Isao Araki

Developmental and injury induced plasticity in the micturition reflex pathway

The storage and periodic elimination of urine are dependent upon neural circuits in the brain and spinal cord that co-ordinate the activity of the urinary bladder, the urethra and the striated urethral sphincter. This study utilized anatomical, electrophysiological and pharmacological techniques to examine: (1) the organization of the parasympathetic excitatory reflex mechanisms that control the urinary bladder of the rat and the cat; and (2) the changes in these reflexes during postnatal development and after spinal cord injury. In normal adult cats and rats, the parasympathetic excitatory input to the bladder is dependent upon a spinobulbospinal reflex pathway that is activated by myelinated (Adelta) bladder afferents and that passes through an integrative center (the pontine micturition center, PMC) in the rostral brain stem. Transneuronal tracing studies using pseudorabies virus as well as physiological methods have revealed that the PMC is located in close proximity to the locus coeruleus. Single unit recordings indicate that neurons in the PMC respond to afferent input from the bladder and are excited prior to or during reflex bladder contractions. Glutamic acid is the major excitatory transmitter in the micturition reflex pathway. Glutamatergic transmission which is mediated by AMPA/kainate and NMDA receptors can be modulated by a variety of other transmitters. In neonatal animals, a spinal micturition reflex is activated by somatic afferent fibers from the perigenital region. This reflex is suppressed during postnatal development, but can be unmasked in adult animals following spinal cord injury. Spinal injury also causes the emergence of a spinal bladder-to-bladder reflex which in the cat is activated by capsaicin-sensitive C-fiber bladder afferents. Patch clamp studies in spinal cord slice preparations indicate that developmental and spinal cord injury induced plasticity in sacral parasympathetic reflex pathways is due in part to alterations in glutamatergic excitatory transmission between interneurons and preganglionic neurons. Changes in the electrical properties of bladder afferent pathways may also contribute to the reorganization of bladder reflexes in paraplegic animals.

Chapter 6 Spinal interneurons and preganglionic neurons in sacral autonomic reflex pathways

Publisher Summary This chapter reviews the autonomic circuitry in the spinal cord that constitutes the final common pathway for the transmission of activity from higher centers in the brain to the pelvic organs. It focuses on the morphological, neurochemical and electrophysiological properties of spinal interneurons and preganglionic neurons that are involved in the parasympathetic control of the pelvic viscera. The major emphasis is on the neurons involved in the regulation of the urinary bladder of the cat and the rat. In the cat, the sacral parasympathetic nucleus (SPN) has a viscerotopic organization; and preganglionic neurons (PGN) innervating different organs can be distinguished by their size, dendritic distribution and axonal conduction velocity. It is not known whether these differences occur in other species. The SPN receives inputs from various sources and in addition has local circuitry consisting of interneuronal-PGN synapses and PGN axon collateral-interneuronal synapses. Local interneurons mediate gamma aminobutyric acid ergic and glycinergic inhibitory as well as glutamatergic excitatory inputs to the PGN. It is possible that the interneurons are also involved as local relays for more distant inputs from primary afferent and supraspinal pathways to the PGN.

Maturation of Bladder Reflex Pathways During Postnatal Development

Neuroanatomical and electrophysiological techniques have provided new insights into the organization of the spinal cord circuitry and the neurotransmitter mechanisms involved in primitive voiding reflexes in neonatal animals. In addition, studies of unitary synaptic transmission in spinal cord slice preparations indicate that developmental and spinal cord injury induced plasticity in sacral parasympathetic reflex pathways is due in part to alterations in glutamatergic excitatory transmission between interneurons and parasympathetic preganglionic neurons. It is proposed that these synaptic changes are due to competition between segmental and supraspinal inputs. Thus synaptic remodeling in the sacral parasympathetic nucleus is likely to be an important factor in the postnatal maturation of voiding reflexes.