Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Turtles”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1987

Band 3 is the basolateral anion exchanger of dark epithelial cells of turtle urinary bladder.

The turtle urinary bladder serves as a model for collecting duct functions in the mammalian kidney. The epithelium of both the turtle bladder and the mammalian collecting duct can generate a steep gradient for H+ ions between blood and urine. Secretion of H+ into the urine is coupled to a basolateral efflux of HCO-3 that appears to be exchanged mainly against Cl-. Here we show that approximately 80% of the dark cells of the bladder contain a 110,000 relative molecular weight (Mr) analogue of the turtle erythrocyte anion exchanger, band 3. The band 3 analogue is confined to the basolateral cell surface and is absent from the apical membrane. A minor population of the dark cells (approximately 20%), which have been previously suggested to represent reverse cells that are involved in HCO-3 secretion rather than absorption, appears not to express a band 3-like anion exchanger, at either the apical or the basolateral membrane. The bladder band 3 protein is colocalized with actin and isoforms of ankyrin (200,000 Mr) and spectrin (230,000 Mr) along the basolateral membrane. Linkage of band 3 via ankyrin to the spectrin-actin lattice may restrict this anion exchanger to the basolateral membrane surface. In view of our previous observation of a band 3-like anion exchanger in the collecting duct epithelium of the rat kidney, these findings point to a common molecular basis for acid-base transport in the mammalian collecting duct and the reptilian urinary bladder.

Animals↗
PubMed1983

Systemic and renal effects of angiotensin II in the freshwater turtle Pseudemys scripta elegans.

This study examined the renal and systemic effects of angiotensin II (ANG II) in the freshwater turtle, Pseudemys scripta elegans. We infused [Asn1, Val5]ANG II at doses of 1, 10, 100, and 500 ng X kg-1 X min-1 in conscious turtles while monitoring blood pressure, glomerular filtration rate (GFR), urine volume, and plasma and urine electrolytes. Saline (0.6%) was infused for two 1-h control periods at 1 ml X kg-1 X h-1 followed by a 1-h infusion of saline with ANG II added. Saline alone was then infused for either two or three 1-h recovery periods. Control values before ANG II infusion averaged 21 mmHg for blood pressure, 1.8 ml X h-1 for urine volume, and 8.0 ml X kg-1 X h-1 for GFR. At 1 (n = 7) and 10 ng X kg-1 X min-1 (n = 6) ANG II produced no significant changes in blood pressure or renal function. Angiotensin infusion at the higher rates of 100 (n = 6) and 500 ng X kg-1 X min-1 (n = 11) significantly elevated blood pressure during ANG II infusion (29 and 44 mmHg, respectively), while electrolyte excretion remained unchanged. Despite the increased blood pressure, GFR and urine volume tended to decrease. At all infusion rates, plasma electrolytes remained unchanged. The results suggest that ANG II is a potent constrictor of preglomerular vessels in the kidney of the turtle.

Angiotensin II↗
PubMed1985

Potassium ion homeostasis and mitochondrial redox status of turtle brain during and after ischemia.

To account for the remarkable capacity of turtle brain to survive without oxygen, microelectrode recordings of extracellular potassium activity (K+o) were made in intact brains of normoxic pentobarbital-anesthetized turtles during and after ischemia. Changes in redox status of brain cytochrome a,a3 were recorded simultaneously by reflection spectrophotometry. Cytochrome a,a3 became fully reduced, and K+o rose at a slow rate for approximately 60 min during complete ischemia. When K+o reached 8-12 mM, an inflection point was observed after which K+o rapidly increased to levels above 30 mM. Full recovery of baseline K+o and cytochrome a,a3 redox state occurred only if brain blood flow was restored within 60 min. These data demonstrate that maintenance of ion homeostasis in turtle brain depends on blood flow and continued delivery of systemic substrates and that viability is threatened if ischemia is prolonged beyond 60 min.

Animals↗
PubMed1985

Central chemical control of ventilation and response of turtles to inspired CO2.

