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Biomedical subjects

C J Cook

Publications and source records attributed to C J Cook.

At least 37 records · Page 2Linked to original sources
PubMed1995

Electroencephalographic studies on the nape shooting of sheep.

The implications of shooting animals in the area of the occipito-atlantal junction was evaluated in three sheep by recording changes in the EEG activity. In one sheep, a shot which entered the occipito-atlantal junction and fractured the first cervical vertebra failed to produce insensibility. In contrast, a shot in another sheep which struck the occipital condyles of the skull resulted in loss of cortical evoked responses, the presence of high amplitude low frequency activity and ultimately all loss of brain activity. These results provide evidence that shooting through the vertebral column does not necessarily transmit sufficient percussive forces to higher brain regions to produce immediate insensibility. This has important implications for the humane destruction of animals, particularly, as in the case of cetaceans, where the occipito-atlantal junction or a high neck position is a recommended target area.

Journal Article↗
PubMed1993

Electrical stunning of red deer (Cervus elaphus).

Eighteen of 23 red deer (Cervus elaphus) at a deer slaughtering premises were successfully stunned with an apparatus modified from that normally used to stun sheep. The five unsuccessful electrical stuns were associated with poor head restraint and poor head contact by the electrodes. The median stunning current was 0.9 A, and in the majority of cases the duration of stunning was less than 1 second. The signs of the electrically induced epileptiform seizures in the deer were dissimilar to those seen in sheep, cattle and pigs, in that the initial tonic phase was less marked, and of shorter duration. A similar shorter and less obvious tonic phase was noted in four deer shot with a captive bolt pistol. Two animals which were electrically stunned, and bled within 10 seconds, showed no signs of recovery while bleeding. The electroencephalograms of four deer stunned with currents of 1.3 A for a duration of either 0.5 or 1.0 seconds were recorded under more controlled conditions. All four animals developed electroencephalograms typical of an epileptiform seizure. The animals exhibited behavioural reactions similar to the other 18 animals in the trial at the deer slaughtering premises and were rendered unconscious for between 54 and 122 seconds. The electroencephalogram activity amplitude was greater than that recorded immediately before stunning and took between 6 and 9 seconds to build up to maximum value. It is concluded that, providing the heads of deer are adequately restrained, head-only electrical stunning can be incorporated into a humane method of slaughter for deer.

Journal Article↗
PubMed1992

Contribution of amino acid transmitters to epileptiform activity and reflex suppression in electrically head stunned sheep.

In sheep, administration of a combination of zolazepam and tiletamine hydrochloride resulted in a dose dependent reduction in the duration of epileptic activity induced by an electric stun applied to the head. The compound also lengthened the normal period of reflex suppression that occurs after a stun. Excitatory amino acid receptor antagonists (2-amino-7-phosphonoheptanoic and 2-amino-5-phosphonovaleric acids) also reduced the duration of epileptic activity following an electric stun. These drugs did not alter the time of pedal and ear pinch reflex suppression. Administration of bicuculline (a gamma amino-4-butyric acid [GABA] receptor antagonist) reduced the period of stun induced reflex suppression and increased seizure duration. Administration of a GABA receptor agonist, baclofen, increased the duration of reflex suppression. The results suggest that the development of epileptiform-like activity following application of an electric current to the head is dependent upon excitatory amino acid receptors. The reflex suppression that also arises following an electric stun is contributed to by the activation of GABA receptor mechanisms.

2-Amino-5-phosphonovalerate↗
PubMed1991

Electroencephalograms and electrocardiograms in young bulls following upper cervical vertebrae-to-brisket stunning.

Passing an electric current (50 Hz, 400 V open circuit, current limited to 1.5 A) from two electrodes acting as a common single electrode set applied on each side of the dorsal surface of the neck (cervical vertebrae C2 to C5 region) to another placed on the brisket of young bulls causes fibrillation of the cardiac muscle, does not induce epileptiform changes in the electroencephalogram, and produces a state of body rigidity. Passing the same electric current through the same neck electrodes, now acting as two separate electrodes, without the brisket electrode, does induce epileptiform activity similar to that seen with head-only stunning, does not fibrillate the heart, and produces a state of limb rigidity lasting for some time after the stun. Given that the presence of epileptiform activity is a criterion for effective electrical stunning and is indicative of insensibility, neck-to-brisket stunning as described here does not appear to be humane.

