Nonlinear dielectric properties and temperature stabilization effect near the ferroelectric phase transition in sodium trihydrogen selenite.

The ferroelectric phase transition of crystalline sodium trihydrogen selenite has been characterized by domain observations and measurements of electric permittivity, pyroeffect and spontaneous polarization. The first-order character of the phase transition is clearly demonstrated by the phase coexistence and temperature autostabilization. The considerable heating effect at 50 Hz ac field is described. The electric field effect on the temperature variation of the electric permittivity, in the phase transition region, shows a considerable domain structure contribution to the permittivity value. It is demonstrated that the dielectric properties of x- and y-samples can be described by classical dielectric state equations: the set of coefficients has been determined. It is concluded that the x-component of spontaneous polarization plays a predominant role in the phase transition.

Microvascular spasm is mediated by vasopressin fibers in the rat hippocampal slice.

Microvessels in the rat hippocampal slice can be used as an in vitro model for the study of cerebral vasospasm. Serum from coagulated blood causes prompt and long-lasting microvascular constriction that is neurogenic in nature. Here we show that a candidate spasmogen, thromboxane B2, has excitatory action on neural elements in the slice. However, spasmogenic serum lacks this excitatory effect. Instead, it is inhibitory for a major population of slice neurons. Thus, neurogenic microvascular spasm is produced by a subpopulation of slice neurons or projection fibers, not all neurons acting in concert. Arginine vasopressin (AVP) is contained in fibers that project to the hippocampus, and hippocampal microvessels contain pressor (V1) receptors for the peptide. AVP causes vasoconstriction in the slice, and a specific V1 antagonist for the peptide blocks the microvascular spasm induced by blood serum. The results are interpreted to mean that neurogenic microvascular spasm is mediated by locally released AVP.

Neurogenic mediation of serum-induced microvascular constriction.

We have used the rat hippocampal slice preparation as a model system for the study of microvascular vasospasm. Penetrating cerebral microvessels in the slice constrict in response to a variety of stimuli, including serum from coagulated blood. Microvascular responses to many stimuli are associated with changes in the activity of nearby neurons, and in some cases can be shown to be neurogenically mediated. Here we use the selective neurotoxin, tetrodotoxin (TTX), to show that serum-induced constriction is also neurogenically mediated. This neural regulation of microvessel caliber may participate in pathological vasoconstriction mechanisms in the whole animal.

Spontaneous and neurogenic constriction of microvasculature in the rat hippocampal slice.

The hippocampal slice is characterized by laminar organization and defined synaptic circuitry and provides an in vitro model system for the study of neuronal membrane properties, the action of putative neurotransmitters, and synaptic plasticity. Because the hippocampus is densely vascularized and hippocampal microvessels respond to a variety of stimuli that also affect the activity of neurons in the slice, the preparation is also especially well suited to investigating the physiologic relationship between neurons and intraparenchymal blood vessels. Here we address the issue of potential neurogenic control of cerebral microvasculature using electrical stimuli and specific neurotoxins. A small proportion of slice microvessels displayed spontaneous rhythmic activity that was independent of any exogenous stimulus. The majority of slices examined contained microvessels that responded to a train of electrical impulses delivered to discrete neural pathways. Under particular stimulus conditions, the vascular response could be completely blocked by 1 microM tetrodotoxin. The results are taken to support the existence of a neurogenic influence on penetrating arterioles.

Blood-borne factors regulating microvascular constriction in the rat hippocampal slice.

Previous work shows that blood serum contains a factor that elicits constriction of large cerebral arteries and may be responsible for cerebral vasospasm in subarachnoid hemorrhage patients. However, few studies have considered the action of potential spasmogens on intraparenchymal resistance vessels. We used a common preparation for neurophysiology, the rat hippocampal slice, to study penetrating arterioles and their response to a variety of potential vasoconstrictors. Dilute serum from clotted rat blood evoked profound microvascular constriction when applied to the slice, but plasma incubated with heparin to prevent coagulation was unable to do so. A variety of potential vasoconstrictor substances were tested to see if they could duplicate the effects of serum. Norepinephrine (10 microM), serotonin (one microM) and prostaglandin E2 (one nM) were ineffective in this regard. However, when a stable eicosanoid, thromboxane B2, was applied at a concentration achieved in the cerebrospinal fluid of subarachnoid hemorrhage patients, it duplicated a portion of the vasoconstriction produced by serum. It is concluded that thromboxane B2 may account for part of the spasmogenic property of serum and that unidentified molecules in the coagulation pathway may also play a role.

Action of vasopressin on neurons and microvessels in the rat hippocampal slice.

Arginine vasopressin is reported to have an excitatory effect on hippocampal neurons in the slice preparation. However, vasopressin also has a classic vasopressor action on mammalian blood vessels. We used the rat hippocampal slice to examine the effects of this peptide on central neural and vascular targets. The hippocampus is densely vascularized and pyramidal cells are enmeshed in a network of microvessels. Vasopressin increased the excitability of impaled neurons without substantially altering membrane potential or resistance. The peptide also caused pronounced vasoconstriction in penetrating microvessels when applied at micromolar concentrations. The concerted action of vasopressin on neurons and blood vessels and the physical proximity of these cell types suggest mechanisms whereby these responses may be associated.