The role of central chemosensors in the overall ventilatory response of freshwater turtles (Chrysemys scripta elegans) to the addition of CO2 in inspired gas was measured. Centrally mediated ventilatory responses were isolated in the unanesthetized animal by combining CO2 breathing and brain ventricular perfusion with mock cerebrospinal fluid (CSF) of varying acid-base status. Breathing 4.5% CO2 resulted in increases in both ventilatory frequency (f) and tidal volume (VT), with increases in VT providing most of the overall ventilatory change. Alterations in the acid-base status of the perfusate produced highly significant changes in f. VT changes were divorced from the acid-base status of the mock CSF perfusate. We therefore conclude that ventilatory changes in turtles, mediated by central chemosensors, are primarily affected by alterations in f. VT changes, associated with acid-base homeostatic mechanisms, are mediated by receptors outside the blood-brain barrier in these animals. On the basis of these data, we hypothesize that the increase in f observed when turtles breathe 4.5% CO2 is primarily mediated by the central chemosensors.

Acid-Base Equilibrium↗
PubMed1986

Effect of autonomic agents on renin release in the turtle, Pseudemys scripta.

Experiments were conducted in the freshwater turtle, Pseudemys scripta, to study the effect of autonomic agents on the control of renin in this primitive species. The unique finding in these studies was that, unlike mammals, isoproterenol infusion fails to increase renin activity even though heart rate and arterial pressure patterns indicated that systemic responses were similar to that in mammals. On the other hand, acetylcholine (ACh) infusion resulted in a prompt threefold elevation (P less than 0.01) of renin activity. This response was blocked by propranolol but not atropine. Other experiments demonstrated that ACh elicited a prompt elevation of circulating norepinephrine and epinephrine in these turtles and led to the hypothesis that the renin response to ACh was secondary to the release of endogenous catecholamines. This hypothesis was supported by the fact that, in reserpinized turtles, ACh failed to elicit the usual renin response. Further evidence stemmed from the fact that epinephrine administration led to a prompt fourfold increase (P less than 0.01) in renin, which could be blocked by propranolol. On the other hand, phenoxybenzamine failed to block the response under identical conditions. Taken as a whole, these data suggest that in this primitive species renin activity is elevated by endogenous catecholamines even though isoproterenol, a classical beta-adrenergic agonist, is without effect. These data illustrate again the need for caution when assuming analogy when comparing responses in primitive species with that of mammals.

Acetylcholine↗
PubMed1987

Acid-base status and electrolytes in red blood cells and plasma of turtles submerged at 3 degrees C.

Two groups of adult Chrysemys picta bellii were studied; control turtles were maintained at 24 degrees C with free access to air, and diving animals were continuously submerged for 8.5-9.5 wk in aerated water at 3 degrees C. Cold submergence elicited a substantial lactic acidosis (blood pH 7.70; plasma [lactate-] 42.5 meq/l H2O). This acid load was largely balanced by changes in plasma strong ions; [Cl-] decreased, and [Ca2+] and [Mg2+] increased. Phosphorus nuclear magnetic resonance showed a significant reduction in the transerythrocyte pH gradient of diving animals (control, delta pH 0.66-0.90; diving, 0.00-0.11). This relative alkalosis of submerged turtle red cells was related to changes in blood cell (RBC) volume and composition; mean corpuscular concentration of hemoglobin [( Hb]) and RBC H2O content measurements revealed a 39% increase in RBC volume. Cell volume change was effected by a proportionally greater influx of K+ than Cl-, providing ionic compensation for the lactic acidosis. The obligatory H2O influx, which decreased the effective concentration of protein anion, and a 77% reduction of RBC [ATP] further contributed to the relative alkalosis. The combined effects of RBC alkalization and reduced [ATP] account for the observed Hb-O2 binding properties previously reported for submerged turtles at 3 degrees C (15).

Acid-Base Equilibrium↗
PubMed1990

Stimulation of H+ secretion by CO2 in turtle bladder: role of intracellular pH, exocytosis, and calcium.

We studied the interaction of intracellular pH, exocytosis, and cell calcium on the stimulation of H+ secretion by CO2 in turtle bladder. Intracellular pH was continuously monitored by the fluorescent dye 6-carboxyfluorescein and exocytosis was monitored by the release of mucosal fluorescein dextran. The initial stimulation of H+ secretion by 1 or 5% CO2 added to the serosal solution was accompanied by a similar and temporally related increase in exocytosis. Furthermore, a decrease in intracellular pH seems necessary for the early increase in H+ secretion and exocytosis. Because calcium plays an important role in exocytosis, we measured intracellular calcium in isolated cells with the fluorescent dye quin2. An increase in intracellular calcium (from 50 to 100 nM) was observed in isolated turtle bladder epithelial cells gassed with 5% CO2. To further evaluate the role of intracellular calcium on H+ secretion and exocytosis we utilized agents that alter cell calcium such as trifluoperazine and lanthanum. In the presence of CO2 these agents blocked partially the increase in H+ secretion and exocytosis but did not affect the decrease in intracellular H+. In conclusion, exocytosis, intracellular pH, and intracellular calcium play a key role in mediating CO2-stimulated H+ secretion in the turtle bladder.

