Overshoot in <Emphasis Type="Italic">V̇</Emphasis>O<Subscript>2</Subscript> following the onset of moderate-intensity cycle exercise in trained cyclists

We have previously observed that following the onset of moderate intensity cycle ergometry, the pulmonary O₂ uptake (O₂) in trained cyclists often does not increase towards its steady-state value with the typical mono-exponential characteristics; rather, there is a transient overshoot. The purpose of this study was to systematically examine this phenomenon by comparing the O₂responses to two moderate-intensity work rates and one high-intensity work rate in trained and untrained subjects. Following a ramp exercise test to the limit of tolerance for the determination of the gas exchange threshold (GET) and O_2peak, seven trained cyclists [mean (SD); O_2peak 66.6 (2.5) ml·kg^–1·min^–1] and eight sedentary subjects [O_2peak 42.9 (5.1) ml·kg^–1·min^–1] completed six step transitions from baseline cycling to work rates requiring 60% and 80% GET and three step transitions from baseline cycling to a work rate requiring 50% of the difference between GET and O_2peak (50%). O₂ was measured breath-by-breath and modelled using standard techniques. The sedentary subjects did not overshoot the steady-state O₂ at any intensity. At 60% GET, six of the seven cyclists overshot the steady-state O₂ [by an integral volume of 164 (44) ml between ~45 and 125 s]. At 80% GET, four of the seven cyclists overshot the steady-state O₂ [by an integral volume of 185 (92) ml between ~55 and 140 s]. None of the cyclists showed an overshoot at 50%. These results indicate that trained cyclists evidence an overshoot in O₂ before steady-state is reached in the transition to moderate-intensity exercise. The mechanism(s) responsible for this effect remains to be elucidated, as does whether the overshoot confers any functional or performance benefit to the trained cyclist.     

The V̇O2 response for an exhaustive treadmill run at 800-m pace: a breath-by-breath analysis

Recent research in which data were averaged over 10 or 30 s suggests that the O₂ response of aerobically fit individuals plateaus below O_{2 max} in an exhaustive square-wave run lasting ~2 min. To investigate this phenomenon we examined the breath-by-breath O₂ response of trained runners to an exhaustive treadmill run at 800 m pace. Eight male competitive runners completed two treadmill tests on separate days: a ramp test to exhaustion and an exhaustive square-wave run at 800-m pace. For the ramp test, the breath-by-breath data were smoothed with a 15-s moving average and the highest of the smoothed values was taken as O_{2 peak} [mean (SD): 68.9 (5.6) ml kg^–1 min^–1]. For the square-wave, the breath-by-breath data were interpolated to give one value per second and modelled using a monoexponential function. Following a delay of 11.2 (1.5) s, O₂ increased quickly [phase-2 time constant of 10.7 (2.7) s] towards an asymptote that represented just 85 (6)% of O_{2 peak} from the ramp test. Expressed in ml kg^–1 min^–1, this asymptote was independent of O_{2 peak} (r=0.04, P=0.94). However, as a percentage of O_{2 peak} it was negatively correlated with O_{2 peak} itself (r=–0.96, P<0.001). It is concluded that in an exhaustive square-wave treadmill run lasting ~2 min the O₂ of aerobically fit runners increases quickly to plateau at a level that is lower than, but independent of, O_2max     

Performing at extreme altitude: muscle cellular and subcellular adaptations

This review reports on the collaborative efforts of the Department of Physiology of the University of Geneva headed by Paolo Cerretelli, the Research Institute at the Federal School of Physical Education in Magglingen and the Department of Anatomy of the University of Bern to elucidate the functional and structural conditions for and consequences of climbing successfully at altitudes in excess of 8000 m. Using a combination of physiological whole body measurements with biochemical, histochemical and morphometric analyses of muscle biopsy samples we were able to establish specific phenotypical alterations of muscle tissue exposed to extreme hypoxia and stress for prolonged periods of time. The decline in aerobic work capacity could be shown to be a consequence of a loss of muscle mass as well as of muscle tissue oxidative capacity whereby muscle capillarity was found to be maintained. The degradation of muscle tissue was further characterized by an increase in muscle lipofuscin. The latter is believed to be the consequence of lipid peroxidation eventually related to mitochondrial loss. Current work ensuing from our long-term collaboration suggests that Sherpas might be protected against the damaging effect of hypoxia by antioxidant mechanisms protecting their muscles under the conditions of extreme altitude.     

