By K. Barrack. Westminster College, Fulton Missouri.
The mode in which action because the K channels open more slowly in response to potentials propagate and the speed with which they are depolarization purchase kamagra super 160mg overnight delivery. This increase in Na permeability com- conducted along an axon depend on whether the axon is pared to that of K causes the membrane potential to move myelinated cheap 160mg kamagra super with amex. The diameter of the axon also influences the toward the equilibrium potential for Na purchase 160 mg kamagra super overnight delivery. The net effect of inactivating channels are distributed uniformly along the length of the Na channels and opening additional K channels is the axonal membrane safe kamagra super 160mg. An action potential is generated when repolarization of the membrane (Fig. The hillock acts as a “sink” where Na afterhyperpolarization is a result of K channels remaining ions enter the cell. The “source” of these Na ions is the ex- open, allowing the continued efflux of K ions. The entry of way to think about afterhyperpolarization is that the mem- Na ions into the axon hillock causes the adjacent region brane’s permeability to K is higher than when the neuron of the axon to depolarize as the ions that entered the cell, is at rest. Consequently, the membrane potential is driven during the peak of the action potential, flow away from the even more toward the K equilibrium potential (Fig. This local spread of the current depolarizes the adja- The changes in membrane potential during an action cent region to threshold and causes an action potential in potential result from selective alterations in membrane that region. These membrane conductance of the axon, the action potential propagates or moves along changes reflect the summated activity of individual volt- the length of the axon from point to point, like a traveling age-gated sodium and potassium ion channels. This in- phases to both the decrease in sodium conductance and the crease in ion flow in the cytoplasm causes greater lengths increase in potassium conductance, and afterhyperpolariza- of the axon to be depolarized, decreasing the time needed tion to the sustained increase of potassium conductance. Recall CHAPTER 3 The Action Potential, Synaptic Transmission, and Maintenance of Nerve Function 43 +50 Depolarizing Repolarizing phase phase 0 E (mV) B C m Resting Resting state Afterhyper- state -50 A polarization A D -100 Time Voltage-gated Na+ Channel Voltage-gated K+ Channel Na+ A Resting state Resting state K+ Na+ B Active state Resting state FIGURE 3. A, At the resting membrane potential, both channels are in a closed, resting state. B, Dur- ing the depolarizing phase of the K+ action potential the voltage-gated sodium channels are activated Na+ (open), but the potassium channels C Inactive state Active state open more slowly and, therefore, have not yet responded to the depo- larization. C, During the repolariz- ing phase, sodium channels become inactivated, while the potassium channels become activated (open). D, During the afterhyperpolariza- tion, the sodium channels are both closed and inactivated, and the K+ potassium channels remain in their Na+ active state. Eventually, the potas- Closed and sium channels close and the sodium D Active state inactive state channel inactivation is removed, so that both channels are in their rest- ing state and the membrane poten- tial returns to resting membrane po- tential. Note that the voltage-gated potassium channel does not have an inactivated state. In this case, the local stimulus is the inward cause the internal axoplasmic resistance, Ra, decreases, al- sodium current that accompanies the action potential. The lowing the current to spread farther down the inside of the larger the space constant, the farther along the membrane axon before leaking back across the membrane. Affected individuals generally have no neurons and muscle cells and in synaptic transmission. The defect in membrane repolar- nel properties derived from biophysical studies of isolated ization could be a result of a prolonged inward sodium cells or their membranes. The advent of molecular ap- current or a reduced outward potassium current. In fact, proaches resulted in the cloning of the genes for a variety mutations in potassium channels account for two differ- of channels and the subsequent expression of these genes ent LQT syndromes, and a third derives from a sodium in a large cell, such as the Xenopus oocyte, for further char- channel mutation. Myotonia is a condition characterized by a delayed re- This approach also allowed experimental manipulation laxation of muscle following contraction. There are several of the channels by expressing genes that were altered in types of myotonias, all related to abnormalities in muscle known ways.