Animals↗
PubMed1990

Changes in turtle brain neurotransmitters and related substances during anoxia.

Freshwater turtles (Pseudemys scripta elegans) were exposed to 0.5-13 h of anoxia at 25 degrees C, whereupon the brain concentrations of 14 amino acid and monoamine neurotransmitters and related substances were measured. Monoamines are of particular interest, because their synthesis and (in part) degradation require molecular oxygen. During anoxia, the level of the inhibitory transmitter gamma-aminobutyric acid (GABA) increased (2.3-fold after 13 h) and the level of the excitatory transmitter Glu fell. Furthermore, anoxia caused increases in the levels of Ala (14 times after 13 h), Tau, Gly, and Ser, whereas the Gln level fell. The increase in Ala is likely to inhibit pyruvate kinase, thereby mediating the decreased rate of glycolysis seen after prolonged anoxia. The increased level of Tau might protect the turtle brain against Ca2(+)-mediated anoxic damage. The monoamine metabolites almost vanished within a few hours of anoxia, indicating a halt in monoamine synthesis and breakdown, and the dopamine level fell. Nevertheless, serotonin, norepinephrine, and epinephrine levels were maintained during 13 h of anoxia, at levels extremely high compared with mammals, suggesting adaptive mechanisms such as stockpiling. It is hypothesized that the pattern of change in levels of amino acids (notably GABA and Glu) and monoamines is of functional significance, because it promotes the decrease in brain activity and energy consumption seen in anoxic turtles.

Amino Acids↗
PubMed1991

Release of inhibitory neurotransmitters in response to anoxia in turtle brain.

In mammals a massive release of the excitatory neurotransmitter glutamate, occurring within a few minutes of anoxia/ischemia, is thought to be a major mediator of anoxic brain damage. In contrast to the mammalian brain, the turtle brain is exceptionally anoxia tolerant. Using intracerebral microdialysis in turtle brain striatum, we have found a large increase in the extracellular level of the inhibitory neurotransmitter gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level after 240 min, whereas no substantial release of glutamate occurred. Moreover, the inhibitory neurotransmitters/neuromodulators glycine and taurine also displayed increased extracellular levels during anoxia. Increased extracellular levels of inhibitory amino acids may be one of the hitherto elusive mechanisms that underlie the decreased activity and energy consumption characterizing the anoxic turtle brain.

Alanine↗
PubMed1992

Metabolic and cardiodynamic responses of isolated turtle hearts to ischemia and reperfusion.

We used 31P and 1H nuclear magnetic resonance spectroscopy to measure intracellular pH, high energy phosphates, and lactate levels in hearts of turtles (Chrysemys picta bellii) subjected to 1.5 h of global ischemia followed by reperfusion. We simultaneously monitored maximum ventricular developed pressure (Pmax), maximal rate of pressure development (dP/dtmax), rate-pressure product (RPP), cardiac output, and heart rate and also measured lactate efflux from the hearts during reperfusion. Our goal was to test the hypothesis that turtle hearts would prove tolerant of prolonged global ischemia at 20 degrees C and would recover completely on reperfusion without any indication of ischemia-or reperfusion-related injury. The 1.5 h of ischemia resulted in decreases in phosphocreatine and ATP to 31.4 +/- 2.8 and 87.3 +/- 6.3% of control, respectively, while Pi rose to 236.6 +/- 26.3%. Intracellular pH decreased during this period from 7.38 +/- 0.02 to 6.87 +/- 0.04. Most of these changes occurred during the first 30 min. Tissue lactate rose during 1.5 h of ischemia from approximately 1.5 to 22.3 mumol/g wet tissue wt. However, the rate of lactate production was much higher during the first 21 min of ischemia (0.41 mumol.g-1.min-1) than during the remaining 70 min (0.10 mumol.g-1.min-1). With the onset of ischemia, Pmax, dP/dtmax, RPP, and heart rate all decreased dramatically with roughly the same time course as the changes in high-energy phosphates and intracellular pH. On reperfusion, turtle hearts rapidly restored high-energy phosphates, intracellular pH, lactate, and cardiodynamics to control levels, usually within 15-30 min, with no evidence of reperfusion injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of temperature and anoxia on regional cerebral blood flow in turtles.