Effects of active recovery between series on performance during an intermittent exercise model in young endurance athletes

Abstract The purpose of our study was to compare time to exhaustion (t_lim) and time spent at a high level of oxygen uptake (O₂) during two high-intensity short intermittent exercises (30 s-30 s) realized with or without series. Eleven young endurance-trained athletes [16.6 (0.4) years] took part in three field tests until exhaustion: (1) a maximal graded test to measure their maximal aerobic velocity (MAV) and maximal oxygen uptake (O_2max); (2) and (3) two randomized intermittent exercises (30 s at 110% of MAV alternated with 30 s at 50% of MAV): one alternating repetitions non-stop (IE) and another including 4 min recovery every six repetitions (IEs). The mean t_lim measured during IEs was significantly longer than IE [respectively 960.0 (102.0) s vs 621.8 (56.2) s]. The time spent at O_2max(t_O2max) and the time spent above 90% of O_2max(t_90%O2max) did not differ significantly according to the type of exercise: with or without series [respectively t_O2max was 158.2 (59.7) s vs 178.0 (56.5) s and t_90%O2max was 290.4 (84.3) s vs 345.0 (61.6) s] but when expressed as a relative value, t_90%O2max during IEs was significantly lower than during IE [respectively 36.4 (10.4)% t_lim vs 58.3 (8.7)% t_lim]. Despite a significant decrease (P<0.005) of time to achieve 90% of O_2max at the start of each series during IEs [respectively 165.0 (43.1) s for the first series and 82.5 (15.8) s for the second series (n=6)] the time spent under 90% of O_2max limited the t_90%O2max during each series. In conclusion, our results showed that intermittent exercise with series does not permit an increase in the time spent at a high level of O₂; however, the athletes performed more repetitions of short intense exercise.     

Factors limiting maximal performance in humans

Theoretical best performance times (t_theor) in track running are calculated as follows. Maximal metabolic power (Ė_max) is a known function of maximal oxygen uptake (O_2max), of maximal anaerobic capacity (AnS) and of effort duration to exhaustion (t_e): Ė_max=f (t_e). Metabolic power requirement (Ė_r) to cover the distance (d) in the performance time t_p is the product of the energy cost of locomotion per unit distance (C) and the speed: Ė_r=C×d/t_p. The time values for which Ė_max (t_e)=Ė_r (t_p), assumed to yield t_theor, can be obtained for any given subject and distance provided that O_2max, AnS and C are known, and compared with actual best performances (t_act). For 15 mint_e100 s, the overall ratio t_act/t_theor was rather close to 1.0. To estimate the relative role of the different factors limiting O_2max, several resistances to O₂ transport are identified, inversely proportional to: alveolar ventilation (R_V*), O₂ transport by the circulation (R_Q), O₂ diffusion from capillary blood to mitochondria (R_t), mitochondrial capacity (R_m). Observed changes of O_2max are accompanied by measured changes of several resistances. The ratio of each resistance to the overall resistance can therefore be calculated by means of the O₂ conductance equation. In exercise with large muscle groups (two legs), R_Q is the major (75%) limiting factor downstream of the lung, its role being reduced to 50% during exercise with small muscle groups (one leg). R_t and R_m account for the remaining fractions. In normoxia R_V* is negligible; at high altitude it increases progressively, together with R_t and R_m, at the expense of R_Q.     

Influence of muscle fibre type and pedal rate on the V̇O2-work rate slope during ramp exercise

We hypothesised that the ratio between the increase in oxygen uptake and the increase in work rate (O₂/WR) during ramp cycle exercise would be significantly related to the percentage type II muscle fibres at work rates above the gas exchange threshold (GET) where type II fibres are presumed to be active. We further hypothesised that ramp exercise at higher pedal rates, which would be expected to increase the proportional contribution of type II fibres to the total power delivered, would increase the O₂/WR slope at work rates above the GET. Fourteen healthy subjects [four female; mean (SD): age 25 (3) years, body mass 74.3 (15.1) kg] performed a ramp exercise test to exhaustion (25 W min^–1) at a pedal rate of 75 rev min^–1, and consented to a muscle biopsy of the vastus lateralis. Eleven of the subjects also performed two further ramp tests at pedal rates of 35 and 115 rev min^–1. The O₂/WR slope for exercise <GET (S ₁) was significantly correlated with O₂ peak in ml kg^–1 min^–1 (r=0.60; P<0.05), whereas the O₂/WR slope for exercise >GET (S ₂) was significantly correlated to percentage type II fibres (r=0.54; P=0.05). The ratio between the O₂/WR slopes for exercise above and below the GET (S ₂/S ₁) was significantly greater at the pedal rate of 115 rev min^–1 [1.22 (0.09)] compared to pedal rates of 35 rev min^–1 [0.96 (0.02)] and 75 rev min^–1 [1.09 (0.05), (P<0.05)]. The greater increase in S ₂ relative to S ₁ in subjects (1) with a high percentage type II fibres, and (2) at a high pedal rate, suggests that a greater recruitment of type II fibres contributes in some manner to the xs O₂ observed during ramp exercise.     