The lesion in the chi- the PPRF would most likely produce a bilateral horizontal gaze asm would result in a bitemporal hemianopsia 160 mg kamagra super sale. Answer C: A fracture through the jugular foramen would po- ﬁned to the subthalamic nucleus on the side contralateral to the tentially damage the glossopharyngeal (IX) 160 mg kamagra super fast delivery, vagus (X) generic kamagra super 160 mg amex, and spinal deﬁcit 160mg kamagra super sale. These movements are violent, ﬂinging, unpredictable, and accessory (XI) nerves. The abnormal movements are contralateral to the loss of the efferent limb of the gag reﬂex and a paralysis of the ip- lesion because the expression of the lesion is through the corti- silateral trapezius and sternocleidomastoid muscles (drooping of cospinal tract. Lesions in the left subthalamic nucleus would result the shoulder, difﬁculty elevating the shoulder especially against re- in a right-sided problem. Damage in the motor cortex would be sistance, difﬁculty turning the head to the contralateral side). In- seen as a contralateral weakness, and cell loss in the substantia ni- volvement of facial muscles would suggest damage to the internal gra would result in motor deﬁcits characteristic of Parkinson dis- acoustic or stylomastoid foramina; this would also be the case for ease (resting tremor, bradykinesia, stooped posture, festinating the efferent limb of the corneal reﬂex. Answer B: The inability to perform a rapid alternating move- nerve (which supplies muscles of the tongue) passes through the ment, such as pronating and supinating the hand on the knee, is hypoglossal canal. This is one of several cardinal signs of cere- bellar disease or stroke. Dysmetria is an inability to judge power, distance, and accuracy during a movement, and dysarthria is difﬁ- 64. Answer E: The constellation of signs and symptoms experi- culty speaking. A resting tremor is seen in diseases of the basal nu- enced by this boy are characteristic of Wilson disease, also called clei, and an intention tremor is seen in cerebellar lesions. These may include movement dis- 208–211) orders, tremor, the Kayser-Fleischer ring at the corneoscleral margin, and eventual cirrhosis of the liver. Answer B: The tremor that worsens as this man attempts to Parkinson diseases are predominately motor problems in the early bring his index ﬁnger to his nose is called an intention tremor, stages and Pick disease is a degenerative disease of the cerebral cor- sometimes referred to as a kinetic tremor. This type of tremor is tex affecting mainly the frontal and temporal lobes; dementia is one cardinal sign of cerebellar lesions. Sydenham chorea is seen in children follow- diseases of the basal nuclei and a static tremor (postural tremor) is ing an infection with hemolytic streptococcus; after treatment seen in the trunk and extremities in a static position. Dysmetria is for the infection, the choreiform movements usually resolve. The rebound phenomenon is an inability of agonist and an- tagonist muscles to rapidly adapt to changes in load. Answer A: A tumor impinging on the midline of the optic chi- asm would damage crossing ﬁbers from both eyes that are coming 71. Answer C: The signs and symptoms in this man clearly indicate from the nasal retinae and would reﬂect a loss of all, or part of both a lesion in the cerebellum on the left side. Between 60% and 70% of pituitary ade- on the left (lesion side) project to the contralateral thalamus nomas are prolactin-secreting tumors. Right or left homonymous (right) and from here to motor cortical areas (also right). The mo- hemianopsia (the nasal visual ﬁeld of one eye and the temporal vi- tor cortex projects, via the corticospinal tract and its decussation, sual ﬁeld of the other eye) are seen following lesions of, respec- back to the side of the body, excluding the head, on which the le- tively, the left and right optic tracts. The man’s left- sided deﬁcits are not consistent with a right cerebellar lesion, and 66. Answer C: The ﬂocculonodular lobe and the fastigial nucleus re- the deﬁcits are not consistent with a midbrain lesion. Lesions of ceive input from the vestibular apparatus (primary vestibulocere- the basal nuclei would result in a different set of motor disorders. In turn, the Purkinje cells of the ﬂocculonodular cortex and cells of the fastigial nucleus project to the vestibular nu- 72. Answer B: The superior cerebellar artery serves the cortex on clei as cerebellar corticovestibular and cerebellar efferent ﬁbers, the superior surface of the cerebellum and most of the cerebellar respectively. While other areas of the cerebellar cortex may have nuclei on the same side; in this case, it is the left artery.