Regional cerebral blood flow (CBF) was measured in isoflurane-anesthetized turtles (Pseudemys scripta) by the hydrogen clearance method. Teflon-coated platinum electrodes (25 microns) were implanted in the olfactory bulbs, midcerebral cortex and cerebellum in eight adult turtles. The electrodes were voltage clamped at +0.30 V relative to a Ag-AgCl electrode implanted in the dorsal neck muscles. Washout kinetics of H2 gas administered via controlled ventilation was used to calculate local blood flow for electrodes exhibiting monoexponential washout kinetics of hydrogen (92 of 104 determinations). Data were obtained in animals with body temperatures of 15, 25, and 35 degrees C under normocapnic conditions during ventilation with 21% O2 and during ventilation with 100% N2. During normoxia, mean blood flows were 1.9 +/- 0.8, 5.0 +/- 1.9, and 6.1 +/- 1.3 (+/- SD) ml.100 g-1.min-1 at 15, 25, and 35 degrees C, respectively. There were no differences between CBF values in the different brain regions. During 1-3 h of anoxia, CBF was 3.0 +/- 2.1, 7.0 +/- 3.7, and 6.6 +/- 2.9 ml.100 g-1.min-1 at 15, 25, and 35 degrees C, respectively (normoxia-anoxia difference not statistically different). Hypercarbia (ventilation with 10-20% CO2 in air or N2), or the transition from anoxia to normoxia, increased CBF up to 80% at each of these temperatures. Maintenance of CBF during anoxia likely contributes to the anoxia tolerance of the turtle brain.

Animals↗
PubMed1992

Roles of catecholamines and corticosterone during anoxia and recovery at 5 degrees C in turtles.

The roles of the catecholamines and corticosterone in glucose regulation during 28 days of submergence anoxia and air-breathing recovery at 5 degrees C in the turtle Chrysemys picta were examined. Anoxia resulted in an increase in mean plasma epinephrine and norepinephrine levels (from 42 and 49 to 966 and 3,826 pg/ml, respectively) and a decrease in hepatic glycogen levels. Despite the increase in plasma catecholamine levels, plasma glucose levels did not change, and the percent of the alpha form of hepatic glycogen phosphorylase was decreased compared with normoxic controls. Plasma levels of lactate increased from 1.5 to 95 mM, and corticosterone decreased during anoxia. During recovery in air, corticosterone returned to control levels within 1 day, and plasma lactate levels slowly decreased. In contrast to a previous study on anoxic turtles at 22 degrees C, at 5 degrees C the catecholamines do not stimulate hepatic glycogenolysis by increasing the level of glycogen phosphorylase alpha. The results do not support the hypothesis that corticosterone enhances lactate clearance from turtle plasma during recovery from anoxia.

Air↗
PubMed1994

Substrate and acute temperature effects on turtle heart and liver mitochondria.

The oxidative properties of heart and liver mitochondria from the Western painted turtle (Chrysemys picta bellii) were characterized on the basis of substrate preferences and temperature sensitivity. Turtle heart and liver mitochondria oxidize most substrates at 2- and 10-fold less, respectively, than rates obtained from the corresponding rat mitochondria. Krebs cycle intermediates, ketone bodies, and glutamate were oxidized at similarly high rates by turtle heart mitochondria (70.0-121.2 nmol O.min-1.mg protein-1). Fatty acylcarnitines were oxidized at approximately one-half of the above rates, and rates of amino acid oxidation were either not detectable or very low. Heart mitochondria oxidize ketone bodies at rates as high as pyruvate plus malate. Liver mitochondria oxidized Krebs cycle intermediates, amino acids, and fatty acids at similarly low rates (3.0-8.0 nmol O.min-1.mg protein-1). Typically, succinate was oxidized at the highest rates, 20.6 +/- 4.0 and 121.2 +/- 1.2 nmol O.min-1.mg protein-1, for liver and heart, respectively. Values for the rate of change of oxidation with a 10 degrees C increase (Q10) from heart and liver mitochondria oxidizing glutamate were calculated over the range 25-5 degrees C in 5 degrees C intervals; over the range 10-5 degrees C, Q10 values were 3.2 and 19.8, respectively. Q10 values calculated over the higher temperature intervals were lower. It is suggested that the large difference in temperature sensitivity between mitochondria from these two tissues and the ability of the heart mitochondria to oxidize ketone bodies at high rates are adaptations to recover from the long anoxic overwintering bouts experienced by this species.