Oxygen uptake kinetics: old and recent lessons from experiments on isolated muscle in situ

The various mechanisms responsible for ATP resynthesis include phosphocreatine (PCr) hydrolysis, anaerobic glycolysis and oxidative phosphorylation. Among these, the latter represents the most important mechanism of energy provision. However, oxidative phosphorylation is characterized by a lower maximal power and a slow attainment of a steady state in response to increased metabolic demand. The rate of adjustment of oxidative metabolism during metabolic transitions, which can be evaluated on the basis of the analysis of O₂ uptake (O₂) kinetics, has implications for exercise tolerance and muscle fatigue. Analysis of O₂ kinetics represents a valid tool for the functional evaluation of healthy subjects, athletes and patients. Over the last 35 years experiments conducted on isolated muscle preparations in situ have allowed us to gain insights into several key aspects of skeletal muscle O₂ kinetics. Their main limiting factor resides in an intrinsic slowness of intracellular oxidative metabolism when adjusting to augmented metabolic needs. The rate of adjustment of oxidative phosphorylation in mitochondria can be functionally related to PCr hydrolysis occurring in the cytoplasm.     

Metabolic and hormonal responses to exhaustive supramaximal running with and without Β-adrenergic blockade

Summary The metabolic and hormonal responses to exhaustive short-term supramaximal exercise were studied in 10 male physical education students. The exercise task was a single bout of running on the treadmill at 22 km·h^–1 and 7.5% slope. It was performed with single oral doses of 100 mg Bupranolol (non-selective -blockade), 100 mg Metoprolol (-1-selective blockade), and placebo. Arterialized capillary and venous blood were sampled until 30 min post exercise.Time to exhaustion was 52.0±2.6, 47.6±2.0, and 46.0±1.9 s in the control, Metroprolol, and Bupranolol experiments. At cessation of exercise, adrenaline and noradrenaline were grossly elevated in all three conditions. Lactate and glucose increased markedly, this being accompanied by increasing insulin in the control and Metoprolol, but not the Bupranolol trials. Glycerol increased moderately, while FFA were depressed. Growth hormone showed a delayed increase at 15 and 30 min post exercise. Cortisol was unaffected by exercise. -blockade reduced the increases of lactate, glucose, glycerol, insulin, and growth hormone, exaggerated the depression of FFA and had no effect on cortisol.The results demonstrate that the strong sympatho-adrenal response to exercise of this nature is a major determinant of the increase of glucose at cessation of exercise. The hyperglycemia in concert with -2-adrenergic stimulation leads to elevation of insulin. Furthermore, lipolysis is controlled by -adrenergic stimulation. The delayed increase of growth hormone seems to be triggered by the declining glucose level during recovery.Supported by Bundesinstitut für Sportwissenschaft, Köln-Lövenich     

Control of metastatic properties of BL6 melanoma cells by H-2Kb gene: immunological and nonimmunological mechanisms

