Memory

Reference: chapter 57, 59.

 Reticular Formation
Diffused mass of neurons and nerve fibers forming an ill-defined meshwork of reticulum in the central portion of the brainstem.

Various nuclei: 1) Nuclei of medullary reticular formation 2) Nuclei of pontine reticular formation 3) Nuclei of midbrain reticular formation Signals: - Downwards into spinal cord - Upwards up to thalamus and subthalamus

Connections of Reticular Formation

Fig. 1 -Afferent connections of reticular formation

Fig. 2 Efferent connections of reticular formation

Functional divisions of Reticular Formation

Ascending Reticular Activating System - ARAS Receives fibers from the sensory pathways via long ascending spinal tracts. Alertness, maintenance of attention and wakefulness. Emotional reactions, important in learning processes. Tumor or lesion sleeping sickness or coma.

Fig.3 Brain section.

Descending Reticular System

Inhibitory:
- Smoothness and accuracy of voluntary movements - Reflex movements - Regulates muscle tone - Maintenance of posture

Facilitatory:
- Maintains the muscle tone - Facilitates autonomic functions

Sleep centers:
1) LOCUS CERULEUS: Location: At junction of midbrain & pons. Neurons in this locus secrete nor epinephrine at nerve endings of nerve fibers. Nerve fibers from these neurons pass to reticular formation.

Sleep centers:
This center (Locus Ceruleus) is involved in REM sleep, when brain is highly active. So perhaps nor-epinephrine secreting neurons are involved (sympathetic stimulation in REM sleep)

Ach secreting neurons in reticular formation of upper brain-stem are also involved.

PGO spikes
In REM sleep there are PGO spikes (large phasic potentials in groups of 3-5). These spikes are due to Acetylcholine secreting neurons in this pathway of producing REM sleep. Only the tone of neck muscles is dec., other muscles keep their tone. But at the same time there is locus ceruleus dependent inhibition of voluntary act.

Sleep centers:
2) RAPHE MAGNUS NUCLEUS: Midline linear nuclei in lower pons & medulla. Fibers from here pass to reticular formation, hypothalamus, limbic system & also spinal cord. These fibers synapse with pain-inhibitory neurons in dorsal horn of spinal cord (analgesia system).

Sleep centers:
There is release of serotonin at nerve endings of these fibers. Raphe Magnus Nucleus is involved in Deep Slow Wave sleep (NREM sleep). Serotonin inhibitors wakefulness.

Stimulation of SCN of Anterior hypothalamus, certain thalamic nuclei & portion of nucleus of tractus solitarius NREM sleep.

Definition of Memory:
Ability to store information or experiences & recall these consciously or unconsciously. Memory is stored in brain, in the form of facilitated neuronal pathway (memory trace) Memory forms the basis of learning

Habituation:
A type of negative memory. Brain can ignore the information with no consequence. Mechanism involved, is inhibition of synaptic pathways for this type of information. Resulting effect is called habituation.

Memory sensitization:
A type of positive memory. Brain enhances & stores the memory traces that have important consequences like pain or pleasure.

Mechanism is facilitation of synaptic pathways.

Special areas in basal limbic region of brain determine whether the information is important or not & make the subconscious decision whether to store the thought as a sensitized memory trace or to suppress it.

Types of Memory:
Immediate memory / short-term memory. Intermediate memory. Long term memory.

Immediate memory / short-term memory

Memory of some words, numbers or information lasting for seconds to a few minutes. It is forgotten unless it is converted into intermediate or long term memory. Short term memory involves hippocampus

Example of short term / immediate memory:

A person consults a telephone directory for a telephone number & then dials that number & forgets the number. By immediate memory, we can take into mind 7 or 10 digits of number. It involves continuous neuronal activity. Memory persists as long as impulses are conducted along nervous pathways.

Mechanisms of immediate memory:

1) impulses travel along nervous pathways having reverbrating circuits (impulses go on travelling along same pathway again & again). 2) pre-synaptic inhibition or facilitation. 3) post-tetanic facilitation.

pre-synaptic inhibition or facilitation

At presynaptic terminal there are additional synapses, which may be inhibitory or facilitatory.

INTERMEDIATE MEMORY:
Memory of some words or information lasting for hours, days or weeks. It is difficult to be recalled & easy to be forgotten, unless converted into long-term memory.

Example of intermediate memory:

We prepare for a test & keep it in mind for weeks (if prepared well) & then forget, unless we revise & convert it into longterm memory.