Animals↗
PubMed1997

Electroencephalogram activity in the anoxic turtle brain.

The anoxia-tolerant turtle brain slowly undergoes a complex sequence of changes in electroencephalogram (EEG) activity as the brain systematically downregulates its energy demands. Following N2 respiration, the root mean square voltage rapidly fell, reaching approximately 20% of normoxic levels after approximately 100 min of anoxia. During the first 20- to 40-min transition period, the power of the EEG decreased substantially, particularly in the 12- to 24-Hz band, with low-amplitude slow wave activity predominating (3-12 Hz). Bursts of high voltage rhythmic slow (approximately 3-8 Hz) waves were seen during the 20- to 100-min period of anoxia, accompanied by large sharp waves. During the next 400 min of N2 respiration, two distinct patterns of electrical activity characterized the anoxic turtle brain: 1) a sustained but depressed activity level, with an EEG amplitude approximately 20% of the normoxic control and with total EEG power reduced by one order of magnitude at all frequencies, and 2) short (3-15 s) periodic (0.5-2/min) bursts of mixed-frequency activity that interrupted the depressed activity state. We speculate that the EEG patterns seen during sustained anoxia represent the minimal or basic electrical activities that are compatible with the survival of the anoxic turtle brain as an integrated unit, which allow the brain to return to normal functioning when air respiration resumed.

Animals↗
PubMed1998

ATP-sensitive K+ channel activation provides transient protection to the anoxic turtle brain.

There is wide speculation that ATP-sensitive K+ (KATP) channels serve a protective function in the mammalian brain, being activated during periods of energy failure. The aim of the present study was to determine if KATP channels also have a protective role in the anoxia-tolerant turtle brain. After ouabain administration, rates of change in extracellular K+ were measured in the telencephalon of normoxic and anoxic turtles (Trachemys scripta). The rate of K+ efflux was reduced by 50% within 1 h of anoxia and by 70% at 2 h of anoxia, and no further decrease was seen at 4 h of anoxia. The addition of the KATP channel blocker glibenclamide or 2,3-butanedione monoxime prevented the anoxia-induced decrease in K+ efflux during the first hour of anoxia, but the effect of these blockers was diminished at 2 h of anoxia and was not seen after 4 h of anoxia. This pattern of change in KATP channel blocker sensitivity can be related to a previously established temporary fall and subsequent recovery of tissue ATP during early anoxia. We suggest that activated KATP channels are involved in the downregulation of membrane ion permeability (channel arrest) during the initial energy crisis period but are switched off when the full anoxic state is established and tissue ATP levels have been restored. We also found that, in contrast to those in mammals, KATP channels are not a major route for K+ efflux in the energy-depleted turtle brain.

Adenosine Triphosphate↗
PubMed1989

NBD-taurine uptake by alpha-type carbonic anhydrase cells of turtle bladder.

The uptake of the fluorescent anion, N-(7-nitrobenz-2-oxa-1,3 diazol-4-yl)aminoethanosulfonic acid-taurine (NBD-T) was examined in sheets of turtle bladder epithelial cells after either serosal or mucosal exposure to the fluorescent anion. Serosal uptake of NBD-T into a population of epithelial cells was demonstrated in thin epithelial sheets scraped from bladder sacs exposed to low (0.5 mM) concentrations of NBD-T sufficient to cause fluorescence in turtle erythrocytes. In nine sheets NBD-T fluorescence was observed in 14.4 +/- 1.3% of epithelial cells; by phase-contrast microscopy of the same fields, these cells were nongranular or carbonic anhydrase (CA) cells. An additional 8.1 +/- 1.0% of cells was nongranular, but failed to exhibit fluorescence after serosal NBD-T exposure, consistent with a beta-CA cell population. Apical uptake of NBD-T into epithelial cells was demonstrable only at high (5 mM) mucosal concentrations in both thin sheets and superfused bladder segments. In thin sheets, NBD-T fluorescence was observed in 15.8 +/- 0.7% of cells and appeared to have a punctate subapical distribution; phase-contrast of the same fields (n = 46) revealed a nongranular cell population of 21.9 +/- 0.9%. Nongranular cells corresponded closely to CA cells as identified with carboxyfluorescein fluorescence. Hence, apical NBD-T was taken up primarily by alpha-CA cells. In conclusion, NBD-T is transported by alpha-CA cells either across the basolateral membrane with high affinity comparable to that of turtle red cell band 3 protein or across the apical membrane with low affinity via a less-specific mechanism such as endocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Turtle hippocampal cortex contains distinct cell types, burst-firing neurons, and an epileptogenic subfield.

