Biomedical subjects

Shawn G Hayes

Publications and source records attributed to Shawn G Hayes.

6 recordsLinked to original sources

PubMed2003

Two epochs in the development of gamma-aminobutyric acidergic neurons in the ferret thalamus.

These studies chart the development of gamma-aminobutyric acid (GABA)-ergic neurons in the three divisions of the thalamus (ventral thalamus, dorsal thalamus, and epithalamus). GABAergic neurons were identified by in situ hybridization to localize mRNA for 67-kDa glutamic acid decarboxylase (GAD(67)) and related to the morphological maturation of the thalamus in fetal and postnatal brains and to expression of transcription factors Gbx-2 and Tbr-1. Origins of GABAergic neurons were sought in in vitro slice preparations incubated in bromodeoxyuridine or injected with a carbocyanine dye. GABA neurons of ventral thalamus (reticular nucleus, ventral lateral geniculate nucleus, zona incerta, and nucleus of the fields of Forel) and of epithalamus appear at least 14 days before those intrinsic to dorsal thalamus. Ventral thalamus GABA cells are derived from a region connecting the ventricular zone of the third ventricle to the caudal ganglionic eminence. This region is delimited ventrally by the Tbr-1-expressing prethalamic eminence and dorsally by the Gbx-2-expressing part of the dorsal thalamus. GABA neurons of epithalamus are derived from the embryonic pretectum. Neurons continue to be added to the ventral thalamus, perireticular nucleus, entopeduncular nucleus, and substantia nigra from the ganglionic eminence as development proceeds. GAD(67)-expressing cells of dorsal thalamus become detectable only at birth and populate the thalamus from posterior to anterior over the first week of life. Although a very small number reaches the dorsal lateral geniculate nucleus from the caudal ganglionic eminence, there is no obvious new source of proliferating neurons at this stage. Intrinsic GABA cells of dorsal thalamus may, therefore, derive from an early generated population of cells that turns on a GABAergic phenotype only late in development.

Animals↗

PubMed2002

Discharge properties of group III and IV muscle afferents.

Stimulation of group III and IV muscle afferents has been shown to have important reflex effects on both the somatic and autonomic nervous systems. These include an inhibitory effect on alpha motoneurones, an excitatory effect on gamma motoneurones and an excitatory effect on the sympathetic nervous system. The purpose of this review is to describe the mechanical and metabolic stimuli that discharge group III and IV muscle afferents. Particular attention will be paid to the responses of these afferents to dynamic exercise induced by electrical stimulation of the mesencephalic locomotor region.

Animals↗

PubMed2002

The exercise pressor reflex.

The exercise pressor reflex is believed to play a role in causing the cardiovascular and ventilatory responses to exercise. This review will discuss the evidence that the reflex is active in both humans and animals. In addition, this review will discuss the nature of the mechanical and metabolic stimuli that evoke the exercise pressor reflex. Particular attention will be paid to the discharge properties of the thin fiber sensory nerves (i. e., group III and IV muscle afferents) whose activation by these mechanical and metabolic stimuli is responsible for evoking the reflex. Finally, some current findings and controversies will be discussed.

Animals↗

PubMed2002

alpha,beta-Methylene ATP elicits a reflex pressor response arising from muscle in decerebrate cats.

In part, the exercise pressor reflex is believed to be evoked by chemical stimuli signaling that blood supply to exercising muscles is not adequate to meet its metabolic demands. There is evidence that either ATP or adenosine may function as one of these chemical stimuli. For example, muscle interstitial concentrations of both substances have been found to increase during exercise. This finding led us to test the hypothesis that popliteal arterial injection of alpha,beta-methylene ATP (5, 20, and 50 microg/kg), which stimulates P2X receptors, and 2-chloroadenosine (25 microg/kg), which stimulates P1 receptors, evokes reflex pressor responses in decerebrate, unanesthetized cats. We found that popliteal arterial injection of the two highest doses of alpha,beta-methylene ATP evoked pressor responses, whereas popliteal arterial injection of 2-chloroadenosine did not. In addition, the pressor responses evoked by alpha,beta-methylene ATP were blocked either by section of the sciatic nerve or by prior popliteal arterial injection of pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (10 mg/kg), a selective P2-receptor antagonist. We conclude that the stimulation of P2 receptors, which are accessible through the vascular supply of skeletal muscle, evokes reflex pressor responses. In addition, our findings are consistent with the hypothesis that the stimulation of P2 receptors comprises part of the metabolic error signal evoking the exercise pressor reflex.

2-Chloroadenosine↗

PubMed2002

MLR stimulation and exercise pressor reflex activate different renal sympathetic fibers in decerebrate cats.

Although mesencephalic locomotor region (MLR) stimulation and the exercise pressor reflex have been shown to increase whole nerve renal sympathetic activity, it is not known whether these mechanisms converge onto the same population of renal sympathetic postganglionic efferents. In decerebrate cats, we examined the responses of single renal sympathetic postganglionic efferents to stimulation of the MLR and the exercise pressor reflex (i.e., static contraction of the triceps surae muscles). We found that, in most instances (24 of 28 fibers), either MLR stimulation or the muscle reflex, but not both, increased the discharge of renal postganglionic sympathetic efferents. In addition, we found that renal sympathetic efferents that responded to static contraction while the muscles were freely perfused responded more vigorously to static contraction during circulatory arrest. Moreover, stretch of the calcaneal (Achilles) tendon stimulated the same renal sympathetic efferents as did static contraction. These findings suggest that MLR stimulation and the exercise pressor reflex do not converge onto the same renal sympathetic postganglionic efferents.

Achilles Tendon↗

PubMed2002

Estrogen attenuates the cardiovascular and ventilatory responses to central command in cats.

Static exercise is well known to increase heart rate, arterial blood pressure, and ventilation. These increases appear to be less in women than in men, a difference that has been attributed to an effect of estrogen on neuronal function. In decerebrate male cats, we examined the effect of estrogen (17beta-estradiol; 0.001, 0.01, 0.1, and 1.0 microg/kg iv) on the cardiovascular and ventilatory responses to central command and the exercise pressor reflex, the two neural mechanisms responsible for evoking the autonomic and ventilatory responses to exercise. We found that 17beta-estradiol, in each of the three doses tested, attenuated the pressor, cardioaccelerator, and phrenic nerve responses to electrical stimulation of the mesencephalic locomotor region (i.e., central command). In contrast, none of the doses of 17beta-estradiol had any effect on the pressor, cardioaccelerator, and ventilatory responses to static contraction or stretch of the triceps surae muscles. We conclude that, in decerebrate male cats, estrogen injected intravenously attenuates cardiovascular and ventilatory responses to central command but has no effect on responses to the exercise pressor reflex.

Animals↗