Mechanism of intermediate memory:

There are temporary chemical changes at synapses & these include Presynaptic facilitation/ Presynaptic inhibition

Long-term memory:
Memory of words, numbers, information or facts which last for years or throughout life. It is so consolidated that it can be recalled rapidly. Difficult to be forgotten. Long term memory involves neocortex

Examples of long-term memory:

Alphabets, names of near relatives, certain facts about universe / religion.

Mechanism of long-term memory:

To convert immediate or intermediate memory into long-term memory, consolidation is required, which involves repetition or rehearsal. Minimum consolidation may occur in 5-10 minutes & maximum occurs in 1 hr or more, e.g., in Hifz-a Quran, same verse of Quran is repeated.

Mechanism of long-term memory:

It involves changes at synapses which are not temporary, but permanent. There is increase in number & size of synaptic terminals.

Increase in number of synaptic vesicles.

Mechanism of long-term memory:

Increase in number of released sites on synaptic knobs. There may be changes in post-synaptic neurons.

It involves protein synthesis. Drugs which inhibit RNA synthesis inhibit memory.

Mechanism of long-term memory:

During consolidation, synapses in thought circuits are permanently facilitated to form a memory trace, i-e., for certain facts in our memory, there is a memory trace.

Mechanism of long-term memory:

In children, a number of extra-neuronal pathways having synapses are available. If these nervous pathways having synapses are facilitated or used, these persist. If not used, they degenerate. (Use it or lose it!)

That is why Hifz-a-Quran is more easy in childhood.

Parts of brain involved in memory process:

1) Temporal lobe: When different parts of temporal lobe are stimulated, past events are recalled. 2) Hippocampi are involved in memory.

3) Thalamic nuclei are also involved.

Loss of recent memory / anterograde amnesia:

Site of lesion: Hippocampi OR Mamillary bodies OR Dorsal medial nuclei of thalamus

Loss of recent memory / anterograde amnesia:

Clinical picture: Past memory remains intact but recent memory is lost. These patients are not able to learn new events. Not able to remember names & faces of person they meet.

Loss of past memory / retrograde amnesia:

Lesion: Lesion of certain thalamic nuclei.

Clinical picture: Loss of past memory but able to store new events.

Drugs which stimulate memory:

Caffeine Nicotine Physostigmine Amphetamine Strychnine

ALZEIMERS DISEASE:
Premature aging of brain. Loss of mental powers. Disease starts at mid-adult age.

In severe cases, picture resembles mental power of a very old person.

Etiology & Mechanism of ALZEIMERS DISEASE:

Thought to be hereditary. Gene which controls formation of Apolipoprotein E (a blood protein that transports cholesterol to the tissues) is defective. This protein is concerned with transport of cholesterol in blood. Deposition of amyloid material in brain (cerebral cortex, basal ganglia, hippocampus, thalamus, cerebellum). A metabolic degenerative disease.

Etiology & Mechanism of ALZEIMERS DISEASE:

Patients with Trisomy 21 (Down syndrome) have 3 copies of the gene for amyloid precursor protein & develop neurological characteristics of Alzeimers disease by midlife. Cerebrovascular disease caused by hypertension, atherosclerosis, diabetes, hyperlipidemia may play a role. Main clinical feature is loss of memory.

Working memory:
Is a form of mainly short-term memory, that keeps information available usually for very short period, while action plan is based on it. Is used during the period of intellectual reasoning. Terminated as each stage of problem is resolved.

Classification of memories on the basis of the type of information stored:

Declarative memory: Memory of various details of an integrated thought, like memory of an important experience including: Memory of surroundings, time relationships, causes of the experience & ones deductions / conclusions that were left in the persons mind. Skill memory: Associate with motor activity like skills developed for hitting a tennis ball, including automatic memories to: Sight the ball Calculate the relationship & speed of the ball to racquet Deduce rapidly the motion of the body, arms & racquet to hit the ball as desired.

1) 2) 3)

This skill memory is based on previous learning of the gamethen moving on the next stroke of the game while forgetting the details of the previous stroke.

post-tetanic facilitation
Through a synapse, impulses are rapidly conducted, then a short rest is given & then impulses are again conducted through same synapse. Now response of post-synaptic neuron is greater, due to more availability of calcium ions in pre-synaptic terminal release of neurotransmitter EPSP Response by postsynaptic neuron. By repeated stimuli in seconds, there is inc. no of calcium channel opening.