The effect of class I H-2 antigen expression on the metastatic properties of BL6 melanoma cells was investigated. The BL6-8 clone isolated from the highly metastatic BL6 melanoma did not express H-2K b gene. Following transfection with the H-2K^b gene, BL6-8 cells displayed a low metastatic potential in the immunocompetent as well as immunosuppressed (X-irradiated) or triple-immunodeficient mice with impaired T, B and natural killer (NK) cells function. The expression of H-2K^b gene and the low metastatic ability of transfected BL6 melanoma cells were associated with appearance of cell membrane soybean agglutinin (SBA) and Griffonia simplicifolia 1B₄ (GS1B₄) lectin-binding carbohydrataes. These alterations in cell surface carbohydrates were found to be a result of reduction in sialylation of SBA binding sites and upregulation of the 1.3 galactosyltransferase (1.3GT) gene. To assess the importance of H-2K^b-induced alterations in cell surface carbohydrates for metastasis formation, BL6-8 melanoma cells were transfected with H-2K^b gene without neo^r gene cotransfection and selected for adherence to SBA-lectin-conjugated agarose beads. The transfected clones that expressed SBA and GS1B₄ lectin-binding carbohydrates were low metastatic. Further analysis of these clones showed that presence of SBA and GS1B₄ lectin-binding carbohydrates rather than expression of H-2K^b molecules per se might be responsible for low metastatic potentials of H-2K^b-transfected cells in the immunocompromized mice. Studies of the possible mechanisms responsible for low metastatic ability of H-2K^b-transfected melanoma cells revealed that these cells displayed a reduced ability to adhere to murine pulmonary endothelial cells as well as to laminin and collagen IV. We hypothesized that the observed nonimmunological effects of H-2K^b gene in BL6 melanoma cells is a result of an interaction between the H-2K^b gene and B16 melanoma-specific ecotropic retrovirus. It results in inhibition of this retrovirus production with consecutive alteration in the expression of cellular genes controlling cell surface glycosylation and adhesion properties essential for the metastatic phenotype of BL6 melanoma.     

Biphasic short-circuit current response to noradrenaline mediated by Ca2+ and cAMP in cultured rat epididymal epithelium

A study was carried out to investigate the short-circuit current (I _sc) response to noradrenaline (NA) and the signal transduction mechanisms involved in cultured rat cauda epididymal epithelium. In normal Krebs-Henseleit solution, NA (10 mol · l^–1) added basolaterally elicited a biphasic I _sc response consisting of a transient spike followed by a second sustained response. The biphasic response was almost abolished by removing ambient Cl^–. Preloading the tissues witha cell-permeant Ca²⁺ chelator, 1,2-bis(2-aminophenoxy) eth-ane-N,N,N,N,-tetraacetic acid acetoxymethyl ester (BAPTA/AM), or pretreating them with thapsigargin (Tg), a microsomal adenosine triphosphatase inhibitor abolished the initial spike in the I _sc response to NA, but had little effect on the second component. Pretreating the tissues with a non-selective -antagonist, nadolol, reduced the second I _sc response in a dose-dependent fashion but the initial spike was not affected. Microfluorimetric studies showed that NA (100 mol · l^–1) elicited single Ca²⁺ spikes in isolated epididymal cells, which could be abolished by prior treatment with Tg. Biochemical assays showed that NA (10 mol · l^–1) increased intracellular cyclic adenosine monophosphate concentration ([cAMP]_i) and the response was abolished by prior treatment with nadolol (50 mol · l^–1). The results showed that NA elicited a biphasic I _sc response mediated by a rise in intracellular Ca²⁺ concentration ([Ca²⁺]_i) followed by a rise in [cAMP]_i. The Ca²⁺-mediated I _sc response had a faster onset and more transient action than the cAMP counterpart. It is suggested that NA released from noradrenergic nerve endings regulates transepithelial Cl^– secretion in the epididymis thereby providing the specialized millieu vital for sperm storage and maturation.     

Stress hormonal response to exercise after sleep loss

Summary While prolonged loss of sleep is unpleasant and demanding, it remains unclear if it blunts or enhances the physiological stress imposed by subsequent exercise. To investigate this, we deprived eight subjects of sleep prior to exercise to see if this altered the stress hormonal response to that exercise. In a first series of experiments, two fragmented nights of sleep preceded 30 min of heavy treadmill walking exercise. While sleep loss disturbed mood before and during exercise (p<0.05), it left stress hormonal levels (cortisol and -endorphin) in blood identical to control. In a second series, subjects performed light treadmill walking exercise for 3 h after 36 sleepless hours. As before, sleep deprivation disturbed mood before and throughout exercise (p<0.05), but failed to change blood levels of stress hormones. In both series, sleeplessness left heart rate, oxygen uptake, minute ventilation, and body core temperature unchanged in exercise. We conclude that sleep loss provokes psychological changes during subsequent exercise without measurably altering the stress hormonal response to that exercise.     