Journal Article↗
PubMed1991

Electrophysiological responses of the fetus to hypoxia and asphyxia.

To study the effect of transient hypoxia on neural function in utero, we examined brainstem auditory and somatosensory evoked potentials in chronically instrumented fetal sheep subject to altered maternal inspired gases. Moderate hypoxia without acidosis for 1 h, in 10 fetuses (fetal arterial pH = 7.37 +/- 0.03, PaO2 = 1.4 +/- 0.27 kPa) caused a transient depression of the later components of the evoked potentials. These recovered within 1 h. However, in 6 fetuses exposed to a second, acidotic, insult 2 days later, associated with a higher inspired PCO2 (fetal pH = 7.25 +/- 0.05, PaO2 = 1.17 +/- 0.28 kPa), there was greater impairment of the later components of the evoked potentials, with significant changes still observable 72 h later. In 4 fetuses a non-acidotic hypoxia was repeated instead and in these fetuses no persisting deficit was seen. These data suggest that there is a narrow threshold between a degree of intrauterine hypoxaemia associated with no sequelae and an insult causing persistent cerebral impairment, and that even mild acidosis may contribute to this.

Acidosis↗
PubMed1990

Excitatory amino acid projections to the periaqueductal gray in the rat: a retrograde transport study utilizing D[3H]aspartate and [3H]GABA.

The afferents to the periaqueductal gray utilizing excitatory amino acid transmitters have been described in rat brain by autoradiography following microinfusion and retrograde transport of D[3H]aspartate. Parallel experiments employing injections of [3H]GABA established that the retrograde labelling found with D[3H]aspartate was transmitter-selective. Following infusion of D[3H]aspartate, perikaryal labelling was found in nine subcortical areas, particularly infralimbic and cingulate cortices, with a predominance of ipsilateral labelled perikarya. Heaviest cortical labelling was localized in perirhinal cortex, in an extensive band of cells adjoining the rhinal sulcus. The hypothalamus contained the heaviest perikaryal labelling within brain: D[3H]aspartate labelled cells in 11 hypothalamic and mammillary nuclei. Intense bilateral labelling was obtained in ventromedial hypothalamus, although the number of perikarya was lower contralaterally. D[3H]Aspartate also produced heavy ipsilateral labelling of perikarya in posterior hypothalamus. Labelling patterns in cortex and hypothalamus were precise and topographic, and [3H]GABA never labelled cells in these regions. Other telencephalic and diencephalic areas containing prominent, retrogradely labelled cells were the lateral septum, amygdala, zona incerta and lateral habenula. The relative density of labelled cells in mesencephalic areas was much lower than that found in cortex and hypothalamus, although D[3H]aspartate labelled a moderate number of perikarya in the inferior colliculus and cuneiform nucleus. A smaller number of heavily labelled cells was found in the parabrachial nuclei, Kolliker-Fuse nucleus and laterodorsal tegmental nucleus. Only occasional labelled perikarya were observed in the myencephalon. Low densities of labelled cells were found after the injection of [3H]GABA into the periaqueductal gray, and the only regions in which a small number of perikarya were labelled by both [3H]GABA and D[3H]aspartate were the dorsal raphe and parabrachial nuclei. Overall, the retrograde transport of D[3H]aspartate revealed a complex topographic and convergent network of afferent pathways to the periaqueductal gray likely to utilize an excitatory amino acid transmitter. Our findings confirm the selectivity of this neurochemical mapping technique and provide evidence that hypothalamic, habenular, subthalamic and cuneiform afferents to the periaqueductal gray utilize an acidic amino acid as their transmitter. They also confirm that corticofugal afferents to periaqueductal gray utilize an excitatory amino acid.

Afferent Pathways↗
PubMed1989

The effects on central dopamine function of chronic L-dopa (methyl ester hydrochloride) treatment of mice.

