following baseline measurements the rats were administered an alcohol or sucrose-containing liquid diet and 19--22 days later were withdrawan. Two postwithdrawal stimulation sessions were conducted on each animal. Separate groups of ethanol-dependent and control rats were given primary stimulation sessions at 8 h, 24 h, 72 h, or 1 week postwithdrawal. Secondary stimulation sessions were conducted 1 week or 2 weeks postwithdrawal. The results from the primary stimulations indicated that ethanol-dependent animals exhibited significant neural hyperexcitability for at least 72 h, but not 1 week, postwithdrawal. Results from the secondary stimulations demonstrated the presence of a relative neural hypoexcitability in ethanol-dependent groups as compared to controls. The pattern of results suggests, however, that the observed relative neural hypoexcitability was not the direct result of ethanol withdrawal.

Alcoholism↗
PubMed1978

Ethanol dependence in the rat: role of non-specific and limbic regions in the withdrawal reaction.

Chronic bipolar electrodes were implanted in cortical, limbic, diencephalic and mesencephalic regions of the rat. Following recovery from surgery the rats were maintained for 14--26 days on a liquid diet in which 35--42% of total calories were provided by ethanol. Following ethanol withdrawal, electrographic and behavioral monitoring was continued for 8--10 h. The withdrawal of ethanol resulted in the time-dependent appearance of a variety of withdrawal signs including tail arching, ataxia, rigidity, tremor and spontaneous and audiogenic convulsions. These behavioral signs were accompanied by the development of epileptiform abnormalities across wide-spread brain regions. Analysis of preconvulsive spike activity revealed a greater spike frequency in limbic, mesencephalic and non-specific diencephalic regions, as compared to those in cortex and specific diencephalon. Seizure discharge during the tonic-clonic phase of the primary audiogenic convulsion was initiated in the mesencephalon or amygdala, but spread rather extensively to the remainder of the brain. In those instances, however, where multiple convulsions occurred following the audiogenic convulsions, there was a marked decline in spread of seizure discharge to the cortex. These results were interpreted to support the notion that some degree of neuroanatomical specificity exists in the genesis of epileptiform abnormalities during ethanol withdrawal. A comparison of these results with those studying the neural mechanisms underlying other forms of generalized epilepsy was made. It is hypothesized that central pacemaking regions such as medial thalamus or reticular formation may serve to organize isolated epileptiform activity into coherent patterns of paroxysmal activity throughout the brain during the ethanol withdrawal syndrome.

Alcoholism↗
PubMedDate not supplied

Ethanol dependence in the rat: a parametric analysis.

Rats were maintained on liquid diets as their sole source of calories and fluid for 10, 15, 20, and 30 days. The diets consisted 35-40% of total calories in the form of ethanol. This procedure resulted in substantial ethanol intake leading to behavioral intoxication. Blood ethanol concentrations were found to be elevated throughout the day with a peak during the dark phase of the light cycle. The removal of ethanol resulted in evidence of physiological dependence, including behavioral manifestation of autonomic and somatic dysfunction and an increased susceptibility to audiogenic convulsions. Ten days of ethanol exposure was found to be sufficient for the reliable induction of ethanol dependence. Further increases in ethanol exposure resulted in increased hyperexcitability as measured by susceptibility to audiogenic convulsions. The severity of withdrawal behavior was found to be correlated with the blood ethanol concentration measured upon ethanol removal. A behavioral rating scale for the evaluation of alcohol withdrawal intensity in rats is described.

Animals↗