The responses of the catecholamines and β-endorphin to brief maximal exercise in man

Summary The responses to brief maximal exercise of 10 male subjects have been studied. During 30 s of exercise on a non-motorised treadmill, the mean power output (mean±SD) was 424.8±41.9 W, peak power 653.3±103.0 W and the distance covered was 167.3±9.7 m. In response to the exercise blood lactate concentrations increased from 0.60±0.26 to 13.46±1.71 mmol·l^–1 (p<0.001) and blood glucose concentrations from 4.25±0.45 to 5.59±0.67 mmol·l^–1 (p<0.001). The severe nature of the exercise is indicated by the fall in blood pH from 7.38±0.02 to 7.16±0.07 (p<0.001) and the estimated decrease in plasma volume of 11.5±3.4% (p<0.001). The plasma catecholamine concentrations increased from 2.2±0.6 to 13.4±6.4 nmol·l^–1 (p<0.001) and 0.2±0.2 to 1.4±0.6 nmol·l^–1 (p<0.001) for noradrenaline (NA) and adrenaline (AD) respectively. The plasma concentration of the opioid-endorphin increased in response to the exercise from <5.0 to 10.2±3.9 p mol·l^–1. The post-exercise AD concentrations correlated with those for lactate as well as with changes in pH and the decrease in plasma volume. Post-exercise-endorphin levels correlated with the peak speed attained during the sprint and the subjects peak power to weight ratio. These results suggest that the increases in plasma adrenaline are related to those factors that reflect the stress of the exercise and the contribution of anaerobic metabolism. In common with other situations that impose stress,-endorphin concentrations are also increased in response to brief maximal exercise.     

CD4+ Th2 cell response cytokine production in bacterial meningitis

There has been a growing body of evidence suggesting that CD4+ Th1/Th2 cell responses participate in pathologic and immunologic processes in infectious disease. Bacterial meningitis is a fatal disease of children and is associated with a spectrum of clinical syndromes. This study provides evidence of CD4+ enhanced interleukin (IL)-4 and IL-6 but decreased IL-2 and interferon- (IFN-) production, the induction of characteristic Th2 cell response cytokines in bacterial meningitis, which may play an important role in disease mechanism. Additionally, monocyte-induced enhanced IL-6, IL-8, and tumor necrosis factor- production may be associated with distinct clinical features such as fever, seizures, and neurological sequelae. A striking finding was also the highly deficient monocyte-induced granulocyte-macrophage colony-stimulating factor production. Of particular interest, the CD8+-enhanced IFN- production may be required for the cytolytic activity or protective response to be maintained in this disease. Taken together, these data reveal that monocytes and CD4+ (Th2) and CD8+ subsets produce distinct cytokines in bacterial meningitis, which may exert an immunoregulatory and immunopathologic effect and thus mediate some of the clinical manifestations of the disease.     

Development of the response of rabbit fetal tissues to thyroxine

The development of the response of rabbit fetal tissues to thyroxine was investigated by determining changes in -glycerophosphate dehydrogenase activity of the liver mitochondria of pregnant rabbits and their fetuses during administration of thyroxine at different times of pregnancy. Until the 23rd day the activity of this enzyme increased only in the mitochondria of the maternal liver, whereas in the fetuses it remained at the control level. After the 24th day of pregnancy an increase in activity of this enzyme was observed in the fetuses also, where it can be explained by the appearance of the response of the rabbit fetal tissues to maternal thyroxine at this stage of development, and increasing until the end of pregnancy.Institute of Biochemistry, Academy of Sciences of the Uzbek SSR, Tashkent. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 12, pp. 721–723, December, 1978.     

The isolated frog skin epithelium: Presence of α and β adrenergic receptors regulating active sodium transport and water permeability