Mice were treated for 28 days with drinking water containing L-DOPA methyl ester hydrochloride (DME) plus carbidopa, carbidopa alone, or with the vehicle. All mice were then given the vehicle for 1 day and behavioural and biochemical assessments made on the 29th day. On average, mice consumed between 181 and 302 mg/kg of DME (expressed as the base) each day. In behavioural experiments DME- and carbidopa-treated mice were subsensitive to the locomotor stimulating effects of apomorphine, after their pretreatment with reserpine plus alpha-methyl-p-tyrosine to remove endogenous stores of dopamine and to stop its synthesis. Even mice pretreated for only one day with chronic DME or carbidopa displayed some subsensitivity to apomorphine challenge, but the effect was more marked the longer the chronic treatment. Other mice were chronically treated for 28 days with alpha-methylDOPA or vehicle, and these mice when challenged with apomorphine after dopamine depletion (as described above), were also markedly subsensitive to the locomotor activating effects of apomorphine. There were no changes in sensitivity of drug-treated mice to the hypothermic effects of apomorphine, to the stereotypy-inducing effects of apomorphine or d-amphetamine, or to the locomotor activating effects of L-DOPA itself or to bromocriptine. There were, however, some changes in the basal grooming behaviour of both DME- and carbidopa-treated mice, and in their response to SKF38393 challenge. Striatal binding studies with [3H]-spiperone and [3H]-SCH23390 indicated that there were no marked changes in Kd or Bmax of either D-1 or D-2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Perinatal cerebral asphyxia: pharmacological intervention.

Perinatal asphyxia is associated with an increased risk of cerebral palsy and significant mortality. We investigated the use of flunarizine, a calcium antagonist and MK-801, an excitatory amino acid antagonist, in preventing the sequelae of severe hypoxic/ischemic insults. Flunarizine was neuroprotective in the infant rat subjected to unilateral carotid ligation and 2 h of hypoxia. Preliminary analysis of experiments in a novel model of cerebral ischemia in the fetal sheep suggests that prophylactic treatment with flunarizine greatly modified the outcome after 30 min of total ischemia. Treatment with MK-801 prevented post-ischemic seizures. The background to these developments is outlined and future prospects considered.

Animals↗
PubMed1988

Precocial neural function in the growth-retarded fetal lamb.

Clinical studies suggest that growth-retarded prematurely delivered infants are neurologically precocious. We investigated this paradoxical observation in the fetal lamb. Somatosensory and brainstem auditory-evoked potentials were studied in chronically instrumented fetal lambs in late gestation with varying degrees of growth retardation induced by preconception uterine carunclectomy. The components of the brainstem auditory-evoked response appeared earlier (p less than 0.05) in fetuses at least 2 SD less than the mean weight for gestational age (n = 5) compared to normal controls (n = 8) or carunclectomized fetuses of normal size (n = 7). Several waveforms of both the somatosensory (N20, P/N 30, and P200) and the brainstem auditory-evoked response (I, III, IV, and V) demonstrated shorter (p less than 0.05) latencies in growth-retarded fetuses relative to normal-sized fetuses. The ability to follow increasing stimulus rates for both stimuli also demonstrated precocial maturation (p less than 0.05) in growth-retarded as compared to normal-sized fetuses. Growth retardation is thus associated with precocial neurologic maturation in utero.

Animals↗
PubMed1987

Radioreceptor binding reveals the potencies of N,N-disubstituted 2-aminotetralins as D2 dopamine agonists.

The affinity of a series of N,N-disubstituted 2-aminotetralins for the rat striatal D2 dopamine receptor labelled by [3H]spiperone has been determined. Displacement data for the more potent 2-aminotetralins were better described by a model where the compounds competed for [3H]spiperone at two sites. The high affinity component accounted for approximately 80% of the total sites. Displacement curves for all 2-aminotetralins were shifted to the right by 100 microM guanosine-5'-triphosphate; a result attributable to the redistribution of 13-47% of the sites to a low affinity form. These data are consistent with the N,N-disubstituted 2-aminotetralins being agonists at the D2 dopamine receptor. In particular, the affinities of the 5-hydroxy-2-aminotetralins were as high as those of traditional dopamine agonists.

Animals↗
PubMed1987

Excitatory amino acid projections to the nucleus accumbens septi in the rat: a retrograde transport study utilizing D[3H]aspartate and [3H]GABA.