The designated dominant follicle is selected between droxylase and subsequently decreases androstenedione days 5 and 7 discount 160 mg kamagra super, and increases in size and steroidogenic activ- production by the dominant follicle generic 160mg kamagra super mastercard. Between days 8 and 10 generic kamagra super 160 mg mastercard, plasma estradiol levels rise cline purchase kamagra super 160 mg with visa, 17-hydroxyprogesterone increases, and progesterone sharply, reaching peak levels above 200 pg/mL on day 12, levels plateau. As the corpus luteum matures, it increases prog- ciding pulses of GnRH are released about every hour. LH level increases and further supports follicular steroido- During the luteal phase, circulating FSH levels are sup- genesis, especially since FSH has increased the number of pressed by the elevated steroids. During the midfollicular reduced during the early luteal phase, but the amplitude is to late follicular phase, rising estradiol and inhibin from the higher than that during the follicular phase. The decline in tant at this time for maintaining the function of the corpus FSH, together with an accumulation of nonaromatizable luteum and sustaining steroid production. In the late luteal androgens, induces atresia in the nonselected follicles. The phase, both LH pulse frequency and amplitude are reduced dominant follicle is saved by virtue of its high density of by a progesterone-dependent, opioid-mediated suppres- FSH receptors, the accumulation of FSH in its follicular sion of the GnRH pulse generator. The reduction surge to occur, estradiol must be maintained at a critical in ovarian steroids acts centrally to remove feedback inhi- concentration (about 200 pg/mL) for a sufficient duration bition. The FSH level begins to rise and a new cycle is ini- (36 to 48 hours) prior to the surge. In addition, in the presence of elevated progesterone, high concentrations of estradiol Estradiol and Progesterone Influence Cyclic do not induce an LH surge. Paradoxically, although it ex- Changes in the Reproductive Tract erts negative feedback on LH release most of the time, pos- itive feedback by estradiol is required to generate the mid- The female reproductive tract undergoes cyclic alterations cycle surge. The Estrogen exerts its effects directly on the anterior pitu- most notable changes occur in the function and histology itary, with GnRH playing a permissive, albeit mandatory, of the oviduct and uterine endometrium, the composition role. This concept is derived from experiments in monkeys of cervical mucus, and the cytology of the vagina whose medial basal hypothalamus, including the GnRH- (Fig. At the time of ovulation, there is also a small but producing neurons, was destroyed by lesioning, resulting in detectable rise in basal body temperature, caused by prog- a marked decrease in plasma LH levels. All of the above parameters are clinically useful of exogenous GnRH at a fixed frequency restored LH re- for diagnosing menstrual dysfunction and infertility. When estradiol was given at an optimal concentration The oviduct is a muscular tube lined internally with a cil- for an appropriate time, an LH surge was generated, in spite iated, secretory, columnar epithelium with a deeper stromal of maintaining steady and unchanging pulses of GnRH. Fertilization occurs in the oviduct, after which the The mechanism that transforms estradiol from a nega- zygote enters the uterus; therefore, the oviduct is involved tive to a positive regulator of LH release is unknown. One in transport of the gametes and provides a site for fertiliza- factor involves an increase in the number of GnRH recep- tion and early embryonic development. Estrogens maintain tors on the gonadotrophs, increasing pituitary responsive- the ciliated nature of the epithelium, and ovariectomy ness to GnRH. Estrogens also increase the motil- age pool of LH (perhaps within a subpopulation of ity of the oviducts. Exogenous estrogen given around the gonadotrophs) to a readily releasable pool. Estrogen may time of fertilization can cause premature expulsion of the also increase GnRH release, serving as a fine-tuning or fail- fertilized egg, whereas extremely high doses of estrogen safe mechanism. A small but distinct rise in progesterone can cause “tube locking,” the entrapment of the fertilized CHAPTER 38 The Female Reproductive System 679 egg and an ectopic pregnancy. The epithelial layer contains glands edematous, and the spiral arteries become tortuous (see that penetrate the stromal layer. Peak secretory activity, edema formation, and secretory columnar epithelium. The pro- to 8 after ovulation in preparation for implantation of the liferative phase coincides with the midfollicular to late fol- blastocyst. Progesterone antagonizes the effect of estrogen licular phase of the menstrual cycle.
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