Summary The effects of stimulation of and adrenergic receptors on short circuit current (S.C.C.), Na⁺ and Cl^– fluxes and osmotic water permeability were studied on isolated frog skin epithelial layers separated from the dermis.Low norepinephrine doses (final concentrations in the incubation medium ranging from 5×10^–9 to 10^–8 M) produced increased water permeability and S.C.C. The latter was entirely accounted for by an increase in the active Na⁺ influx. Na⁺ outflux and Cl^– fluxes were not modified. Both these effects disappeared after treatment with the blocking agent, Propranolol. Higher norepinephrine doses (final concentrations: 10^–7 to 10^–6 M) produced: 1. an increase in water permeability lower than that produced by low doses, the highest doses failing to increase water permeability, and 2. a triphasic change in S.C.C.: after an initial increase, S.C.C. dropped to its resting value and then rose again to a sustained value. Na⁺ and Cl^– flux measurements showed that the variation in S.C.C. reflected variations in active Na⁺ transport. When the same high norepinephrine doses were applied after treatment with the blocking agent Phentolamine, the effects observed were identical to those obtained with low doses.On blocked preparations, large doses of norepinephrine inhibited the water permeability and sodium transport increases induced by theophylline or oxytocin but did not modify those induced by 35-cyclic AMP. The inhibition was suppressed after blocking receptors.From the foregoing, it was concluded that both and adrenergic receptors are present in frog skin epithelial cells and are involved in the regulation of water and sodium permeability.It is suggested that the inhibitory effect of stimulation resulted from the inhibition of cyclic-AMP generating system, the activity of which is under the positive control effect of oxytocin and stimulation.     

Diameter and flow velocity changes of feline small pulmonary vessels in response to sympathetic nerve stimulation

Using an X-ray television system, we measured directly changes in the internal diameter (ID), flow velocity, and volume flow of the small pulmonary vessels (100–500 m ID) in response to electrical sympathetic nerve stimulation (SNS) in anaesthetized cats before and after adrenergic receptor blockade. Flow velocity was obtained by measuring the distance that the leading edge of the contrast medium moved per 0.1 s in the small arteries. Volume flow was obtained from the product of flow velocity and cross-sectional area calculated from the ID of the small arteries. SNS was accolmplished with 10- to 15-V square-wave pulses of 2-ms duration at 20–30 Hz for 20-s periods. In response to SNS, arterial ID decreased significantly by 8–13% in the 200- to 500-m vessels but not in the 100- to 200-m vessels. In the veins, on the other hand, there was no significant ID decrease in any of the 100- to 500-m vessels. After -receptor blockade (phentolamine, 2 mg/kg i.V.), there were significant ID increases (4–9%) in the 100- to 500-m arteries in response to SNS, the maximum increases being in the 100- to 200-m arteries. After -blockade (propranolol, 2 mg/kg i.V.), the ID decrease due to SNS in the 200- to 500-m arteries was enhanced (24–27%) and, in addition, the 100- to 200-m arteries exhibited a significant ID decrease (18%). Combined and -blockade completely abolished the ID decrease due to SNS. In the veins, on the other hand, no ID change occurred even after - or -blockade. The results indicate that SNS selectively constricts 200- to 500-m arteries. The data suggests that SNS has -mediated vasoconstrictor and -mediated vasodilator effects on the 100- to 500-m arteries and that the ID response pattern to SNS depends chiefly on the balance between -mediated vasoconstriction and -mediated vasodilation. Associated with the ID decrease due to SNS, flow velocity was increased by 21%. However, SNS did not affect volume flow, because the increase in velocity was compensated by the reduction in the cross-sectional area (due to the decreased ID).     

Functional reorganization of the noradrenergic system after partial fornix section: a behavioral and autoradiographic study

Previous experiments revealed that the cholinergic deficit in rats with a partial fornix section was accompanied by an increase in turnover of noradrenaline (NE) in the hippocampus. This noradrenergic hyperactivity contributed to the cognitive deficit in lesioned rats, probably by interaction with the cholinergic system. The present experiment examines the reorganization of the noradrenergic system after the damage induced by partial fornix section and attempts to determine if the increase in NE turnover is of locus coeruleus (LC) origin, or if it is a result of local regulation at the noradrenergic terminals. Rats were submitted to knife-cut section of the fornix, resulting in a decrease in choline acetyltransferase activity in the hippocampus, correlated with a significant behavioral deficit in a spatial memory task. Lesioned rats learned a nonspatial memory task normally. Sections of brains of these rats were submitted to quantitative autoradiography. [¹²⁵I]Iodopindolol binding was assessed in the dorsal and ventral hippocampus to determine availability of receptors. This was found to be significantly lower in lesioned rats. [¹²⁵I]Iodoclonidine was used to determine ₂ receptors binding in dorsal and ventral hippocampus and in LC. There was no difference in ₂ receptors in LC, a significant decrease in dorsal regions of the hippocampus, and a significant increase in ventral regions. Muscarinic M1 receptors in the hippocampus showed no changes after the lesion.