Afferents to the nucleus accumbens septi utilizing glutamate or aspartate have been investigated in the rat by autoradiography following injection and retrograde transport of D[3H]aspartate. Parallel experiments with the intra-accumbal injection of [3H]GABA were employed to establish the transmitter-selective nature of the retrograde labelling found with D[3H]aspartate. The topography of cortical and thalamic perikarya labelled by D[3H]aspartate was extremely precise. D[3H]Aspartate labelled perikarya were found in layer V of agranular insular cortex; bilaterally within prelimbic and infralimbic subareas perikarya, but predominantly ipsilaterally. Ipsilateral labelling was observed in dorsal, ventral and posterior agranular insular cortices, and in perirhinal cortex. Injections into ventral accumbens labelled perikarya in ipsilateral entorhinal cortex, while infusion of D[3H]aspartate into anterior caudate-putamen resulted in labelling of perikarya in ipsilateral cingulate and lateral precentral cortices. Following infusion of D[3H]aspartate, ipsilateral midline thalamic nuclei contained the highest density of labelled perikarya; infusions centred on nucleus accumbens resulted in heavy retrograde labelling of the parataenial nucleus, but labelling was sparse from a lateral site and not observed after injection into anterior caudate-putamen. Less prominent labelling of perikarya was seen in other thalamic nuclei (mediodorsal, central medial, rhomboid, reuniens and centrolateral), mostly near the midline. Perikaryal labelling was also found in the ipsilateral amygdaloid complex, particularly in basolateral and lateral nuclei. Only weak labelling resulted in ventral subiculum. Numerous labelled cells were present bilaterally in anterior olfactory nucleus, although perikarya were more prominent ipsilaterally. Labelled perikarya were not consistently observed in other regions (ventral tegmental area, medial substantia nigra, raphe nuclei and locus coeruleus) known to innervate nucleus accumbens. Presumptive anterograde labelling was detected in ventral pallidum/substantia innominata, ventral tegmental area and medial substantia nigra. [3H]GABA was generally not retrogradely transported to the same regions labelled by D[3H]aspartate; an exception being the anterior olfactory nucleus, where large numbers of labelled perikarya were found. [3H]GABA failed to label perikarya in thalamus and amygdala, and a topographic distribution of label was absent in neocortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed1987

Cholinoreceptors in the isolated costo-uterine muscle of the rat.

1 The aim of this study was to examine the cholinoreceptor population in the rat costo-uterine muscle. 2 The nicotinic cholinoreceptor agonists nicotine and DMPP, and the ganglionic muscarinic cholinoreceptor stimulant McNeil A-343, had no effects upon isolated preparations of this tissue. 3 Acetylcholine was more potent than carbachol and approximately equipotent with methacholine (the mean EC50 values were 7.0, 6.3 and 6.7 respectively) in producing contractions of the preparation; each was a full agonist. The potencies of carbachol and methacholine were similar in preparations taken from animals in oestrus and in dioestrus. 4 Atropine competitively antagonised the effects of carbachol and methacholine, the pA2 values were 9.37 and 9.41 respectively. The pA2 value for pirenzepine with carbachol as the agonist was 6.69. 5 Pilocarpine produced phasic contractions of the tissue (EC50 value = 4.17), and competitively antagonised the effects of carbachol with a pA2 value of 5.26. The anticholinesterase, physostigmine, produced only a small potentiation of the effects of acetylcholine. 6 It is concluded that the cholinoreceptors which mediate contraction of the rat costo-uterine muscle are muscarinic, homogeneous in nature and unaffected by fluctuating levels of ovarian hormones occurring during the oestrous cycle. The consequences of inhibition of cholinesterase activity in isolated preparations of the tissue are minimal.

Animals↗
PubMed1987

Brainstem auditory evoked potentials in the fetal sheep, in utero.

We studied brainstem auditory evoked potentials (BAEPs) in 8 fetal sheep in utero, ranging in gestational age from 105 to 142 days gestation (normal term 147 days). We could not elicit BAEPs prior to 117 days of gestation. After this age rapid maturation was seen, with three discernible peaks observed prior to 120 days and five peaks after 120 days. A significant (P less than 0.05) gestational age related fall in peak latencies and interpeak latencies was observed. The rate of stimulus presentation that could be tolerated without significant changes in wavepeak latency or amplitude also increased with advancing gestational age. In older fetuses (greater than 125 days), where a differentiated electrocorticogram (ECOG) was observed, differences were seen in latency and amplitude of several of the BAEP wavepeaks dependent upon the state. In high voltage ECOG states the amplitudes of wave IV and V were significantly (P less than 0.05) greater than in the low voltage ECOG state and the latencies of wave I, II and V were significantly (P less than 0.05) longer in low as compared to high voltage ECOG state. The BAEP, being obtainable over very short periods of time, appears to provide a useful indice of neural maturation for the sheep fetus in utero.

Acoustic Stimulation↗