The dorsal and medial telencephalon of reptiles consists of a simple trilaminar cortex. The turtle dorsal cortex has been identified as a favorable physiological preparation that may bear a phylogenetic relationship to mammalian neocortex. While anatomical studies have likened the reptilian medial cortical region to mammalian hippocampus, its physiological properties have not been explored. We therefore used intracellular and extracellular recording techniques to examine the cellular and synaptic physiology of turtle "hippocampal" or medial cortex. Turtle medial cortex contains two principal classes of neurons, pyramidal cells and stellate neurons. Recordings with Lucifer yellow CH (LY)-filled microelectrodes allowed us to correlate the physiological properties of medial cortical neurons with their cellular morphology. Pyramidal neurons were situated in a single cellular layer and had spiny apical dendrites extending into the molecular layer. These cells fired relatively long-duration action potentials (APs) and showed frequency adaptation to suprathreshold current pulse injections. Stellate cells were usually found in the subcellular and molecular layers and had aspiny dendrites. In contrast to pyramidal cells, they fired brief APs and displayed no frequency adaptation. A discrete population of cells in the dorsal portion of medial cortex (DMC) was capable of bursting endogenously or in response to synaptic activation. Bursts usually contained an underlying slow depolarization and often occurred at regular intervals. Intracellular LY injections confirmed that these cells were pyramidal in morphology. Electrical stimulation of afferent fibers revealed that pyramidal cells and stellate neurons differed in their synaptic responses. In ventral medial cortex (VMC), afferent stimulation evoked a multiphasic response in most pyramidal cells, whereas stellate cells were synaptically excited. Orthodromic activation of DMC bursting cells resulted in a powerful excitation--often a short burst--and subsequent inhibition. Stellate neurons in DMC also had a biphasic synaptic response consisting of both an early excitation and a late inhibition. Experiments using intracellular chloride (Cl-) injection or focal bicuculline application suggested that part of the inhibitory component of the pyramidal cell synaptic response was dependent on a gamma-aminobutyric acid (GABA)-mediated increase in Cl- conductance. These results correlated with our immunohistochemical studies that revealed the presence of GABAergic neurons in medial cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

Morphological identification of physiologically characterized afferents innervating the turtle posterior crista.

The turtle posterior crista consists of two hemicristae. Each hemicrista extends from the planum semilunatum to the nonsensory torus and includes a central zone (CZ) surrounded by a peripheral zone (PZ). Type I and type II hair cells are found in the CZ and are innervated by calyx, dimorphic and bouton afferents. Only type II hair cells and bouton fibers are found in the PZ. Units were intraaxonally labeled in a half-head preparation. Bouton (B) units could be near the planum (BP), near the torus (BT), or in midportions of a hemicrista, including the PZ and CZ. Discharge properties of B units vary with longitudinal position in a hemicrista but not with morphological features of their peripheral terminations. BP units are regularly discharging and have small gains and small phase leads re angular head velocity. BT units are irregular and have large gains and large phase leads. BM units have intermediate properties. Calyx (C) and dimorphic (D) units have similar discharge properties and were placed into a single calyx-bearing (CD) category. While having an irregular discharge resembling BT units, CD units have gains and phases similar to those of BM units. Rather than any single discharge property, it is the relation between discharge regularity and either gain or phase that makes CD units distinctive. Multivariate statistical formulas were developed to infer a unit's morphological class (B or CD) and longitudinal position solely from its discharge properties. To verify the use of the formulas, discharge properties were compared for units recorded intraaxonally or extracellularly in the half-head or extracellularly in intact animals. Most B units have background rates of 10-30 spikes/s. The CD category was separated into CD-high and CD-low units with background rates above or below 5 spikes/s, respectively. CD-low units have lower gains and phases and are located nearer the planum than CD-high units. In their response dynamics over a frequency range from 0.01-3 Hz, BP units conform to an overdamped torsion-pendulum model. Other units show departures from the model, including high-frequency gain increases and phase leads. The longitudinal gradient in the physiology of turtle B units resembles a similar gradient in the anamniote crista. In many respects, turtle CD units have discharge properties resembling those of calyx-bearing units in the mammalian central zone.

Algorithms↗